From info at hf-symposium.org Sat Apr 1 00:16:38 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Sat, 1 Apr 2006 00:16:38 -0300 Subject: [HF-FORUM] Opening speech Message-ID: <200604010016.38491.info@hf-symposium.org> Dear Colleagues, The International Society for Holter and Noninvasive Electrocardiography (ISHNE), pioneer in distance cardiology education through the Internet, is proud to present this new conference. We start today the worldwide conference on heart failure, just as we have been doing it over the last four years, with the same strength, joy and expectations as in the prior events. The excellent response from the previous editions and the great number of registrants, which by now is well over 10,000, encourages us to continue working on these presentations in which you, with your comments, questions and concerns, constitute the very essence. This time we have Dr. Arthur J. Moss as the Honorary Chair. He is from Rochester, NY, USA, and is a world renowned investigator of arrhythmias and sudden death. There are 45 lecturers, which will provide an updated approach to incidence, evaluation and treatment of Heart Failure. These publications will be available on our site starting tomorrow and will continue through the first 10 days of April. During this time the Forum will be open for the questions, answers, comments and discussions from all participants. Among the innovations, we want to highlight the following: For the first time, we have included the translation into Chinese and Russian, in addition to our usual policy of translation into Portuguese and Spanish. This presents a great challenge and work for the whole team, but we think this is the best way to reach several distant areas of the planet in their native languages. CME credits (Continuous Medical Education) will be provided by the ACCME of the USA, to anyone who requires such credits and has answered correctly the questions we will publish about each presentation in due time. This is the first time we have received this type of accreditation for an Internet activity, thus it demonstrates a very important commitment. In addition to the presentations, we will have clinical cases, bibliography and treatment guidelines so that you may have all the necessary elements to evaluate this subject. Dr. Moss has written 10 questions about Heart Failure that Dr. Anthony DeMaria has gladly answered. These same questions were posed by our experts to the most distinguished colleagues from China, India, Russia, Argentina and Brazil in order to obtain a more comprehensive picture of this disease. Surely these questions will also be present in the subsequent discussion. In this way, we feel we may offer a different, interactive conference with a very high scientific level, in which participation by each one of you is the special spice to make it more interesting. We would like to take this opportunity to thank everyone who has supported us in this project, and special thanks to Dr. Moss for his dedication and enthusiasm, to the guests for their presentations and comments, to the Board of Trustees of the ISHNE for their ongoing help and St. Jude Medical, who with their support made this event possible. To everyone, thank you very much. We are pleased to begin this conference. Dr. Wojciech Zareba Dr. Sergio Dubner Dr. Edgardo Schapachnik Dr. Andr?s P?rez Riera Dr. Li Zhang -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 1 00:20:30 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Sat, 1 Apr 2006 00:20:30 -0300 Subject: [HF-FORUM] Instructions Message-ID: <200604010020.30953.info@hf-symposium.org> Lectures During the first week of the month of April, we will publish new lectures daily, coming from the different faculties that participate in the Symposium. There will be communications in due time about this lectures, through this Forum. They will be available in the LECTURES area in two formats: For reading straight from the PC screen For this modality, you should access the LECTURES hall, pick the lecture in the language selected, and click on the corresponding hyperlink, indicated by the sign VIEW THE PRESENTATION, with which a window will open from where you may read. For printing and delayed reading in PDF format Those that prefer downloading the PDF file, should press the right button of the mouse, on the respective hyperlink, according to the language selected. By doing so, you may download the PDF file, and save it on the corresponding folder. IN ALL CASES, EACH TIME THE SYSTEM REQUIRES IT, THE RESPECTIVE PASSWORDS SHOULD BE ENTERED, WHICH WERE PROVIDED IN THE PROPER TIME. LPM Radio Likewise, in the LPM Radio sector, you may listen to interviews. To listen to them, you will need to have either the Winamp or the Real Audio software installed (the Real Media Player software, provided with the Windows system, is not suitable). Those of you that do not have the advised programs, may download them for the site itself. You will have to select the language in which you wish to listen to the interview, and click on the corresponding hyperlink. You have to take into account that according to the different types of connections to the Internet you may have, the procedure of downloading the interview may last a variable amount of time. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 1 00:30:05 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Sat, 1 Apr 2006 00:30:05 -0300 Subject: [HF-FORUM] Passwords Message-ID: <200604010030.05451.info@hf-symposium.org> Dear Colleagues: If you don't remember your personal passwords, you can use the following ones: USER ID: heartf PASSWORD: HEARTF Best regards Edgardo and Sergio -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 1 02:27:24 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Sat, 1 Apr 2006 02:27:24 -0300 Subject: [HF-FORUM] Today's Scientific Activity Message-ID: <200604010227.24621.info@hf-symposium.org> Dear colleagues, As of today, in the Conference Room, the following Presentations are available: http://www.hf-symposium.org/lectures.php - ICD and CRT in Heart Failure Prof. Dr. Arthur Moss - The New York Heart Failure registry Dr. Marrick Kukin - Cardiac sympathetic terminal function in congestive heart failure Dr. Chang-Seng Liang In the sector corresponding to the Clinical Cases, you can see the following ones http://www.hf-symposium.org/clinicalcases.php - A Young Patient with Dilated Cardiomyopathy and Out-of-Hospital Sudden Death: >From Randomized Trials and Guidelines to Real Life Patients. Dr. Sami Viskin -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 2 00:05:30 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Sun, 2 Apr 2006 00:05:30 -0300 Subject: [HF-FORUM] Today's Scientific Activity Message-ID: <200604020005.30714.info@hf-symposium.org> Dear colleagues, As of today, in the Conference Room, the following Presentation is available: http://www.hf-symposium.org/lectures.php - Controversies in the pharmacologic therapy of patients with heart failure Dr. Bertram Pitt In the sector corresponding to the LPM Radio, you can see the following webcast http://www.hf-symposium.org/lpmradio.php - The interaction of Anemia, Heart Failure and Renal Failure - The Cardio Renal- Anemia Syndrome Dr. Dov Wexler / Dr. Donald Silverberg / Dr. Dan Tzivoni -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 3 00:08:11 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Mon, 3 Apr 2006 00:08:11 -0300 Subject: [HF-FORUM] Today's Scientific Activity Message-ID: <200604030008.11648.info@hf-symposium.org> Dear colleagues, As of today, in the Conference Room, the following Presentations are available: http://www.hf-symposium.org/lectures.php - Conflicting aspects of the assessment of Heart Rate Variability in Patients with Cardiac Diseases Leonid Makarov - The Prognostic Value of Holter Monitoring in Congestive Heart Failure Iwona Cygankiewicz, Wojciech Zareba and Antoni Bayes de Luna - Origin and Determinants of ANF and BNP Production by the Heart under Normal and Pathophysiological Conditions Adolfo J. de Bold -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 3 22:16:27 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Mon, 3 Apr 2006 22:16:27 -0300 Subject: [HF-FORUM] Passwords Message-ID: <200604032216.27949.info@hf-symposium.org> Dear doctors, If you don't remember your personal passwords, you can use the following ones USER ID: heartf PASSWORD: HEARTF Best regards -- Susana Torok B. S. Administrative Secretary for the ISHNE HF World-Wide Internet Symposium. AKROS Group From info at hf-symposium.org Tue Apr 4 00:06:19 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Tue, 4 Apr 2006 00:06:19 -0300 Subject: [HF-FORUM] Today's Scientific Activity Message-ID: <200604040006.19677.info@hf-symposium.org> Dear colleagues, As of today, in the Conference Room, the following Presentations are available: http://www.hf-symposium.org/lectures.php - Heart rate turbulence in patients with nonishhemic heart failure Makarov, L. / Komoliatova, V. / Gorlitskaya O. / Tutelman K. / Kalachanova E.P. - Creation of a New Bioartificial Myocardium: Dream or Reality? Juan Carlos Chachques, MD, PhD - Device Management of heart failure patients with atrial fibrillation Professor Dr. Andreas Schuchert In the sector corresponding to the Clinical Cases, you can see the following ones http://www.hf-symposium.org/clinicalcases.php - Tachycardia-Induced Cardiomyopathy. Dr. Michael Eldar -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 5 00:29:34 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Wed, 5 Apr 2006 00:29:34 -0300 Subject: [HF-FORUM] Today's Scientific Activity Message-ID: <200604050029.34815.info@hf-symposium.org> Dear colleagues, As of today, in the Conference Room, the following Presentations are available: http://www.hf-symposium.org/lectures.php - Prediction of Response to Cardiac Resynchronization Therapy Johnson Francis, Sunil Roy T.N.and Roy John - Can Implantable Biventricular Pacing Systems Without Defibrillation Capability Be Justified in Heart Failure Patients? David G Benditt and Cengiz Ermis - Potential of Natriuretic Peptides as Therapeutic Agents in Cardiovascular Disease Mercedes L. Kuroski de Bold, William P. Sheffield and Adolfo J. de Bold IIn the sector corresponding to the LPM Radio, you can listen to the following interview http://www.hf-symposium.org/lpmradio.php - Dr. Carlos Bertolasi, Dr. Raul Oliveri, Dr. Hernan Doval (from Argentina) -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 6 19:48:35 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Thu, 6 Apr 2006 19:48:35 -0300 Subject: [HF-FORUM] Today's Scientific Activity Message-ID: <200604061948.35376.info@hf-symposium.org> Dear colleagues, As of today, in the Conference Room, the following Presentations are available: http://www.hf-symposium.org/lectures.php - Electromechanical Therapy. A historical perspective of device therapy in the failing heart Raffaelle Corbisiere - The Management of Heart Failure after Biventricular Pacing Juan M. Aranda, Jr. - Role of the AV Interval in DDD Pacing:Insights into Programming with Respect to Ventricular Function when AV Nodal Conduction is Intact Paul A. Levine IIn the sector corresponding to the LPM Radio, you can listen to the following interview http://www.hf-symposium.org/lpmradio.php - Jacob Jose (from India) -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 7 00:13:01 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Fri, 7 Apr 2006 00:13:01 -0300 Subject: [HF-FORUM] Today's Scientific Activity Message-ID: <200604070013.01783.info@hf-symposium.org> Dear colleagues, As of today, in the Conference Room, the following Presentations are available: http://www.hf-symposium.org/lectures.php - Interview Leonid Makarov / Viacheslav Mareev - Ischemic Cardiomyopathy and Treatment of Heart Failure by ACE Inhibitors and ?-Receptor Blockers Yongxin Lu, MD / Runlin Gao, MD - Implantable Cardioverter Defibrillator Therapy in MADIT II Patients with Signs and Symptoms of Heart Failure Wojciech Zareba IIn the sector corresponding to the LPM Radio, you can listen to the following interview http://www.hf-symposium.org/lpmradio.php - Dialog About Heart Failure, From China II Dr. Dayi Hu -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 8 00:18:09 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Sat, 8 Apr 2006 00:18:09 -0300 Subject: [HF-FORUM] Today's Scientific Activity Message-ID: <200604080018.09668.info@hf-symposium.org> Dear colleagues, As of today, in the Conference Room, the following Presentations are available: http://www.hf-symposium.org/lectures.php - The Genetic Causes of Heart Failure. A focus on sudden death: from the molecular mechanisms to clinical approach. Andr?s Ricardo P?rez Riera / Edgardo Schapachnik / Sergio Dubner - Use of the Method of Heart Rate Variability Analysis for the Assessment of Functional-Clinical State of Patients with Chronic HF, its Prognosis and the Effectiveness of the Standard Treatment. Vasyuk Y.A / Yuschuk E.N / Shupenina E.Y / Serova ?.?. - Cardiac Resynchronisation Therapy in Heart Failure Prof. Ali Oto, IIn the sector corresponding to the LPM Radio, you can listen to the following interviews http://www.hf-symposium.org/lpmradio.php - Dialog About Heart Failure, From U.S.A. Dr. Arthur Moss / Dr. Anthony DeMaria - Dialog About Heart Failure, From China Dr. Yongxin Lu -- Susana Torok B. S. Administrative Secretary for the ISHNE HF World-Wide Internet Symposium. AKROS Group From info at hf-symposium.org Sun Apr 9 00:07:09 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Sun, 9 Apr 2006 00:07:09 -0300 Subject: [HF-FORUM] Today's Scientific Activity Message-ID: <200604090007.09340.info@hf-symposium.org> Dear colleagues, As of today, In the sector corresponding to the Clinical Cases, you can see the following one http://www.hf-symposium.org/clinicalcases.php - Ischemic Cardiomyopathye Robert Styperek - In the sector corresponding to the LPM Radio, you can see the following webcast http://www.hf-symposium.org/lpmradio.php Heart Failure: Atrial Fibrillation Jonathan Steinberg -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 10 00:23:05 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Mon, 10 Apr 2006 00:23:05 -0300 Subject: [HF-FORUM] Today's Scientific Activity Message-ID: <200604100023.05780.info@hf-symposium.org> Dear colleagues, As of today, in the Conference Room, the following Presentations are available: http://www.hf-symposium.org/lectures.php - Heart Failure, From an Electrophysiological Perspective Device Therapy in the Failing Heart Raffaelle Corbisiere - Cardiac Resynchronization Therapy for Heart Failure Robert Styperek - Cardiac Remodeling Peter S. Rahko - When to Consider Heart Transplant Mariell Jessup - The Value of 24 H Heart Rate Variability in Predicting the Mode of Death in Patients With Heart Failure and Systolic Dysfunction in Beta- Blocking Era Arbolishvili G. / Mareev V. In the sector corresponding to the LPM Radio, you can see the following webcast http://www.hf-symposium.org/lpmradio.php - Cardiac Amyloidosis Rodney Falk -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 10 19:22:43 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Mon, 10 Apr 2006 19:22:43 -0300 Subject: [HF-FORUM] To open the deliberations Message-ID: <200604101922.43224.info@hf-symposium.org> Dear colleagues and friends, With this message we open the period of deliberations of the Symposium. This Forum will be the channel to which you may send all kinds of questions, opinions, replies, counter-replies, etc. We hope that this new stage of the event will be enriching for all of us. Cordially, Sergio and Edgardo -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 10 23:08:00 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Mon, 10 Apr 2006 23:08:00 -0300 Subject: [HF-FORUM] Beta blockers. Dr. Arenzo Message-ID: <200604102308.00248.info@hf-symposium.org> Dear colleagues, First of all, I would like to congratulate you for developing a new and important event to contribute to the exchange of ideas, and letting us seize the experience of the group of experts, so as to improve the treatment of our patients. My question is the following: Is there a maximal dose of carvedilol, or it may be adjusted according to the patient's tolerance seeking a complete beta blocking effect? What is the opinion of the experts about the use of beta blockers in COPD and bronchial asthma associated to HF; and do we have functional tests or other evaluations that would enable us to predict which cases may have an adverse response to this medication? Thank you, "Julio Arenzo" -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 11 13:46:50 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Tue, 11 Apr 2006 13:46:50 -0300 Subject: [HF-FORUM] 1P. Cardiac amyloidosis. Dr. Perez Riera Message-ID: <200604111346.50631.info@hf-symposium.org> Dear Dr. Rodney Falk, I'm Andres Ricardo Perez Riera from Sao Paulo, Brazil. First, I would like to congratulate you for the magnificent presentation in PowerPoint on the subject of cardiac amyloidosis. It is one of the most brilliant presentations I have read. My question is: low voltage of QRS complexes is present in approximately 50% of cases of cardiac amyloidosis, explained by the fact that infiltrated amyloid material substitutes the myocardium that produces voltage. Low voltage of amyloidosis usually happens only in the frontal plane. Do you have an explanation for the reasons of this FP predilection reported in literature? (Dubrey AW et al Am J Cardiol 1996:77:313) Dr. Andres R. Perez Riera -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 11 14:06:02 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Tue, 11 Apr 2006 14:06:02 -0300 Subject: [HF-FORUM] 2S. Functional class IV. Dr. Rodriguez Artuza Message-ID: <200604111406.02125.info@hf-symposium.org> Congratulations, extraordinary lectures, but now let's go into the real world and let me ask my first questions to the forum. What to do with the great number of patients in functional class IV who do not respond to optimal therapy, and do not respond to resynchronization? Could it be that the therapy in this new setting of resynchronization, ACEI, B-blockers and Spironolactone may be associated to dobutamine or levosimendan? What to do with those patients in terminal stage with no access to heart transplantation? In Venezuela we still have many patients in this real world. Dr Carlos Roidriguez Artuza Maracaibo Venezuela -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 11 17:04:10 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 11 Apr 2006 17:04:10 -0300 Subject: [HF-FORUM] 3S. Cellular Cardiomyoplasty. Dr. Pereira Message-ID: <2CEDFA08-ABFB-4681-8E93-AB7319DCC7F8@hf-symposium.org> The topic of cellular cardiomyoplasty, which for some time now I have seen and heard developed by Dr. J.C. Chachques, is truly fascinating. I would like to ask him, based on his presentation, which were the bases for his work team to choose bone marrow autologous cell transplantation? I mean, what are the advantages of it in comparison to the other current possibilities of myocardial regeneration therapy? Kind regards, Dr. Luciano Pereira - Paraguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 11 17:53:54 2006 From: info at hf-symposium.org (Heart Failure Symposium) Date: Tue, 11 Apr 2006 17:53:54 -0300 Subject: [HF-FORUM] 4E. ACEI therapy in CHF. Dr. Sosnowski Message-ID: <200604111753.54954.info@hf-symposium.org> Dear colleaques, Many thanks for opportunities opened aiming unrestricted exchange of scientific and clinical experience and excellence. I would like to know experts opinion about objective methods, other than blood pressure response, allowing for evaluation the effectiveness of ACE inhibition and its (their) clinically usefulness in patients with HF. Kind regards Maciej Sosnowski maciej.sosnowski at gmail.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 11 19:25:00 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 11 Apr 2006 19:25:00 -0300 Subject: [HF-FORUM] 5P. RE: Beta blockers. Dr. Perez Riera Message-ID: <5CC05C37-B24A-4372-A1DC-5C437B5DC706@hf-symposium.org> Dear colleague, Dr. Julio Arenzo, The posological scheme we use here in Brazil, is called "in crescendo." Here an expert, Dr. Bocchi from the InCor of Sao Paulo, for patients with refractory heart failure and candidates to transplantation (Bocchi EA. et al. Arq. Bras. Cardiol. 1998; 71:169-173) has proposed the following posological scheme: Start with 6.25 mg/day for 7 to 10 days (3.125 mg 2 x day). In the case of intolerance translated by bradycardia lower than 55 bpm, AV blocks greater than 1st degree, or important worsening of heart failure, the medication should be suspended. If well tolerated, it is increased to 6.25 mg twice a day for more than 10 days until a limit of 50 mg/day for patients up to 75 Kg and 75 mg/day for patients above this weight or who display heart rate above 80 bpm. If at each increase of the dose intolerance appears, there should be a return to the prior dose. In the mentioned paper the median dose used was 42 mg/day. Dose of 25 mg 2 x day is indicated in average for hypertensive patients. In Latin-America we notice that our pattern doses are always more timid than in USA. About the second question, whether it may be used in COPD, I think not. This is a third-generation adrenergic blocker that blocks the three adrenergic receptors: beta1, beta2 and cardioselective: it blocks beta1 and beta2 receptors, with the strength of the beta2 block being tenfold superior to propranolol. Additionally, it does not possess beta2-agonism (ISA activity) as bucindolol and labetalol. COPD is one of the contraindications of the drug together with others: The contraindications for the drug are: 1) Bronchial asthma with or without COPD 2) Significant bradycardia: less than 50 bpm 3) Significant hypotension with systolic pressure below 85 mmHg 4) COPD 5) 2nd or 3rd AV blocks 6) Pregnancy, because it affects the fetus 7) Breast-feeding (it has to be suspended) 8) Sinus node disease 9) Prinzmetal's variant angina: about this, the coronary vessels present in their walls, three types of adrenergic receptors: alpha1, alpha2 and beta2. Alpha1: its stimulus causes vasoconstriction. Carvedilol may block this effect. Alpha2: its stimulus causes vasoconstriction. Carvedilol does not have an effect on this receptor. Beta2: its stimulus causes vasodilatation. Carvedilol may prevent this vasodilatation by block. In brief, the drug by not acting on alpha2 and by blocking beta2, may facilitate vasospasm, even though it blocks alpha1 mediators of vasoconstriction. Side effects 1) Respiratory system: bronchospasm and dyspnea in predisposed patients. Nasal congestion. 2) Neurological: dizziness, headache, fatigue, depression, paresthesia and sleep disorders. 3) Gastrointestinal: nausea, abdominal pain, diarrhea and rarely vomiting and constipation. 4) Cardiovascular: possible worsening of heart failure, intense bradycardia, AV block, hypotension, Reynaud's phenomenon, intermittent claudication, cold limbs, shock. 5) Metabolic: hyperglycemia in diabetic patients, manifestation of latent diabetes, ponderal increase and cholesterol increase. 6) Skin: exantema, hives, pruritus, etc. 7) Effects on the mother/fetus pair: it is contraindicated in pregnant women because of potential to affect the fetus. Women who are breast- feeding should suspend this. It may cause: 1- By decrease in the umbilical artery flow with less weight and height at birth. 2- Fetal bradycardia: by block of cholinergic impulses in sinus node mediated by beta1 and beta2 receptors. 3- Fetal hypoglycemia: by hepatic alpha1 and beta2 block, decreasing glycogenolysis and gluconeogenesis. 4- Fetal hyperbilirubinemia: by beta2 block, thus preventing relaxation of biliary pathways and enabling contraction predominance measured by cholinergic impulse. 5- Mild delay at onset of respiratory movements. 8) Urogenital: impotence and urination difficulties. 9) Ophthalmological: sight disorders, eye irritation, decrease of tears. Pharmacological interaction: similar to propranolol. Best regards, Andr?s Ricardo P?rez Riera Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation - Santo Andr? - S?o Paulo - Brazil -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 12 13:38:08 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 12 Apr 2006 13:38:08 -0300 Subject: [HF-FORUM] 6S. Diastolic failure. Dr. Ansin Message-ID: <9FBCBAD8-A411-408F-BB68-20344247B21D@hf-symposium.org> Congratulations again to the organizers of this interesting event, and especially to the cardiology representatives from the MERCOSUR (suggestion included). I would like to make some reflections so that the experts may comment about them. Recently, at the ACC meeting in Atlanta, the subject of diastolic CHF (DCHF) management did not show substantial advancements in their definition or management. 1- In most papers, DCHF is defined by excluding systolic CHF (SCHF), presenting as a condition a NORMAL EF. Starting from EF being an insufficient indicator both for contractility and cardiac and peripheral vascular syndrome of CHF, although it is a good independent prognosis indicator, DCHF should be defined according to stages 1-2 or 3 of the abnormal echocardiographic pattern of ventricular relaxation, since these depend on end diastolic pressure (EDP). 2- Near 50% of the patients with CHF have normal EF. Diastolic function is closely related with systolic failure and is part of a compensating mechanism of the myocardial impelling aspiration pump function. The basic aspect of CHF is end diastolic pressure, with which the myocardium works in the three-dimensional curve of strength, length and time (HR). The stages of pseudonormalization (2) and mild (3) or severe (4) restriction, may be perfectly determined by echo Doppler, and each one of them depends on the volume-pressure curve. In all of them EDP may be determined, so the way I see it, we should consider a CHF classification with normal or low EF related with high or low EDP and with the extent of remodeling (cardiomegaly) and asynchrony; and pure DCHF should be left for restrictive or hypertrophic cardiomyopathies with restrictive pattern. 3- In view of the previous considerations, we shouldn't be surprised if traditional CHF management, whether systolic or diastolic, should be the same because they are failed compensating mechanisms for the same progressive pathophysiology. On the contrary, the management of pure restrictive cardiomyopathies may be very different and their prognosis and efficacy may be different, too. I think that this would explain the success in using nitrates and hydralazine in black patients, where the prevalence of hypertensive heart disease is very high. Is there some randomized resynchronization study in patients with SCHF vs. DCHF? Dr Juan Carlos Ansin Panam? -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 12 13:38:43 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 12 Apr 2006 13:38:43 -0300 Subject: [HF-FORUM] 7S. Restrictive cardiomyopathy in pediatrics. Dr. Petrozzi Message-ID: Congratulations and thank you for the information. I would like to know what alternatives are there in the medical treatment of restrictive cardiomyopathy in a 2-year-old girl, with FC IV CHF, with ejection fraction in 65%, severe tricuspid regurgitation, severe atrial dilatation and very dilated vena cava. Thank you very much for your reply, Veronica Petrozzi Pediatrician -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 12 15:33:05 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 12 Apr 2006 15:33:05 -0300 Subject: [HF-FORUM] 8S. Beta blockers. Dr. Wolman Message-ID: <82D1F70C-BA70-4E5F-AAF3-E98166CA3E09@hf-symposium.org> Hi friends of the cybernetic science, Congratulations on the remarkable effort made. I would like to ask the following: is it the same using bisoprolol or carvedilol? Is the antioxidative and vasodilatation action of carvedilol important? Thanking you in advance, Luis Wolman -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 12 16:52:00 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 12 Apr 2006 16:52:00 -0300 Subject: [HF-FORUM] 9S. Aminophiline EV. Dr. Melgar Message-ID: <0D7215AA-84CF-4836-AA08-D5EF30BEBCF9@hf-symposium.org> I would like to know the criterion of the colleagues who are experts in arrhythmias, and if they have experience with the use of aminophiline in pills or endovenous, and in which cases would you use it or not. Thank you. Rosendo Rivero Melgar Bolivia. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 12 18:11:31 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 12 Apr 2006 18:11:31 -0300 Subject: [HF-FORUM] 10S. Spongiform myocardium. Dr. Valiente Message-ID: <4891406B-585E-4221-B837-CC02BF4278CF@hf-symposium.org> Dear colleagues of the FORUM, My greetings and congratulations for such an interesting Symposium. I am interested in letting you know about a 36-year-old male patient, carrier of spongiform myocardium, who presents dyspnea at minimal strain and precordial pain with pressure figures of 140/100. Coronariography was conducted on him, and coronary arteries were found to be normal. What would be the management to follow in this patient? Regards and thank you, Dr Juan Carlos Valiente. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 12 18:14:46 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 12 Apr 2006 18:14:46 -0300 Subject: [HF-FORUM] 10E. RE: Functional class IV. Dr. Perez Riera Message-ID: <6B91CA40-CE57-49DB-AA16-654A1F86A298@hf-symposium.org> Dear Dr Carlos Rodriguez Artuza from Maracaibo Venezuela here Andr?s Ricardo P?rez Riera from S?o Paulo Brasil. Levosimendan is a novel inotropic agent indicated for patients with decompensated heart failure(HF). It is a calcium sensitizer indicated for short term treatment of acutely decompensated severe cronic HF (1). The action mechanisms is Ca2+ sensitization for positive inotrope effect by three mechanisms: increasing affinity of cardiac Troponin C for Ca2+; direct stabilization of the calcium-induced conformation of cardiac Troponin and action on other target proteins in the molecular cascade of myocardial contraction. Finally and activation of ATP-dependent K+ channels for vasodilation and cardioprotective effect resultant increase in tension development, myocardial contractility. Does not affect total intracellular Ca2+ concentration. Therefore, enhanced myocardial performance achieved without increasing myocardial O2 consumption and without provoking arrhythmias. Activation of K+ channels in vascular smooth muscle producing venous, arterial and coronary vasodilation. Levosimedan increase in cardiac index, decrease in pulmonary capillary wedge pressure, reduce preload and afterload, improve coronary blood flow, no adverse effect on diastolic function, decreased potential for arrhythmia, improved cardiac function in stunned myocardium(2). It is indicated in decompensated low-output HF (cardiac index <2.5/l/min/m2 or PCWP >16mmHg or LVEF <0.4) (3). Levosimendan produces positive hemodynamic effects without increasing myocardial oxygen demand or causing arrhythmias. Bolus injection followed by infusion 0.05-0.2 ug/kg/min for 24 hours. Outcome benefits included regression of dyspnea, improved hemodynamic index, increased urine output, shortened hospital and ICU stay, and lower 180-day mortality. Effects last for 3-4 days due to long acting metabolite (half-life 80 hours). Repetitive administration at intervals of 4-8 weeks maintained clinical improvement in 6 out of 9 patients in a small study LV failure in acute coronary artery disease: Levosimendan exerts a coronary and systemic vasodilatory effect through its K(ATP) channel-opening properties and may exert other cardioprotective actions through this mechanism. Cardiogenic shock: No formal controlled studies. In several clinical observations, improved hemodynamics if combined with noradrenaline to maintain adequate perfusion pressure . Infusion 0.05-0.2ug/kg/min for 24 hours without bolus L-NAME, a nitric oxide synthase antagonist, represents a promising new approach for the treatment of cardiogenic shock(4). Perioperative treatment in patients undergoing cardiac surgery: Traditionally, perioperatively used inotropic agents, epinephrine, dobutamine, and milrinone, are limited by significant increases in myocardial oxygen consumption, proarrhythmia, or neurohormonal activation. Levosimendan, a new inodilator for the treatment of decompensated HF, has also shown promise in elective therapy of cardiac surgical patients with high perioperative risk or compromised LV function, as well as in rescue therapy of patients with difficult weaning from cardiopulmonary bypass(5). No formal controlled studies. In several clinical observations, improved hemodynamics, improved/prevented postoperative ischemic cardiac depression.Given as bolus 12ug/kg or as infusion 0.2ug/kg/min for 6 hours Post-partum cardiomyopathy: Levosimendan proved a useful agent when used as initial therapy in this case of post-partum cardiomyopathy(6). Dose: Avoid an infusion rate >0.2ug/kg/min Avoid prolong infusion >24 hours for dose dependent adverse effects Treatment of decompensated cardiac failure (level of evidence:B) Adverse effects: Most common adverse reaction is headache and hypotension (5%) . Well tolerated in sick patient population.No increase risk of hypotension and ischaemia in patients with HF due to AMI; No increase risk for arrhythmias No attenuated effects with beta-blockers(7). Levosimendan, improves long-term survival in patients with acute HF and has been incorporated into the European Society of Cardiology guidelines. Improved heart function without increased O2 consumption, anti-ischemic effects, no arrhythmogenic effect and positive effects on intestinal perfusion. Nesiritide, a recombinant brain natriuretic peptide, is an alternative to nitroglycerin and dobutamine and possibly have a benefit for survival. In reference to your second question: What to do with those patients in terminal stage with no access to heart transplantation? In Venezuela we still have many patients in this real world. Please you must read the interview with Dr Jo?o Breda in this Virtual Symposium. They are: 1) Nontransplant Surgical Alternatives for the palliation of HF: Coronary bypass, ventricular reconstruction or left ventricular reduction surgery (PLVR) and valve repair (mitral valve reconstruction or mitral valve annuloplasty,), to be offered to many patients with advanced HF with good short- and long-term results. In 2005, few patients are inoperable (8). By combining operative techniques with optimal medical management of HF, good outcome can avoid or postpone transplantation. This strategy will help to preserve the limited number of donor organs for those patients with no other surgical or medical alternatives. 2) Left ventricular assist devices: Ex The AbioCor artificial heart (Only for rich countries. Very expensive for us). (9). 3) Dynamic cardiomyoplasty (CMP),: In this technique skeletal muscle is wrapped around the heart and stimulated synchronously with the heart itself. 4) The Batista procedure( non more used to day....I think) 5) Cell transplantation approaches have recently emerged as new alternatives to stimulate myocardial regeneration(bone-marrow-derived and cardiac-derived stem/progenitor cells). In parallel to "mechanical" options, "biological" strategies have been designed, which are primarily based on cell therapy. References 1) Ferenc Follath et al. European Experience on the Practical Use of Levosimendan in Patients with Acute Heart Failure Syndromes. The American Journal of Cardiology 2005; 96 (6A) 2) Garcia Gonzalez MJ, Dominguez Rodriguez A. Pharmacologic Treatment of Heart Failure due to Ventricular Dysfunction by Myocardial Stunning : Potential Role of Levosimendan. Am J Cardiovasc Drugs. 2006;6:69-75. 3) Delle Karth et al. Hemodynamic effects of a continuous infusion of levosimendan in critically ill patients with cardiogenic shock requiring catecholamines. Acta Anaesthesiol Scand 2003; 47: 1251-12560. 4) Rauch H, Motsch J, Bottiger BW. Newer approaches to the pharmacological management of heart failure. Curr Opin Anaesthesiol. 2006;19:75-81. 5) Raja SG, Rayen BS. Levosimendan in cardiac surgery: current best available evidence. Ann Thorac Surg. 2006; 81:1536-46. 6) Nguyen HD, McKeown B. post-partum cardiomyopathy. Levosimendan for post-partum cardiomyopathy. Crit Care Resusc. 2005;7:107-110. 7) Mart?n J. Garc?a-Gonz?lez et al.,Utility of Levosimendan, a New Calcium Sensitizing Agent, in the Treatment of Cardiogenic Shock Due to Myocardial Stunning in Patients With ST-Elevation Myocardial Infarction: A Series of Cases. Journal of Clinical Pharmacology, 2005;45:704-708. 8) .McGee EC, Grady KL, McCarthy PM. Nontransplant Surgical Alternatives for Heart Failure. Curr Treat Options Cardiovasc Med. 2005;7:491-501. 9) Morreim EH. End-stage heart disease, high-risk research, and competence to consent: the case of the AbioCor artificial heart. Perspect Biol Med. 2006 Winter; 49:19-34. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. riera at uol.com.br -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 12 20:22:08 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 12 Apr 2006 20:22:08 -0300 Subject: [HF-FORUM] 11S. Digitalis. Dr. Villaverde Message-ID: <9D51ED92-4FCB-4780-A3FA-49C0A1A14B2C@hf-symposium.org> Dear colleagues, I seize this opportunity to congratulate you about the course and its organizers. Very interesting topics are mentioned; I wish we could have more similar activities about different cardiology topics. My question is the following: what do you think about the use of digitalis, specifically Digoxin, in patients with Heart Failure in sinus rhythm? Is it useful? If so, is there some advised scheme to start a therapy? Regards, Dr Homarh Villaverde Lima - Per? -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 12 20:38:49 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 12 Apr 2006 20:38:49 -0300 Subject: [HF-FORUM] 12S RE: Beta blockers. Dr. Arenzo Message-ID: <9D5E1FD2-ACD1-4D84-B42A-A2A16D51B737@hf-symposium.org> Dear Dr. Andres Ricardo Perez Riera, I would like to thank you for your reply to my question, but my question goes beyond what was classically written and known. For instance, in a patient with HF who receives Carvedilol 25 mg, twice a day, and persists with HR of 78 bpm, with normal BP and no signs of pump failure, should the B-blocker dose be increased? About the known contraindication in patients with asthma and COPD, one sees in the practice that many patients with these basic pathologies receive a treatment with atenolol or carvedilol, and in a high percentage they do not present a worsening of their respiratory symptoms. Shouldn't we ask ourselves again, if we should maintain as absolute this contraindication, or should we seek what subset of patients would be in conditions to benefit from the B-blocking therapy? From your point of view, do we have non-invasive functional respiratory tests that may answer this question? Thank you to all those who participate in this conference. Julio Arenzo -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 08:45:41 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 08:45:41 -0300 Subject: [HF-FORUM] 13S. RE: Beta blockers. Dr. Moreno Message-ID: <5EBCA163-1BB5-4139-91C4-8DFD36081470@hf-symposium.org> Dear Dr. Julio Arenzo, The maximal dose of carvedilol is identified depending on the patient's weight. Thus, it is advisable to use up to 50 mg/day (25 mg each 12 hours) in patients with a weight lower than 80 kg and in those who weight 80 or more, up to 100 mg/day may be used (50 mg each 12 hours); of course, according to how the increase of the dose is tolerated, or whether the desired therapeutic effect is obtained. I cannot be accurate about the foundation for this "maximal dose," but I can assure you that I don't know of any report in literature where more than such a dose is needed to achieve the desired beta blocking effect. Kind regards to you and to all those who participate in this forum. And a special greeting for everyone that made it possible for us to exchange our experiences in such pleasing way. Dr. Francisco L. Moreno -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 08:55:19 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 08:55:19 -0300 Subject: [HF-FORUM] 14S. Echocardiographic variables. Dr. Zapata Message-ID: <0308AF52-95BD-4B3C-A11D-4D410FB508DD@hf-symposium.org> Thank you very much to everyone who made this great event possible. I would like to ask the distinguished specialists, what role do echocardiographic indexes of ventricular performance, different from ejection fraction, for instance derived from pulsed Doppler (dP/dT, Tei), of pulsed tissue Doppler of the ring, strain, and so on, have. Do you use some of these to establish a prognosis or to make therapeutic choices? Regards from Chile Mario Zapata, mzapatam at manquehue.net -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 09:10:25 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 09:10:25 -0300 Subject: [HF-FORUM] 15S RE: Cellular cardiomioplasty. Dr. Soto Message-ID: <60316EEC-404A-400A-BE11-790CA71FD750@hf-symposium.org> I think both the presentations and the questions asked are extremely interesting. About cellular cardiomyoplasty, so brilliantly developed by Dr. Chachques, and supplementing the question by Dr. Luciano Pereira, if we take into account that it appears to have substantially advanced regarding the type of cell, we still have doubts about which is best pathway for implantation and what the appropriate number of cells is. On the other hand, maybe this could be a procedure to be used in patients in waiting lists for heart transplantation? Kind regards, Dr. Enrique Soto Uruguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 09:18:24 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 09:18:24 -0300 Subject: [HF-FORUM] 16E RE: Cardiac amyloidosis. Dr. Falk Message-ID: <2EA64E6D-BC8A-472E-88C4-F4233998234E@hf-symposium.org> Dr. Perez Riera correctly indicates that the low voltage in patients with cardiac amyloidosis is almost exclusively seen in the limb leads but not in precordial leads, and asks whether there is an explanation. I'm afraid that, while I have seen this very many times, I do not have a precise explanation as to why this should be. There are , however, a couple of points worth making that may give a clue. The explanation that the low voltage is "explained by the fact that infiltrated amyloid material substitutes the myocardium that produces voltage" is probably only partially true. Interestingly, low voltage is much less common in senile and familial amyloid cardiomyopathy than it is in AL (light-chain associated) amyloid, despite similar echocardiographic wall thickness, suggesting that the infiltration of the myocardium alone may not be the whole answer. Furthermore, after successful treatment of the plasma cell dyscrasia, voltage gradually returns towards normal in AL amyloid even if the wall thickness does not decrease. These observations may reflect a myocyte dysfunction produced by cardiotoxic light chains that is manifest on the ecg as low voltage. Why only in the frontal plane remains unclear, and I welcome suggestions!! Sincerely, Rodney Falk -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 09:57:29 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 09:57:29 -0300 Subject: [HF-FORUM] 17E RE: Cellular cardiomyoplasty. Dr. Chachques Message-ID: There is a tendency to use bone marrow cells for myocardial regeneration since this approach avoids the complex and expensive 3- week cell-culture procedure and the risk of ventricular arrhythmias and sudden death observed after skeletal myoblasts implantation. Another drawback of using skeletal myoblasts is the lack of gap junctions and electromechanical connections between the implanted cells and the host myocardium. Thus, it is uncertain whether an improvement in ventricular performance could be mediated by increased systolic function caused by synchronous contraction of the graft since skeletal myoblasts are known to not contract spontaneously. Furthermore, the "in vitro" cell cultures and multiple passage procedures can attenuate the viability of cell; after implantation these denervated skeletal myoblasts could progressively become atrophic. Bone marrow stem cells are principally used for the induction of angiogenesis in ischemic diseases. Most of these cells are endothelial progenitors and can be obtained from bone marrow. Technically, after aspiration of the ilium bone (200-300 ml), mononuclear bone marrow cells are selected by Ficoll density separation. This simple and cheap cell selection procedure can be performed by hematologists the same day of the cardiologic treatment. New developments include the use of umbilical cord cells and mesenchymal bone marrow cells (called also stromal cells), these cells can differentiate in cardiac cells. Cellular cardiomyoplasty seems to reduce the size and fibrosis of infarct scars, contribute to the recovery of myocardial viability, limit postischemic remodeling, and restore regional myocardial elasticity. Cardiac tissue engineering (using collagen matrix seeded with stem cells) emerges as a new therapeutic tool and extends even more the amazing possibilities of cell therapies in cardiology, becoming a promising way for the creation of a "bioartificial myocardium". I would like to recommend the lecture of this subject in the new periodic publication "Insuficiencia Cardiaca" (Vol. 1, N? 1), edited by Sergio Perrone et al. Best regards, Juan Carlos Chachques, MD, PhD. Paris, France. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 11:01:53 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 11:01:53 -0300 Subject: [HF-FORUM] 18E Statins. Dr. Ilknur Can Message-ID: <725F582A-2D46-49D8-A4FF-1DDE1DC57471@hf-symposium.org> I would like to ask if you advocate use of statins in non-ischemic dilated cardiomyopathy ? Thank you Ilknur CAN, MD Turkey -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 11:08:13 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 11:08:13 -0300 Subject: [HF-FORUM] 19S Rehabilitation. Dr. Samaniego Message-ID: The organization and realization of this Symposium by the Internet has been a great success. My question is for Dr. Bertolasi. We know that all the advancements about diagnostic methods and therapeutic options currently, provide us, cardiologists, with the great chance of improving quality of life and life expectancy for our patients. But we also know that once the acute stage of the cardiological event has passed, the patient always has a feeling of abandonment before the great challenge represented by working again and/or reentering society, and namely concerning physical activity; this is why cardiovascular rehabilitation is so important. I ask my question regarding the possibility of learning about the likely causes as to why in our Latin-American countries we have not advanced in raising awareness about the significance of this important tool? There are many centers devoted to cardiovascular rehabilitation, but in general they are private centers.What happened with the great number of patients in the population that do not have access to this important resource? And what should we do to make this resource reach Public Care? Thank you, Dr. Wagner Samaniego Hospital de URGENCIA de Santiago. Hospital del Trabajador. Santiago de Chile -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 13:15:50 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 13:15:50 -0300 Subject: [HF-FORUM] 20S Dry weight. Dr. Viano Message-ID: What is the precise definition of "dry weight" of a patient with CHF and of course, medicated with diuretics therapy. Francisco E. Viano -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 15:34:06 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 15:34:06 -0300 Subject: [HF-FORUM] 21E RE: Spongiform myocardium. Dr. Towbin Message-ID: <4B596184-42E5-4362-A1A0-8E835994B949@hf-symposium.org> Presuming that his LV is dilated and has systolic dysfunction (ie, dilated cardiomyopathy-like phenotype),he should be on ACE Inhibitor and Beta- Blocker therapy. If systolic function is poor, use of aspirin (or even warfarin) for potential thrombi is also reasonable to consider. Many cases of LV Noncompaction (formerly called spongiform myocardium) will reverse remodel. In some cases these patients present with HF due to diastolic dysfunction in the face of LV hypertrophy (hypertrophic-like phenotype) in which case Beta-Blockers are a reasonable starting point. In approximately 1/3 of children with this disease, they change from 1 form to the other (ie, DCM TO HCM, which we have termed an "undulating phenotype". I hope this is helpful. Jeff Towbin, MD Baylor College of Medicine Texas Children's Hospital Houston, Texas, USA -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 15:57:52 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 15:57:52 -0300 Subject: [HF-FORUM] 22E RE: Spongiform myocardium. Dr. Perez Riera Message-ID: <65573031-AFCD-437A-AED5-7637607E1117@hf-symposium.org> Dear Dr Dr Juan Carlos Valiente. Noncompaction of the myocardium Non-compaction of LV myocardium or Isolated non-compaction of the ventricular myocardium (INVM), LV hypertrabeculation or spongy myocardium, belongs to the "unclassified" cardiomyopathies according to the World Health Organization.Locus Xq28;OMIM NO: 302060,Gene symbol: TAZ Clinical presentation consists of congestive heart failure with depressed LV systolic function, ventricular arrhythmias, arterial thromboemboli from thrombus formation within the inter - trabecular recesses, as well as restrictive physiology from endocardial fibrosis. Three inherited forms have been described. The majority of cases occur sporadically. The X-linked form shows mitochondrial abnormalities similar to Barth syndrome. It is likely that this form is caused by mutations in the G4.5 gene found in Barth syndrome and LV noncompaction. The incidence of the sporadic form has diminished markedly in the U.S. with the giving of vaccine (mumps-measles- rubella) to many in the population. The Barth syndrome has skeletal muscle involvement and white cell abnormalities as well as cardiac abnormalities. But all three have mutations in the G4.5, as does dilated hypertrophic cardiomyopathy. Clinical symptoms include signs of leLV systolic dysfunction even to the point of HF, ventricular arrhythmias, and embolic events(1). Cardiac arrhythmias including VT are common in these cases, and hence ICDs are advised. The causes and electrophysiological mechanisms of arrhythmias in noncompaction are still unknown: grossly irregular branching and connecting of myocardial fascicles in the noncompacted segments, isometric contraction with increased wall stress, and localized coronary perfusion impairment can all induce disorganized or delayed activation and increase the potential for arrhythmias. Buonanno et al reported the first case of noncompaction in which an ICD was used to control life-threatening arrhythmias(2). Several factors could be responsible for the malignant arrhythmias in this entity(3). The prognosis for these patients is poor because of accelerated event rates of fatal arrhythmias, thromboemboli, and profound left ventricular decompensation. Only 7 patients with isolated noncompaction of the left ventricle have been reported to have undergone heart transplantation(4)( untill end 2004). At times, as the problem progresses and cardiac failure occurs,there has been the need to do heart transplants when medication fails. The incidence of cardiovascular complications is high.Anticoagulation is necessary. Dr. Andres R. Perez Riera References 1) Narin N, Celiker A, Uzum K, Poyrazoglu MH, Karakukcu M. Isolated noncompaction of the ventricular myocardium. Turk J Pediatr 2002;44:83-5. 2) Buonanno C, Variola A, Dander B, Gabaldo S, Marafioti V. Isolated noncompaction of the myocardium: an exceedingly rare cardiomyopathy. A case report. Ital Heart J 2000 ;1:301-5. 3) Seres L, Lopez J, Larrousse E, Moya A, Pereferrer D, Valle V. Isolated noncompaction left ventricular myocardium and polymorphic ventricular tachycardia. Clin Cardiol 2003;26:46-48. 4) Stamou SC, Lefrak EA, Athari FC, et al Heart transplantation in a patient with isolated noncompaction of the left ventricular myocardium. Ann Thorac Surg. 2004;77:1806-8. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 16:26:31 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 16:26:31 -0300 Subject: [HF-FORUM] 23E RE: Beta blockers. Dr. Perez Riera Message-ID: Dear Dr. Arienzo: Patients with CHF and COPD tolerated carvedilol well with no significant reversible airflow limitation, but patients with CHF and asthma tolerated carvedilol poorly. The effect of carvedilol on left ventricular dimensions and function in patients with concomitant airway diseases was similar to that seen in general group of patients. Asthma remains a contraindication to beta-blockade(1). Beta-blocker dose, HR, and blood pressure, achieved during beta- blocker therapy have independent prognostic value in HF. None of these factors influenced the beneficial effects of carvedilol when compared with metoprolol tartrate at the pre-defined target doses used in COMET(2). The Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiaca en Argentina GESICA) studied whether a standardized protocol for the initiation and titration of the beta-blocker carvedilol in a multicenter, open-label program would optimize beta-blocker use in HF patients. The program included: (1) The carvedilol initiation and titration period, and (2) Long-term follow-up at 6 and 12 months. Of 1299 patients in the registry, 504 were excluded due to current therapy; of the remaining 795 eligible patients, 293 were excluded due to contraindications. Of the included patients with follow-up data (n = 316), 93.3% tolerated carvedilol initiation and 47.7% of the patients reached the target dose of 50 mg/day for a mean dose of 39 = 83), of which 53% achieved a target dose for a mean dose of 43.08 mg/day. This protocol improved therapy rates and achieved target doses quickly (average of 4 visits). Concomitant medications did not have to be adjusted and there were low withdrawal rates (10%) and hospital admissions (7.2%) for HF. Patients were able to maintain carvedilol therapy at 6 and 12 months. These results indicate that a standardized titration protocol, as used in GESICA, for the initiation and titration of beta-blockers is well tolerated and may improve beta-blocker use in carefully selected heart failure patients(3). Reference 1) Kotlyar E, Keogh AM, Macdonald PS, et al Tolerability of carvedilol in patients with heart failure and concomitant chronic obstructive pulmonary disease or asthma. : Ann Thorac Surg. 2004;77:1806-8 2) Metra M, Torp-Pedersen C, Swedberg K et al. Influence of heart rate, blood pressure, and beta-blocker dose on outcome and the differences in outcome between carvedilol and metoprolol tartrate in patients with chronic heart failure: results from the COMET trial. Eur Heart J. 2005;26:2259-68. 3) Stamou SC, Lefrak EA, Athari FC, Burton NA, Massimiano PS. Impact of a standardized titration protocol with carvedilol in heart failure: safety, tolerability, and efficacy-a report from the GESICA registry. Cardiovasc Drugs Ther. 2005;19:99-101. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology,School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 23:13:20 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 23:13:20 -0300 Subject: [HF-FORUM] 24S RE: Digitalis. Dr. Pereira Message-ID: <99372AAA-4D5E-40C0-A8D8-FF44469E00DF@hf-symposium.org> Dr. Villaverde, Digitalis, so much used for centuries, and now almost completely relegated, mostly after the DIG study, still has a role in CHF with decreased systolic function, and even more if the patient is in AF. Beyond these current indications and guidelines, in many places of our countries, where access to state-of-the-art medicine is available for a few, I think it will still be used for a long time, taking into account that this drug is cheap and easy to obtain for most people. I'm certain that in rural areas of my country (where most people do not have medical insurance) is still used, and even abused out of necessity, in spite of knowing what the guidelines state. Experience points out that digitalis works pretty well in elderly patients who do not have much mobility, since the effect of the drug is lost with exercise. On the other hand, we have to remember that the therapeutic index of digitalis is very narrow (the effective doses are very close to the toxic doses, and even more if used in combination with thiazide or loop diuretics). In order to answer your question, if the patient is in sinus rhythm, I would advise a daily dose of 0.25 mg/day for five days a week. It should not be suspended for two days in a row, since plasma concentration would fall to non-efficient levels. I think that -if the patient were in sinus rhythm- there would be no hurry for a rapid digitalization, which in the case of fibrillation with high ventricular response would justify initiating with 0.75 mg to 1.5 mg/ day as a single dose (rapid oral digitization). Dr. Luciano Pereira Paraguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 13 23:39:24 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 13 Apr 2006 23:39:24 -0300 Subject: [HF-FORUM] 25E RE: Cardiac Amyloidosis. Dr. Perez Riera II Message-ID: <6E7BDDDF-8CE9-4552-92C1-7CEDF8A44CBF@hf-symposium.org> Dear Dr Rodney Falk: Thanks a lot by your interesting and cleavers explanations. You answer: "The low voltage is explained by the fact that infiltrated amyloid material substitutes the myocardium that produces voltage is probably only partially true". I agree totally with you. The voltage of QRS is dependent of multiple factors: number an size of fibers, increased surface area and grater wall thickness may be expected to increase the solid angle subtended by the precordial electrodes, intracavitary blood volume (Brody effect), proximity of the heart to the chest wall, body build, race, sex, and others factors as obesity, large brest, low or high hematocrit, etc. One model showed that if a low voltage on ECG was present and interventricular septal thickness is >198mm, the diagnosis of cardiac amyloidosis could be made with a sensitivity of 72% and a specificity of 91%. In this model, the positive predictive and negative predictive values were 79% and 88%, respectively. The authors conclude that in patients with suspected cardiac amyloidosis, a combination of noninvasive parameters-namely, a low voltage on ECG and increased intraventricular septal thickness- on ECO is a useful diagnostic tool. Rahman JE, Helou EF, Gelzer-Bell R, Noninvasive diagnosis of biopsy-proven cardiac amyloidosis. J Am Coll Cardiol. 2004;43:410-415. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 14 11:35:07 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 14 Apr 2006 11:35:07 -0300 Subject: [HF-FORUM] 26C Heart failure and coronary thrombus. Dr. Yaolian Deng Message-ID: <6FD96880-F7E6-4CFE-8CEC-1DE27EAC0CA1@hf-symposium.org> In patients with processing heart failure and coronary thrombus after revascularization for 1-3 weeks, how to consider the management of heart failure and selection of thrombolytic regimens? What's the difference from those after acute myocardial infarction? Dr. Yaolian Deng -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 14 11:52:17 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 14 Apr 2006 11:52:17 -0300 Subject: [HF-FORUM] 27S Resynchronization or transplantation. Dr. Serra Message-ID: <1C11F5EF-7F15-484C-A6F5-BFE281F2D4AD@hf-symposium.org> Patients with heart failure in Class III and IV, in spite of maximal and optimal pharmacological therapy, may be considered for management with cardiac resynchronization or transplantation. In those who are, by their clinical characteristics, candidates to both therapies (resynchronization and transplantation): is it right to attempt resynchronization first, before including them in a transplantation waiting list? It should be resynchronization first and then, in case of failing, transplantation? In the end, do physicians who advocate resynchronization compete for the patients against experts in transplantation? Jos? Luis Serra C?rdoba Argentina -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 14 15:43:49 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 14 Apr 2006 15:43:49 -0300 Subject: [HF-FORUM] 28S From Bolivar. Dr. Vergara Message-ID: <48A2085E-1F85-4E6D-A0C0-1454888D9994@hf-symposium.org> Dear colleagues, I practice my profession in the city of Bolivar, in the province of Buenos Aires, Argentina. I am honored to greet you here, and congratulate you for the task and the effort of making this worldwide conference that I have been following closely from this place. Moreover, I have had the chance to be one of the main researchers from PRISMA study along with Drs. Belziti and Muratore, gathering data for this work in Bolivar. I only wish to thank and congratulate again the organizers. dr.arturo vergara -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 14 15:49:22 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 14 Apr 2006 15:49:22 -0300 Subject: [HF-FORUM] 29S Digoxin. Dr. Almenarez Garcia Message-ID: <162F4676-2A01-46A4-962A-3382F3971BD3@hf-symposium.org> I would like to know if in the light of evidence, there is a difference between using digoxin and beta-methyl-dixogin. Thank you, Miguel almenarez garcia chillan chile -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 14 16:07:48 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 14 Apr 2006 16:07:48 -0300 Subject: [HF-FORUM] 31S RE: Rehabilitation. Dr. Perez Gutierrez Message-ID: <5DBBFE3A-D368-48A3-8F2D-6AC12D06CBD9@hf-symposium.org> Dear Dr. Samaniego, Chile As Spanish is also a language in this Forum, I will reply in our language, the one from the South of our America. The final questions of your communication are the very essence of the great health care problems we have to face, except of course, very few exceptions; the health care specialists from our developing countries from all continents, where not only Cardiology and Rehabilitation, which are specialties or services many times well beyond the reach of most of the population (due to the multiple causes that define availability), but even basic Primary Health Care is a faraway goal to be reached by the WHO. The answer to your question is therefore, quite wide, and we would have material for a Forum devoted singly to this matter with many replies. I think my country has found a reply of its own a long time ago and it is walking toward it. Thank you for your concern for less favored people. Dr. Ismael P?rez Guti?rrez Departamento Salud Facultad de Medicina 10 de Octubre Ciudad de la Habana Cuba -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 15 07:49:25 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 07:49:25 -0300 Subject: [HF-FORUM] 32S Diastolic failure. Dr. Arenzo Message-ID: I think the conference is fascinating. I congratulate the organizers and all those who participate with their contributions and experience. I would like to know the opinion of the experts, about the diagnostic criteria for diastolic HF. In what aspects does the management of diastolic failure differ from systolic failure? Dr. Julio Arenzo Buenos Aires, Argentina. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 15 07:51:58 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 07:51:58 -0300 Subject: [HF-FORUM] 33E RE: Dry weight. Dr. Perez Riera Message-ID: Dear friend Francisco E. Viano The definition of "dry weight" is: The plant, animal, or other material containing the chemical of interest is dried to remove all water from the material. The amount of the chemical found in subsequent analysis is then expressed as weight of chemical divided by weight of the dried material which once contained it. Dry weight refers to the weight of animal tissue after it has been dried in an oven at 65 degree Celsius until a constant weight is archived. Dry weight represents total organic and inorganic matter in to the tissue. Unfortunately, there is no standard measure of dry weight and as a consequence it is difficult to ascertain adequacy of fluid removal for an individual patient. It is evident that a better understanding of fluid status and fluid changes during the treatment of HF is required to develop a precise measure of fluid balance. Similar term(s): dw, dried material. All the best Andres Ricardo Perez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andre - Sao Paulo - Brazil. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 15 08:13:57 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 08:13:57 -0300 Subject: [HF-FORUM] 34E RE: Digitalis. Dr. Perez Riera Message-ID: <78794CB2-E486-4C33-8F58-76AECBE2731A@hf-symposium.org> Dear Dr Villaverde: Heart failure (HF) treatment remains a therapeutic challenge. Digoxin is a therapeutic agent with unique effects that inhibits the sarcolemmal NaK-ATPase in many tissues with the effects on cardiac inotropic fibers, conducting tissue, neural tissue and smooth muscle providing the major physiological effects in health and disease. The major indications for its clinical use include systolic HF, where, in addition to angiotensin conversion enzyme inhibitors(ACEIs) betablockers and diuretics, it reduces the incidence of pulmonary edema, and in the management of patients with supraventricular tachycardia, where it reduces the ventricular rate. Digoxin has traditionally been the drug of choice for ventricular rate control in patients with chronic AF, with or without HF with systolic dysfunction. In patients with permanent AF, digoxin monotherapy is ineffective to control ventricular rate during exercise, but the combination of digoxin with a beta-blocker or a non- dihydropyridine calcium channel antagonist can control HR both at rest and during exercise. Only a few randomized, controlled studies have evaluated the adverse effects of digoxin in patients with AF in a systematic way and side effects requiring drug withdrawal have rarely been reported. When reported, the most frequent adverse effects were ventricular arrhythmias, AV block of varying degrees and sinus pauses. This evidence suggested that, in contrast to other antiarrhythmic drugs, digoxin is a safe drug in patients with AF. However, this safety profile can be erroneous due to the short follow- up of the studies and patient selection. Because patients with HF have been excluded in most studies, the safety profile of digoxin in this population has not been directly addressed. Early recognition that an arrhythmia is related to digoxin intoxication as well as recognition of concomitant medications or medical conditions that may directly alter the pharmacokinetic profile of digoxin, or indirectly alter its cardiac effects by pharmacodynamic interactions remain essential for safe and effective use of digoxin in patients with AF(1). Six drugs/drug classes are contemporary treatments in systolic HF: a diuretic, an ACEI or an angiotensin receptor antagonists, a betablocker, spironolactone and, often, digoxin. While digoxin and diuretics are used to reduce the number of episodes of pulmonary edema, they have not been associated with a significant reduction in mortality (2). Some patients with systolic HF also may be candidates for the combination of hydralazine/isosorbide dinitrate as well as nonpharmacological approaches with biventricular pacemakers and/or ICDs. Treatment of diastolic heart failure is less evidence-based, and speculative treatments focus on control of blood pressure, tachycardia, volume overload, and myocardial ischemia(3). Improvement in HF outcomes resulting in reduced morbidity and mortality may be achieved through greater adherence to recognized guidelines(4). Digoxin should be considered in all patients with systolic HF, supraventricular tachycardia, and, in association with other treatment, as a single dose of 750 -1000 mug/70 kg in patients not treated previously with digoxin who have septic shock. It should be avoided in patients with critical coronary artery disease and ischaemic or hypertrophic diastolic failure (5). The incidence of digoxin toxicity has been declining for a variety of reasons, including a lower therapeutic range, the development of more effective drug therapies for HF, and more accurate dosing methods. In addition, digoxin toxicity, once commonly fatal, can now be quickly and effectively treated by the emergency administration of antidigoxin Fab fragments(6). References 1) Tamargo J, Delpon E, Caballero R. The safety of digoxin as a pharmacological treatment of atrial fibrillation. Expert Opin Drug Saf. 2006; 5:453-467. 2) Young R, Worthley LI. Current concepts in the management of heart failure. Crit Care Resusc. 2004; 6:31-53. 3) Crouch MA. Chronic heart failure: developments and perspectives. Consult Pharm. 2005; 20:751-765. 4) Mann JL, Evans TS. A review of the management of heart failure in long-term care residents. Consult Pharm. 2006;21:222-228. 5) Worthley LI, Holt AW. Digoxin in the critically ill patient. Crit Care Resusc. 1999;1:252-264. 6) Bauman JL, Didomenico RJ, Galanter WL. Mechanisms, manifestations, and management of digoxin toxicity in the modern era. Am J Cardiovasc Drugs. 2006; 6:77-86. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 15 08:28:26 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 08:28:26 -0300 Subject: [HF-FORUM] 35E RE: Cellular cardiomioplasty. Dr. Chachques Message-ID: <01FCDF79-1CD6-441C-912F-79A91995973C@hf-symposium.org> Local treatments for myocardial regeneration highlight the need for efficient and practical delivery methods to the heart. New technologies for cell implantation are emerging. Intracoronary and endoventricular catheter-based cell delivery procedures for therapeutic angiogenesis and myogenesis have been performed. Whatever the transmyocardial route, whether via the epicardium or endocardium, one must mention the high mortality of the cells. This mortality is probably linked to the injection itself and the poor vascular supply of chronic postinfarct scars. For this reason it is important to deliver the maximum of available cells (more than 300 millions per procedure). Surgical cell implantation is performed into well-exposed ischemic areas, permitting multiple injection points within and principally around the infarct. Our approach consisted of performing the main implantation in the peri-infarct area (70% of cells), since residual irrigation and collateral myocardial revascularization in this border zone allows for better survival of the implanted cells. The remaining 30% of cells are implanted in the central portion of the scar. Video- assisted thoracoscopic cell implantation was successfully achieved in experimental and clinical cases. Percutaneous selective coronary artery cannulation for cell injection can be used for myocardial regeneration. This intravascular delivery is based on the potential migratory properties of some cells which retain their ability to cross the basal lamina. This approach should be reserved for mononuclear bone marrow cells, since intracoronary delivery of skeletal myoblasts and bone marrow mesenchymal cells could provoke microemboli. In fact, the myoblasts size (length 25-30 mm) and shape (stellar and spindle-shaped) are more prone to embolizations than bone marrow mononuclear cells (spherical and disc- shaped, diameter 8-18 mm). A new diagnostic-therapeutic electrode catheter for local myocardial treatment has been created by our group, called ?Cell-Fix? catheter. This second generation system includes a method and apparatus to identify by electrophysiology the infarcted area and simultaneously to deliver the cells, stabilizing the scar by vacuum at the moment of injection. Hereby a comparative table of delivery techniques: CELL DELIVERY ADVANTAGES DISAVANTAGES EPICARDIAL (surgical) Accuracy of injection. Surgical and anesthetic risks. ENDOCARDIAL (endoventricular catheter) Less invasive. Periodical injections. Difficulty to localize the target area. Loss of cells. INTRACORONARY Easy manipulation. Low cost. Migration of cells to the myocardium unknown. Risk of embolisation. The development of cell therapies for heart failure is progressing according to a rigorous scientific methodology, from observation to experimentation, to a careful evaluation of preliminary clinical results. I believe that catheter-based stem cell transplantation should be used for selected patients waiting heart transplantation. Best regards, Juan Carlos Chachques, Paris, France -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 15 09:18:13 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 09:18:13 -0300 Subject: [HF-FORUM] EXPERTS ASK, EXPERTS ANSWER Message-ID: <346AEC4D-CB74-4AF3-99FE-3F5557C2D027@hf-symposium.org> Dr. Armando Bordalo e S? from Portugal asks: - Is there any place for levosimendan in acute myocardial infarction? Dr. Yongxin Lu from China answers My answer is yes, levosimendan could be safely used in acute myocardial infarction with heart failure. Levosimendan acts as a calcium sensitizer and adenosine triphosphate- dependent potassium KATP channel opener that increases contraction, causes vasodilation, and provides cardioprotective effects. This is accomplished by its dual action mechanism. Levosimendan binds to cardiac troponin C, thereby enhancing calcium myofilament responsiveness and increasing myocardial contraction without increasing intracellular calcium levels. Thus, contraction is increased with no significant increase in myocardial oxygen consumption. The opening of KATP channels by levosimendan causes vasodilation and exerts anti-ischemic, anti-stunning and anti- apoptosis effects on the myocardium. RUSSLAN trial is a randomized, placebo-controlled, double blind study. Levosimendan at different doses (0.1-0.4 microg x kg[-1] x min [-1]) or placebo was administered intravenously for 6h to 504 patients with left ventricular failure complicating acute myocardial infarction. Levosimendan-treated patients experienced a lower risk of death and worsening heart failure than patients receiving placebo during both the 6h infusion (2.0% vs. 5.9%; P=0.033) and over 24h (4.0% vs. 8.8%; P=0.044). Mortality was lower with levosimendan compared with placebo at 14 days (11.7% vs. 19.6%; hazard ratio 0.56 [95% CI 0.33-0.95]; P =0.031). Levosimendan at doses of 0.1-0.2 microg x kg(-1) x min(-1) did not induce hypotension or ischemia, and reduced the risk of worsening heart failure and death in patients with left ventricular failure complicating acute myocardial infarction. De Luca, L., et al., from Italy, reported a small clinical trial of 52 consecutive patients with anterior acute myocardial infarction who were randomized to levosimendan or placebo infusion. Levosimendan, after primary angioplasty in patients with anterior acute myocardial infarction, appeared to improve the Doppler echocardiographic parameters of left ventricular diastolic function. In another trial, they evaluated the acute effects of levosimendan on hemodynamics and coronary flow velocities in patients with left ventricular (LV) dysfunction undergoing percutaneous coronary interventions (PCIs) for an acute myocardial infarction (AMI). The results showed that Levosimendan significantly decreased pulmonary capillary wedge pressure and significantly increased cardiac index resulting in a significant decrease of systemic vascular resistance. Moreover, coronary flow reserve (CFR) on infarct-related artery and on reference vessel significantly improved in patients treated with levosimendan. They demonstrated that Levosimendan, given intravenously after a PCI procedure in patients with AMI and LV dysfunction, significantly improves hemodynamics and CFR. Sonntag, S., et al., from Germany, reported a clinical trial in which 24 patients with an acute coronary syndrome underwent angioplasty followed by double-blinded, randomized treatment with levosimendan or placebo. The number of hypokinetic segments decreased with levosimendan and the single-beat elastance was increased by levosimendan. The pressure-volume area, end-systolic pressure and volume index were decreased by levosimendan. The end-diastolic volume index was decreased by levosimendan. The time constant of isovolumic LV pressure fall decreased with levosimendan. Levosimendan improved the function of stunned myocardium without obvious impairment of diastolic function. Mustapha, F., et al, from Tunis, presented the case of a 54-year-old male patient treated successfully with levosimendan for cardiogenic shock following acute myocardial infarction. Alhashemi, JA, et al, from Sandi Arabia, reported another case with acute myocardial infarction and cardiogenic shock. They thought that levosimendan in combination with a beta-adrenergic antagonist may have beneficial effects in patients with cardiogenic shock who exhibit tachycardia in response to inotropic agents. Other scholars have also reported levosimendan treatment in patients with acute myocardial infarction and cardiogenic shock. I appreciated discussing this issue with you. If something is wrong in my understanding, please let me know. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 15 09:40:42 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 09:40:42 -0300 Subject: [HF-FORUM] 30S RE: Spongiform myocardium. Dr. Valiente Message-ID: <3F8F9480-82F4-4B4C-A86C-9F58BB5AA4CB@hf-symposium.org> Thank you very much for your help. Let me tell you more about the case of the patient. In an echocardiogram we found RV 28 mm, Ao 39 mm, Exc Ao 21 mm, LA 33 mm, IVS 15 mm, PW 12 mm, thickened 58%, LVDd 58 mm, LVSd 51 mm, SF 12%; LVEF 26%; TDV 167; TSV 124; LVEF X longitude area 26%; eccentric LVH, widespread LV hypokinesis with paradoxical septal motion, trivial mitral valve insufficiency, pulmonary acceleration time 127, restrictive relaxation pattern, EA fusion, E wave 121 cm/s, E/E' ratio 20 E' wave 6 cm/s, increase of pulmonary capillary wedge pressure 26 mmHg, prominent post-systolic wave in Strain Rate with post-systolic prolongation of LV contraction, small LV systolic wave < 4 cm/s, excessive trabeculations with color flow that is inserted between such trabeculations; LV compactation disorder; live 3D is made, and initial diagnosis of spongiform cadiomyopathy is verified, which predominate in the lateral septal wall and apex. As I have previously informed, a coronariography was conducted in the patient, and we found normal coronary arteries. As treatment enalapril, warfarin, isosorbide dinitrate (10), diuretics (furosemide, spironolactone), digoxin and aminophilline are indicated. In the physical examination, we found positive BP 140/100 occasionally, sweating and he mentioned dyspnea and precordial pain that is relieved with nitroglycerin. We also found lung sounds in both pulmonary fields. The "asthma-like" symptoms started at the same time as the first cardiovascular symptoms. I wonder, is it feasible to use beta blockers in this patient? What prognosis does he have, taking into account his age (36 years old) and what future management do you suggest? Thank you very much to all the colleagues, and especially to the organizers of the Symposium. Dr Juan Carlos Valiente Reyes Hospital Universitario Cl?nico Quir?rgico Dr Miguel Enrique. Cuba -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 15 11:50:42 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 11:50:42 -0300 Subject: [HF-FORUM] 36S RE: Echocardiographic variables. Dr. Mato Message-ID: First of all I want to thank and congratulate the organizers for this opportunity to have access to lectures and communications. To answer Dr. Zapata, yes, we are working with traditional parameters and besides, with DTI with software that enables us to quantify velocity curves, strain, strain rate and tissue tracking. Currently, our line of work is mostly focused in measuring wall dysynchrony in patients who are possible candidates for CRT, or even in those with PM in whom, due to their heart disease, and faced with a change of generator, CRT is posed as a possibility. In turn, we have already started our experience with groups of electrophysiologists in the change of post-implantation parameters, verifying data with simultaneous DTI for optimization. We measure time to systolic peak, in velocity curves with two samples by wall in the different windows. In our country, the numbers are small, but we are working in this. Regards, Dra. Silvia Mato Hospital Italiano, Montevideo, Uruguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 15 13:29:37 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 13:29:37 -0300 Subject: [HF-FORUM] 38C. Restrictive cardiomyopathy in pediatrics. Dr. Raymond In-Reply-To: References: Message-ID: <5E600853-3B5A-4809-8FA7-55D376F51E4B@hf-symposium.org> Cardiac transplantation Dr. Raymond (from China) -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee El 12/04/2006, a las 13:38, HF Symposium escribi?: > Forum of the ISHNE Heart Failure World-Wide Internet Symposium > ______________________________________________________________________ > > DeFT Response: DFT Management Tools for CRT-D and ICD Patients > http://www.sjm.com/deftresponse > ______________________________________________________________________ > > Congratulations and thank you for the information. I would like to > know what alternatives are there in the medical treatment of > restrictive cardiomyopathy in a 2-year-old girl, with FC IV CHF, with > ejection fraction in 65%, severe tricuspid regurgitation, severe > atrial dilatation and very dilated vena cava. > Thank you very much for your reply, > > Veronica Petrozzi > Pediatrician > > -- > Dr. Sergio Dubner > President of Scientific Committee > > Dr. Edgardo Schapachnik > President of Steering Committee > > > > > _______________________________________________ > Hf-forum mailing list > Hf-forum at hf-symposium.org > http://lists.hf-symposium.org/mailman/listinfo/hf-forum > From info at hf-symposium.org Sat Apr 15 15:07:17 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 15:07:17 -0300 Subject: [HF-FORUM] 37E RE: Digoxin. Dr. Perez Riera Message-ID: <48D1F9CA-9417-4C0B-8723-3A6608076CD9@hf-symposium.org> Dear Dr. Miguel Almenarez Garcia from Chillan - Chile: Beta-methyl digoxin (BMD) is semisynthetic digitalis glycoside with the general properties of digoxin but more rapid onset of action. Its cardiotonic action is prolonged by its demethylation to digoxin in the liver. It has been used in the treatment of congestive heart failure( CHF), Since Megges and Repke [1961] showed that acetylation of the hydroxyl groups in the aglycone or the sugar side chain of the digitalis molecule results in a derivative with enhanced and more complete absorption from the gastrointestinal tract, several new compounds resulting from acetylation or methylation of digoxin molecule have been developed. BMDis a methyl derivative of digoxin. Enhanced and more complete gastrointestinal absorption of tritium labeled BMD [Rennekamp et al. 1972] has been confirmed. Weiss et al. [1975], based on the serum levels following oral administration, calculated that to achieve comparable levels, digoxin dose would have to be increased by 1.55 times compared to that of BMD. These and other studies supported an earlier notion that BMD was a better and desirable cardiotropic agent than the digoxin. Comparison of cardiac effects using equivalent doses of the two compounds however, showed no difference [Das et al. 1977]. Following oral administration, the serum glycoside levels to BMD indeed were significantly greater than those with digoxin. However, these differences in serum levels were not of sufficient magnitude to influence detectable cardiac inotropic effects, hence, the search for a better digoxin should continue (1). The intestinal absorption and urinary elimination rate of total cardioactive material was compared following digoxin and BMD administration to twelve healthy volunteers. Significantly more injected digoxin was recovered in urine. Urinary clearance was more rapid for digoxin, mean half-lives of elimination being 35 hours for digoxin and 40 hours for BMD. Calculated percentage intestinal absorption was lowest for digoxin tablets with a dissolution rate of 77% in one hour, intermediate for BMD tablets, and maximal for an experimental soft gelatin formulation of digoxin in solution. Respective mean values were 75%, 87% and 97%. Similar steady state plasma concentrations followed twice daily ingestion of the 0.25 mg digoxin tablets and 0.20 mg BMD tablets. Mean peak plasma concentration and percentage urinary recovery of ingested dose were higher during continued BMD administration. Between-subject variation in absorption was higher for the digoxin tablets. The comparative intestinal absorption of BMD and digoxin depends upon the formulation. Digoxin is virtually completely absorbed from a solution encapsulated in soft gelatin. Relatively more BMD is eliminated by nonrenal routes (2). The serum digoxin levels of 23 patients were measured by radio immune assay. The patients were divided into 2 groups receiving either 0,5 mg digoxin b.i.d. or 0,25 mg digoxin b.i.d. orally after having been changed from a maintenance dose of 0,2 mg BMD ( Lenoxin). The question was whether typical or reduced maintenance doses of digoxin in the new preparation reached therapeutic digoxin serum levels in the absence of renal insufficiency. Results: 1) The maintenance dose of 0,2 mg BMD produced stable serum digoxin levels within non-toxic range in all patients; 2) The dosage of 0,5 mg digoxin (group 1) induced accumulation to toxic levels (2,14 mg/ml). A change to 0,25 mg digoxin led to therapeutical serum levels; 3) When using the dosage of 0,25 mg digoxin from the onset of the test (group 2) Accumulation was avoided and normal serum digoxin levels were observed during the test period (3). A total of 1109 determinations of digoxin concentration in serum were performed in 317 patients with HF during oral maintenance therapy with digoxin, beta-acetyldigoxin and BMD. It was shown that the optimal therapeutic serum concentration (1.21 to 1.70 ng/ml) can be obtained reliably if the dosage of digoxin and its derivatives is based on the body weight. The daily doses recommended for oral maintenance therapy are 4mug/kg for BMD, 5 mug/kg for beta- acetyldigoxin, and 8 mug/kg for digoxin. For initiating cardiac therapy the double maintenance dose can be prescribed once. Digoxin derivatives should be preferred to digoxin when choosing the drug (4). In a prospective randomised study 12 patients suffering from cirrhosis of the liver (stable phase) and 12 healthy male volunteers were treated with either 0.3 mg BMD (Lanitop) or 0.4 mg beta- acetyldigoxin (Novodigal) daily, orally. Every day the total serum digoxin concentrations of the patients and volunteers were measured by radioimmunoassay. Both digoxin and BMD are measured by this method. In subjects receiving BMD therapy the ratio of BMD to digoxin in the serum was determined by liquid chromatography. The digoxin levels in patients with cirrhosis treated with BMD were statistically significantly higher than in healthy volunteers. In patients with cirrhosis the proportion of serum BMD averaged 77.7% of the total digoxin concentration, whereas the proportion was only 37.5% in healthy volunteers. With beta-acetyldigoxin there was no statistically significant difference between patients with cirrhosis and healthy volunteers. Alterations in pharmacokinetics may cause the higher total serum digoxin concentrations in cirrhotic patients. The following factors seem to be important: longer elimination half life, changes in distribution volume and reduced renal clearance. There is greater danger of digitalis toxicity in patients with cirrhosis of the liver on standard dosage of BMD than on standard dosage of beta- acetyldigoxin(5). References 1) Das G. Beta-methyl digoxin: a better absorbable digoxin. Int J Clin Pharmacol Ther Toxicol. 1989; 27:521-525. 2) Johnson BF, C. E. Bye CE, Jones GE, Sabey GA The pharmacokinetics of beta-methyl digoxin compared with digoxin tablets and capsules Eur Journal of Clinical Pharmacol. 1976; 10: 231 ? 236. 3) Hennersdorf G, Leithauser H. Digoxin therapy in patients with long-term digitalis therapy. Comparison of the digoxin blood level after oral administration of digoxin and beta-methyldigoxin Fortschr Med. 1980;98: 410-412. 4) Schneider J, Ruiz-Torres A. The importance of body weight in treatment with digoxin and digoxin derivatives Dtsch Med Wochenschr. 1977;102:116-118. 5) Rameis H, Bonelli J, Waginger H, Hruby K. Pharmacokinetics of beta-methyldigoxin and beta-acetyldigoxin in patients with cirrhosis of the liver Wien Klin Wochenschr. 1981;93:572-576. All the best Andres Ricardo Perez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology,School of Medicine, ABC Foundation Santo Andre - Sao Paulo - Brazil. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 15 22:10:29 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 22:10:29 -0300 Subject: [HF-FORUM] 39S Aldosterone antagonists. Dr. Bartolomeo Message-ID: First, I would like to congratulate you for the great level of the conference. My question is the following: when should an aldosterone antagonist be used? In asymptomatic patients with no cardiac remodeling? In asymptomatic patients with remodeling? Or in symptomatic patients? In which cases is justified and in which not, and why? Dr. Mario Bartolomeo -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 15 22:29:05 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 22:29:05 -0300 Subject: [HF-FORUM] 40S RE: Spongiform myocardium. Dr. Quinones Message-ID: Dear Dr. Valiente, The patients with spongiform myocardium or non-compaction myocardium, as this disease is also known, have a predisposition to the formation of thrombi in left ventricular myocardial recesses and frequently, they suffer systemic thromboembolic events, where coronary arteries are not excluded, which may justify the crises and the precordial pain, although precordial pain is also described by myocardial ischemia secondary to an inappropriate relationship between the myocardium and blood vessels. Due to the first reason, I would anticoagulate. They also develop ventricular dysfunction, initially diastolic and later systolic, so depending on the phase of evolution, I would indicate beta-blockers with the aim of decreasing oxygen consumption, or I would treat the systolic dysfunction with standard therapy (ACEI, spironolactone, diuretics and digitalis if it was indicated). I would also assess in this patient, the characteristics of his heart rhythm, since they have a tendency to suffer malignant ventricular arrhythmias and present sudden death; and although there is no wide variety of papers about the management to follow with them to define the risk of sudden death (SD), I would like to stratify his risk through the results of a Holter, late potentials, RR variability, LVEF, to define an antiarrhythmic therapeutic management or SD prevention. Regards, Dr. Qui?ones -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 15 23:37:15 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 15 Apr 2006 23:37:15 -0300 Subject: [HF-FORUM] 41E Congratulations. Dr. Yabluchansky Message-ID: <8899D41B-49BA-4E52-BC26-48EF6965ECD0@hf-symposium.org> Dear friends! I am glad to greet and congratulate everyone with participation in this remarkable event. Indeed we had an opportunity to exchange with the results of our researches and to feel the rhythm of heart insufficiency today. For me personally it is also the huge material which I use in educational process with my students and which I plan to place on the pages of Russian-speaking international medical paper for wider familiarization withthe problems of medical society. It would be great if this symposium will become the beginning of regular virtual symposiums. Good luck everyone! Sincerely, Myckola (Nickolay) Yabluchansky Ukrania -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 16 17:54:34 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 16 Apr 2006 17:54:34 -0300 Subject: [HF-FORUM] 43S Levosimendan. Dr. Pereira Message-ID: <05600938-23A1-4F1B-8268-AEABB64CF3A8@hf-symposium.org> I don't know whether we will still want to continue using levosimendan after the conclusions of the SURVIVE W study, which compared this drug with dobutamine. The main difference is in the cost of the first one. And this study showed that there were no significant differences between both. I transcribe it next: Survival of Patients with Acute Heart Failure in Need of Intravenous Inotropic Support (SURVIVE-W) Year Presented 2005 Description The goal of the trial was to evaluate treatment with levosimendan compared with dobutamine among patients with acute heart failure in need of intravenous inotropic support. Drugs/Procedures Used Patients were randomized in a double-blind manner to either treatment with levosimendan (12 µg/kg bolus plus 0.1-0.2 µg/kg/min infusion for 24 hours) (n=663) or dobutamine (³5 µg/kg/min infusion for ³24 hours) (n=664). Principal Findings Baseline characteristics were similar in both groups, with 88% of patients having a history of heart failure, 86% in New York Heart Association class IV heart failure, and a baseline ejection fraction of 24%. Median BNP was 1178 pg/mL and 1231 pg/mL. Levosimendan infusion duration was 23 hours and dobutamine infusion was 39 hours. There was no difference in the primary endpoint of all-cause mortality at 180 days (26.1% in levosimendan group and 27.9% in dobutamine group, hazard ratio [HR] 0.92, p=0.401 ). Likewise, there was no difference at 5 days (4.4% vs 6.0%, HR 0.72, p=NS) or 31 days (11.9% vs 13.7%, HR 0.85, p=NS). BNP at 24 hours was lower in the levosimendan group compared with dobutamine (p<0.001). In the subgroup of patients with history of heart failure, mortality trended lower at 5 days (HR 0.58, 95% CI 0.33-1.01) but was not significantly lower. In a meta-analysis of the LIDO, CASINO and SURVIVE trials, mortality at 6 months was lower in the levosimendan group (relative risk 0.76, p=0.032). Among the adverse events, atrial fibrillation occurred more often in the levosimendan group (9% vs 6%), while cardiac failure occurred less often in the levosimendan group (12% vs 17%). There was no difference in hypotension (16% vs 14%) or ventricular tachycardia (8% vs 7%). Interpretation Among patients with acute heart failure in need of intravenous inotropic support, treatment with levosimendan was not associated with a reduction in mortality at 6 months compared with dobutamine. Patients with acute heart failure in need of inotropic support are a particularly higher risk population, with a high mortality rate (27%) in the present study by 6 months. Levosimendan, a novel drug that acts as a calcium sensitizer, has been proposed as an alternative to standard treatment with dobutamine. Earlier trials such as LIDO and CASINO showed lower rates of mortality with levosimendan, although these were small pilot trials. The much larger SURVIVE study did not confirm these mortality findings at either early or late timepoints, although the relative benefit appeared higher early rather than later after the initial infusion. Conditions ¥ Heart failure Study Design Randomized. Blinded. Parallel. Patients Enrolled:1327 Mean Follow-Up:6 months Mean Patient Age:Mean age 67 years % Female:18 Primary Endpoints All-cause mortality at 6 months Secondary Endpoints All-cause mortality at 31 days, BNP at 24 hours, days alive out of hospital, change in patient dyspnea assessment, change in patient global assessment. Patient Population Hospitalization for acute heart failure, left ventricular ejection fraction ²30%, clinical need for inotropic therapy after intravenous diuretics and/or vasodilators. Related Trials Levosimendan Infusion versus Dobutamine (LIDO) View REVIVE II (REVIVE II) View References Presented by Dr. Alexandre Mebazaa at the American Heart Association Scientific Session, Dallas, Texas, November 2005. Summary Written By Ms. Sabina A. Murphy, M.P.H. Author Disclosure: Research Grants: Astra, Aventis, Boston Scientific, Bristol Myers Squibb, COR Therapeutics, DVI Guidant, Eli Lilly, Genentech, Merck, Millennium Pharmaceuticals, Pfizer, SmithKline Beecham, Sonus, NIH, Percusurge, Pharmadigm, Point Biomedical, TIMI 3 Systems. Summary Reviewed By C. Michael Gibson, M.D., F.A.C.C. Kind regards, Dr. Luciano Pereira Paraguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 16 17:56:00 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 16 Apr 2006 17:56:00 -0300 Subject: [HF-FORUM] 44S RE: Spongiform myocardium. Dr. Virgini Message-ID: I'm treating a family made up by 4 sisters, three of which present this pathology, just as their father. The first symptom the oldest one presented was syncope, and in the Holter made, she presented episodes of Torsade de pointes that cardioverted spontaneously. This sister is for the time being, the only one with cardiomyopathy; the other members of the family show no signs and are asymptomatic. An ICD was implanted in this patient, and as in evolution she presented myocardial dilatation, she was treated with ACEI, diuretics and b-blockers, preparing her to enter in a transplantation plant; but the patient improved her heart failure, and did not present any more arrhythmias since three years ago, and she is in normal functional capacity. My only doubt is if the sisters will not show sudden death as their first symptom? And if so, what do we do? DR GABRIEL GUSTAVO VIRGINI. INSTITUTO CARDIOLOGICO BOLIVAR -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 16 17:59:23 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 16 Apr 2006 17:59:23 -0300 Subject: [HF-FORUM] 45S AF in elderly patients. Dra. Perez Leon Message-ID: <0283DE51-C1F5-4761-B962-9668989D39BC@hf-symposium.org> My greetings and I would like to congratulate all the colleagues that made this scientific exchange, so necessary, possible. I would like to know the current therapeutics (according to the etiology) for atrial fibrillation in elderly patients. Thanking you in advance, Dra. Mariblanca P?rez Le?n. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 16 18:01:23 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 16 Apr 2006 18:01:23 -0300 Subject: [HF-FORUM] 46S RE: Levosimendan. Dr. Reyes Message-ID: <3923E21C-E763-43DD-A77C-128051852494@hf-symposium.org> First, I would like to congratulate the people in charge of this Symposium for the great opportunity of being able to exchange our experience and for the good organization of this event. I do not doubt about the advantages of Levosimendan in acute myocardial infarction, complicated with heart failure, but Dr. Yongxin Lu from China, in her review on this topic, and quoting Sonntag, S et al, from Germany, says that the latter reported about a clinical trial in which 24 patients with acute coronary syndrome underwent angioplasty, followed by a randomized and double-blind treatment with levosimendan or placebo. The number of hypokinetic segments decreased with levosimendan and the elasticity by beat increased with levosimendan. My question is: how could we know whether this is due to Levosimendan and not to opening the vessel responsible by Angioplasty? Dr Raul Reyes. Cuba. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 16 18:24:21 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 16 Apr 2006 18:24:21 -0300 Subject: [HF-FORUM] 42S Spironolactone. Dr. Acuna Message-ID: <5A4BE060-AF97-42FB-9988-A4499BE120C5@hf-symposium.org> Congratulations for the enterprise and for realizing this Forum. My question is: should we continue today, before the evidence, waiting for patients to reach FC III to start with spironolactone, and could we institute it in patients with FC I and II? Thank you, Dr. Acu?a de Uruguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 16 18:34:01 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 16 Apr 2006 18:34:01 -0300 Subject: [HF-FORUM] 49S RE: Spongiform myocardium. Dr. Sporidis Message-ID: About Dr. Valiente's patient: I do not understand why the patient is receiving aminophilline, if the bronchospasm seems to be caused by the relative compression of the bronchioles by blood stagnancy of small circulation, and not by the bronchium itself. Due to arrhythmogenicity and the present constellation it would be rejected. I would like to know more about this case. Sincerely, Dr. Dimitrios Sporidis Cardiocentro Aleman de Berlin Alemania -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 16 18:50:58 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 16 Apr 2006 18:50:58 -0300 Subject: [HF-FORUM] 53E RE: Digitalis. Dr. Marcus Message-ID: It is well documented that digitalis has an additive effect to beta blockers in achieving rate control in atrial fibrillation.This regimen is known to induce a marked reduction in adrenergic activity and augmentation in vagal activity. Ref. Farshi R. et al. Ventricular Rate Control in Chronic Atrial Fibrillation During Daily Activity and Programmed Exercise: A Crossover Open-Label Study fof Five Drug Regimens J. Am Coll. Cardiol 1999;33;304-310. Frank Marcus -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 16 19:51:18 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 16 Apr 2006 19:51:18 -0300 Subject: [HF-FORUM] 47S RE: Restrictive cardiomyopathy in pediatrics. Dr. Virgini Message-ID: <9651175F-01DD-42C3-8757-1E3EDB01F16D@hf-symposium.org> About the case presented by Dr. Petrozzi, I think just as the colleague from China: TRANSPLANTATION. Dr. Gabriel Virgini -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 16 19:59:21 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 16 Apr 2006 19:59:21 -0300 Subject: [HF-FORUM] 48E RE: Aldosterone antagonists. Dr. Perez Riera Message-ID: Dear Dr. Mario Bartolomeo: Spironolactone (SPIR) binds to cytoplasmic mineralocorticoid receptors (MR) and functions as an aldosterone antagonist. Many patients with HF should receive aldosterone receptor antagonists. These drugs binds to cytoplasmic MR and functions as aldosterone antagonists, ie, either SPIR or the newer agent eplerenone -in addition to an ACE, inhibitor or an angiotensin II receptor blocker (ARB) or both, and a beta-blocker (1). SPIR is a nonselective aldosterone antagonist, and eplerenone is selective to the aldosterone receptor. SPIR may be useful as a cardioprotective agent to prevent cardiovascular remodeling via the angiotensin-converting enzyme (ACE)/ epidermal growth factor receptor (EGFR)/ extracellular signal- regulated kinases ERK pathway, nicotinamide adenine dinucleotide phosphate NAD(P)H oxidase/lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) pathway, and Rho-kinase pathways(2). The drug was shown to have an early suppressive effect on several immunoactive and proinflammatory cytokines. To elucidate the mechanism behind this, the four MR-binding steroids SPIR, canrenone, 7alpha-thiomethyl-spironolactone and aldosterone (ALDO) were investigated for effects on lipopolysaccharide- and phytohemagglutinin-A-activated human blood mononuclear cells. Gene expression was examined after 4 h using microarrays, and SPIR affected 1018 transcripts of the (=) 22,000 probed. In contrast, the SPIR-related steroids affected 17 or fewer transcripts. Combining SPIR and ALDO resulted in 940 affected transcripts, indicating that SPIR has an early gene-regulatory effect independent of MR. The affected genes encode a large number of signalling proteins and receptors, including immunoinflammatory response genes and apoptosis and antiapoptosis genes. Apoptosis was evident in CD3-, CD14- and CD19-positive cells, but only after 18 h of exposure to SPIR.The transcriptional network involving the differentially regulated genes was examined and the results indicate that SPIR affects genes controlled by the transcription factors NF-kappaB, CEBPbeta and MYC.These observations provide new insight into the non-MR-mediated effects of SPIR(3). Williams et al show that the nonspecific mineralocorticoid receptor (MR) antagonist, SPIR, protects from caspase-3 activation induced by serum deprivation in contrast to the selective MR antagonist, eplerenone, that is non-protective. The authors also demonstrate that progesterone, hydrocortisone and dexamethasone all protect Human umbilical vein endothelial cells (HUVECs) from serum-deprivation induced caspase-3 activation, whereas aldosterone and dihydrotestosterone have no effect. SPIR has been demonstrated to display agonist activity only to the progesterone receptor and the authors additionally show that SPIR and progesterone, but not eplerenone, inhibit mitochondrial cytochrome c release and cleavage of nuclear poly (ADP-ribose) polymerase (PARP) and increase cell viability. Additionally, the PR antagonist mifepristone (RU486) partially blocked the inhibitory effect of both SPIR and progesterone on caspase-3 activation, cytochrome c release and nuclear PARP cleavage. Nitric oxide protects HUVECs from apoptosis in response to various stimuli including serum-deprivation; however, the nitric oxide synthase inhibitor N-monomethyl-L-arginine, did not abolish inhibition of caspase-3 activation or PARP cleavage by SPIR. Thus, the authors demonstrate that SPIR protects HUVECs from serum- deprivation induced apoptosis by inhibition of caspase-3 activity, cytochrome c release and PARP cleavage by a NO-independent mechanism; further, this effect is likely mediated by the agonist properties of SPIR toward the progesterone receptor(4). Treatment fo HF is directed not only towards improving symptoms, but also to preventing the development from asymptomatic systolic dysfunction to symptomatic HF, to preventing cardiac remodelling, renal dysfunction and to reducing mortality. The approved oral 6 drugs category can be given at the same time if the patient tolerates them, because their beneficial effect is additive. Patients with systolic HF or diastolic HF should be treated with diuretics if fluid retention is present, with an ACE inhibitor or an angiotensin II receptor blocker (ARB) if the patient cannot tolerate an ACE inhibitor because of cough, angioneurotic edema, rash, or altered taste sensation, and with a beta blocker unless contraindicated. Aldosterone receptor antagonists have proven to be a valuable treatment tool in the management of HF due to systolic dysfunction. If severe systolic HF persists, an aldosterone antagonist should be added. The degree of left ventricular dysfunction (LVD) is a key factor for determining clinical management strategies in the patient post MI. Addition of an aldosterone antagonist is also advised in patients with LVD(5). SPIR and eplerenone are life-saving agents in patients with advanced HF and may benefit patients with mild HF. Both have been shown to improve morbidity and mortality in patients with advanced HF. K+ and renal function must be routinely assessed to minimize the risk of life- threatening hyperkalemia. Blocking the effects of aldosterone can improve many of the functions that are deranged in patients with HF, as well as promote excretion of Na+ and water and preservation of K+ and H+ in the distal renal tubule. These medications can be especially effective at removing fluid from the periphery and soft tissues. The "Randomized Aldactone Evaluation Study" (RALES) trial results in patients with severe HF NYHA class III or IV and a left ventricular EF of no more than 35 % showed that administration of a sub- hemodynamic dose of SPIR (25 mg a day) as an add on therapy to ACE-I plus standard treatment resulted in a significant mortality reduction due both to decreased death from progressive HF and SCD. These findings support the pivotal role of aldosterone in the pathophysiology of progressive HF. Although it is an effective antialdosterone agent, widespread use of SPIR in humans is limited by its tendency to produce undesirable sexual side effects. Impotence and gynaecomastia can be induced in men, whereas pre-menopausal women may experience menstrual disturbances. Adverse effects of both spironolactone and eplerenone include potentially life-threatening hyperkalemia, which can be induced by renal insufficiency, diabetes mellitus, advanced HF, advanced age, and concurrent drug therapy(6).A selective aldosterone receptor antagonist, eplerenone, appear promising for the effective blockade of aldosterone and its harmful effects without the sexual disturbances of SPIR. Eplerenone was successfully introduced for the treatment of hypertension and HF. Growing number of experimental studies are finding a broader role for Aldosterone in driving the pathophysiology of both HF and hypertension. When added to conventional therapy aldosterone receptor blockers show benefits which are in addition to those conferred by ACE-I and/or aII receptor blockers(7). References 1) Pitt B, Rajagopalan S. Aldosterone receptor antagonists for heart failure: current status, future indications. Cleve Clin J Med. 2006; 73:257-260. 2) Nakano S, Kobayashi N, Yoshida K, Ohno T, Matsuoka H. Cardioprotective mechanisms of spironolactone associated with the angiotensin-converting enzyme/epidermal growth factor receptor/ extracellular signal-regulated kinases, NAD(P)H oxidase/lectin-like oxidized low-density lipoprotein receptor-1, and Rho-kinase pathways in aldosterone/salt-induced hypertensive rats. Hypertens Res. 2005; 28:925-936. 3) Sonder SU, Mikkelsen M, Rieneck K, Hedegaard CJ, Bendtzen K. Effects of spironolactone on human blood mononuclear cells: mineralocorticoid receptor independent effects on gene expression and late apoptosis induction. British Journal of Pharmacology advance online publication, 6 March 2006;doi:10.1038/sj.bjp.0706700. 4) Williams TA, Verhovez A, Milan A, Veglio F, Mulatero P. Protective effect of spironolactone on endothelial cell apoptosis. Endocrinology. 2006 Feb 23; [Epub ahead of print]. 5) Rudo TJ, Kowey PR. Real-world algorithms for the optimal use of drugs and devices in the patient post myocardial infarction and the future of post myocardial infarction management. Clin Cardiol. 2005;28:I58-163. 6) Marcy TR, Ripley TL. Aldosterone antagonists in the treatment of heart failure. Am J Health Syst Pharm. 2006;63:49-58. 7) Dieterich HA, Wendt C, Saborowski F. Cardioprotection by aldosterone receptor antagonism in heart failure. Part I. The role of aldosterone in heart failure. Fiziol Cheloveka. 2005;31:97-105. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology,School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 16 22:02:51 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 16 Apr 2006 22:02:51 -0300 Subject: [HF-FORUM] 54C RE: Diastolic failure. Dr. Richard In-Reply-To: <9FBCBAD8-A411-408F-BB68-20344247B21D@hf-symposium.org> References: <9FBCBAD8-A411-408F-BB68-20344247B21D@hf-symposium.org> Message-ID: <8CA63959-E955-460A-820B-D7574AFF0369@hf-symposium.org> Actually we have no consistent conclusions either in my or other heart centers. If possible, we hope you and your team can organize some clinic trials and follow up to validate it. Dr. Richard > Forum of the ISHNE Heart Failure World-Wide Internet Symposium > ______________________________________________________________________ > > DeFT Response: DFT Management Tools for CRT-D and ICD Patients > http://www.sjm.com/deftresponse > ______________________________________________________________________ > > Congratulations again to the organizers of this interesting event, and > especially to the cardiology representatives from the MERCOSUR > (suggestion > included). I would like to make some reflections so that the > experts may > comment about them. > Recently, at the ACC meeting in Atlanta, the subject of diastolic CHF > (DCHF) > management did not show substantial advancements in their > definition or > management. > > 1- In most papers, DCHF is defined by excluding systolic CHF (SCHF), > presenting as a condition a NORMAL EF. Starting from EF being an > insufficient indicator both for contractility and cardiac and > peripheral > vascular syndrome of CHF, although it is a good independent prognosis > indicator, DCHF should be defined according to stages 1-2 or 3 of the > abnormal echocardiographic pattern of ventricular relaxation, since > these > depend on end diastolic pressure (EDP). > 2- Near 50% of the patients with CHF have normal EF. Diastolic > function > is closely related with systolic failure and is part of a compensating > mechanism of the myocardial impelling aspiration pump function. The > basic > aspect of CHF is end diastolic pressure, with which the myocardium > works in > the three-dimensional curve of strength, length and time (HR). The > stages of > pseudonormalization (2) and mild (3) or severe (4) restriction, may be > perfectly determined by echo Doppler, and each one of them depends on > the > volume-pressure curve. In all of them EDP may be determined, so the > way I > see it, we should consider a CHF classification with normal or low EF > related with high or low EDP and with the extent of remodeling > (cardiomegaly) and asynchrony; and pure DCHF should be left for > restrictive > or hypertrophic cardiomyopathies with restrictive pattern. > 3- In view of the previous considerations, we shouldn't be > surprised if > traditional CHF management, whether systolic or diastolic, should > be the > same because they are failed compensating mechanisms for the same > progressive pathophysiology. On the contrary, the management of pure > restrictive cardiomyopathies may be very different and their > prognosis and > efficacy may be different, too. I think that this would explain the > success > in using nitrates and hydralazine in black patients, where the > prevalence of > hypertensive heart disease is very high. > > Is there some randomized resynchronization study in patients with > SCHF vs. > DCHF? > > Dr Juan Carlos Ansin > Panam? > > -- > Dr. Sergio Dubner > President of Scientific Committee > > Dr. Edgardo Schapachnik > President of Steering Committee > > > > > > _______________________________________________ > Hf-forum mailing list > Hf-forum at hf-symposium.org > http://lists.hf-symposium.org/mailman/listinfo/hf-forum > > -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 17 15:24:21 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 17 Apr 2006 15:24:21 -0300 Subject: [HF-FORUM] 55C RE: Heart failure and coronary thrombus. Dr. Yongxin Lu Message-ID: Dr. Yao asked: In patients with processing heart failure and coronary thrombus after revascularization for 1-3 weeks, how to consider the management of heart failure and selection of thrombolytic regimens? What's the difference from those after acute myocardial infarction? Thanks for your question. For patients with heart failure and coronary thrombus after revascularization for 1-3 weeks, If EKG show STEMI, fibrinolytic therapy is not different from those with AMI, but, selection of fibrinolytic agents is dependent on whether patients have been management with SK or rSK, repeated selection of SK or rSK is not recommended. If patients with NSTEMI or unstable angina, it is not necessary to use thrombolytic agents. Repeated PCI should be considered for these patients. Reperfusion therapy is key issue for saving the ischemic myocardium. For treatment of HF, ACE inhibitors or ARB, beta-blocker and diuretics are recommended, antithrombolic therapy should be aggressived, anti-angina medicine should be chosen. No use of digoxin is better. Dr. Yongxin Lu ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 17 15:24:38 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 17 Apr 2006 15:24:38 -0300 Subject: [HF-FORUM] 56C RE: Aldosterone antagonists. Dr. Yongxin Lu Message-ID: <381D2696-2DD5-44A9-B72B-F2741D364320@hf-symposium.org> Dr. Bartolomeo asks My question is the following: when should an aldosterone antagonist be used? In asymptomatic patients with no cardiac remodeling? In asymptomatic patients with remodeling? Or in symptomatic patients? In which cases is justified and in which not, and why? Thanks for your question. For patients with hypertension, asymptomatic and no evidence of cardiac remodeling, aldosterone antagonist could be used as a diuretic, not only a anti-hypertensive drug, but also a anti- remodeling drug. If hypertensive patient with primary aldosteronism, CT or MRI show bilateral hyperplasia, aldosterone antagonist should be chosen. For patients with cardiac remodeling related with myocardial infarction, and reduced LVEF, aldosterone antagonist should be used. EPHESUS trial demonstrated it is benefit for these patients. For patients with moderately severe or severe symptoms of HF, if their renal function and potassium concentration are normal, low-dose aldosterone antagonist should be considered according RALES study. If there is renal dysfunction or hyperkalemia, aldosterone antagonist should not be used. Dr. Yongxin Lu from China ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 17 15:42:37 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 17 Apr 2006 15:42:37 -0300 Subject: [HF-FORUM] 50S SCD in obese patient with risk factors. Dr. Valdes Garcia Message-ID: <78368E5A-DC1E-4304-A2CF-004BAE56CEC9@hf-symposium.org> Here I present my case: 62-year-old female patient, morbid obesity. Her height is 1.55 m and her weight is 110 kg. She has been a diabetic with a 10-year evolution [glibenclamide-metformin], HBP with a 15-year evolution [candesartan-hycrochlorothiazide], hypothyroid [normal values of T3, T4, TSH], old anteroseptal and inferior myocardial infarction [2 vessels, it seems], QRS 140 ms. Dilated cardiomyopathy [probably ischemic]. EF 30%. NYHA Class III. She is also treated with 25 mg of atenolol, spironolactone 50 mg and furosemide 80 mg a day. She came to Mexico DF to visit relatives and presented an episode of Acute Pulmonary Edema. After 10 days of hospitalization, she went to her home. Currently in Class II. What do you think would be the best management choice? Continuing with the medical management or using devices? Thank you, Dr. Jose Angel Valdes Garcia Mexico DF Thanks everyone and congratulations for this brilliant event. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 17 16:17:52 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 17 Apr 2006 16:17:52 -0300 Subject: [HF-FORUM] 51E RE: Digoxina. Dr. Safer Message-ID: <048805D4-CE55-4A26-A1F7-54B756B3B9AD@hf-symposium.org> Digoxin is a natural drug substance which was extracted for probably hundreds of years from Digitalis purpurea plant, while Beta- Methyldigoxin (BMD) is a semisynthetic digitalis glycoside. The latter has all the general properties of Digoxin. The difference is in the pharmacokinetic properties: BMD bioavailability is enhanced, due to a higher absorption rate of BMD from the digestive tract. BMD onset of effect is faster, drug maximum concentration peak tends to be lower and later, and the cardiotonic action is prolonged, since the liver demethylates BMD to Digoxin. Intra- and interindividual plasma level variability is decreased condiderably by BMD, which eases dose finding and maintenance. Since I had been involved in the planning and evaluation of a clinical phase-3 study in Germany 30 years ago, I still remember some, but by far not all details. As most details from this study vanished from my memories, I had to look for the efficacy data from literature. Ito et al (1975) give the equivalence of efficacy as: patients who were switched from other digitalis preparations to BMD "...revealed that 1 mg of beta-methyldigoxin is equivalent to 1.8 mg of digoxin or to 0.59 mg of digitoxin. The usefulness and ease of beta-methyldigoxin in maintenance was evaluated as being somewhat superior to other cardiac glycosides, according to the global judgement of the physicians. The observed side effects were similar to those of other glycosides in frequency and character." Best regards Dr. Anton Safer (Weisenheim, Germany) Literature: Ito Y, Seki K, Kimura E. (1975): Multiclinical open studies on the effect of beta-methyldigoxin on congestive heart failure with atrial fibrillation. Jpn Heart J. 1975 Sep;16(5):538-47. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 17 16:35:34 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 17 Apr 2006 16:35:34 -0300 Subject: [HF-FORUM] 52S RE: Digitalis. Dr. Gorini Message-ID: <2CB3D76C-596A-48CB-AF9F-0AEBBC319162@hf-symposium.org> Greetings for everyone, and my congratulations to the organizers. The reason for my comment may be a little off topic from the approached issue, since it has more to do with "evidence" than anything else. Just as Dr. Perez Riera stated, there is no "evidence" that diuretics or digoxin reduce mortality in Heart Failure. Nevertheless, and with an approach more "epistemological" than purely methodological, we should wonder what this means. So as to avoid abstractions, I will only pose one question: How many people with heart failure could live if we would never administer diuretics? About digitalis, it reduces hospitalizations as well, besides some episodes of Acute Pulmonary Edema, and of course, it presents all the mentioned drawbacks (more noticeable in elderly women and other special situations). Therefore, and using EBM as a starting point, I'm for using digitalis when there are no doubts about the clinical benefits in a given patient: if using it is not difficult, if there is no intolerance or Renal Failure, and if withdrawal is perceived by the patient as a worsening in his/her symptoms or impairment in functional capacity, in such cases I do use digitalis. Regarding diuretics, and just as it is advised, I leave them for when they are "evidently" necessary; i.e. before signs of systemic and/or pulmonary venous congestion, or symptoms that suggest this. Once again, regards and congratulations. Dr. N?stor Gorini Argentina -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 17 19:03:31 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 17 Apr 2006 19:03:31 -0300 Subject: [HF-FORUM] INSTRUCTIONS FOR CME'S CREDITS TESTING Message-ID: <3619CEE6-CFB3-4C25-A724-5475901D3E5D@hf-symposium.org> As of April 20th, in the CREDITS section, there will be questions uploaded about each lecture presented in this symposium and identified with the name of the faculty. Each question has replies suggested with a correct one. Each member that is registered in this symposium will be able to answer the number of questions he/she wishes of the lectures either heard or read. Each 5 questions replied correctly, 1 credit will be obtained with a maximum of 10. These questions may be answered until October 1st, 2006, and they are automatically submitted to the server of the symposium. Once the replies are received and analyzed, a certificate is generated with the number of granted credits, which will be sent via e-mail, in .PDF format. All those who request it, should fill in their name and e-mail. Since CME credits are granted by the ACCME from USA, we consider that they should be completed in English, and therefore will not be translated into the other languages. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 17 20:42:12 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 17 Apr 2006 20:42:12 -0300 Subject: [HF-FORUM] 57S RE: Beta blockers. Dr. Vazquez-Tanus Message-ID: <57D037BF-20A6-43F6-B78E-5723E27BA594@hf-symposium.org> Congratulations for such excellent symposium on Heart Failure. I support these activities in their maximal splendor and I am a regular observer. About Dr. Arenzo's statement, it is appropriate to say that maybe it should be a relative contraindication, customizing each particular case. My experience is basically the same, and I have many patients with asthma who use Carvedilol in maximal tolerated doses, just as Atenolol. We should not forget that I had to withdraw them in other patients because of asthma worsening; however, they are really a few cases. Dr Vazquez-Tanus -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 17 22:01:38 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 17 Apr 2006 22:01:38 -0300 Subject: [HF-FORUM] 58S Chagasic cardiomyopathy. Dr Juri Message-ID: <48F3B69A-BE8D-4C09-B247-F3B20032402C@hf-symposium.org> Dear friends, I want to thank you for the chance given me to participate in such enriching symposiums (ARVD, AF and now this on HF). Besides, I would like to congratulate you for the excellence of the lecturers and for the work and effort these events imply. Now, I would like to pose a topic that, although it has not been proposed between the central issues of this symposium, I think is very important for Latin-American people especially, and for the rest of the colleagues in general, and this is CHAGASIC CARDIOMYOPATHY (in its acute and chronic forms), which as those who know me know, it is an issue of permanent concern to me. The questions that arise are innumerable, but I will just ask a few: The evolution is the same as cardiomyopathies with another etiology? The medical treatment should be the same? And if someone has experience on the use of resynchronizers and/or ICD, can they tell about it? Thanking you in advance for your replies or other questions. Dr. Juan Carlos Juri Mendoza - Argentina -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 11:10:26 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 11:10:26 -0300 Subject: [HF-FORUM] What's new for 'heart failure, congestive' in pubmed Message-ID: This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM). Do not reply directly to this message. Sender's message: Search: heart failure, congestive Sent on Saturday, 2006 Apr 15 Search heart failure, congestive[MeSH] Click here to view complete results in pubmed. (Results may change over time.) To unsubscribe from these e-mail updates click here. Entrez pubmed Results Items 1 - 36 of 36 1: G Ital Cardiol (Rome). 2006 Mar;7(3):228-33. Related Articles, Books Comment on: G Ital Cardiol (Rome). 2006 Mar;7(3):224-7. [Of defibrillators and guidelines] [Article in Italian] Tavazzi L. Publication Types: Comment Editorial PMID: 16572989 [PubMed - indexed for MEDLINE] 2: G Ital Cardiol (Rome). 2006 Mar;7(3):206-16. Related Articles, Books [Administrative databases as a basic tool for the epidemiology of cardiovascular diseases] [Article in Italian] Monte S, Fanizza C, Romero M, Rossi E, De Rosa M, Tognoni G. Laboratorio di Farmacoepidemiologia, Centro Studi SIFO, Consorzio Mario Negri Sud, S. Maria Imbaro (CH). monte at negrisud.it The broader availability of administrative databases, characterized by increasing data reliability, related to the various steps of the healthcare process, has became also in Italy an important resource for epidemiological studies. Specifically, the methodological developments in the handling and analysis of drug prescription files can be seen as the original and highly informative backbone of a comprehensive monitoring of healthcare delivery processes. The area of chronic cardiovascular treatments occupies a privileged space in these developments, which are illustrated in the paper, with a synthetic presentation of the methodology supported by a model analysis of the epidemiology of heart failure in a healthcare district and by a reference list which has been conceived to provide to the reader a comprehensive perspective on an area so far largely unexplored. PMID: 16572986 [PubMed - indexed for MEDLINE] 3: G Ital Cardiol (Rome). 2006 Mar;7(3):186-91. Related Articles, Books [Chronic heart failure as a crisis event of the family] [Article in Italian] Rocchi S, Boraso A, Bettinardi O, Ghidelli C. Servizio di Psicologia, Fondazione S. Maugeri, Clinica del Lavoro e della Riabilitazione, IRCCS, Gussago (BS). srocchi at fsm.it The family greatly influences any of its members and significantly contributes to the patient rehabilitation. A limited and superficial interest from the family as well as an overprotective and anxiogenic behavior may lead to chronicization, relapse or even to progression of the disease. The close relationship between the patient and the physician is an illusion, since family members deeply affect this interaction. They may first influence the cardiologist's choice and later, through comments or actions, treatment expectations, diagnosis and therapy by sustaining or, on the contrary, minimizing the patient- physician interaction. A therapeutic triangle, which includes the family, the patient and the physician, develops from the beginning; thus the physician needs to be aware of it to use these interactions in the best interest of the patient himself. In this context clinical psychologists play a pivotal role first in identifying dysfunctional relations within the family and then in supporting the family to overcome crisis events. Publication Types: Review PMID: 16572984 [PubMed - indexed for MEDLINE] 4: Schweiz Rundsch Med Prax. 2006 Mar 15;95(11):399. Books, LinkOut [Cardiomyopathy] [Article in German] Brunckhorst CB. Abteilung Kardiologie, Departement Innere Medizin, Universitatsspital Zurich. Publication Types: Case Reports PMID: 16570645 [PubMed - indexed for MEDLINE] 5: Circulation. 2006 Mar 28;113(12):e659. Related Articles, Books, LinkOut Images in cardiovascular medicine. Severe left atrial edema and heart failure after atrial fibrillation ablation. Steel KE, Roman-Gonzalez J, O'Bryan CL 4th. Department of Cardiology, Wilford Hall Medical Center, Lackland AFB, Texas, USA. Kevin.Steel at lackland.af.mil PMID: 16567573 [PubMed - indexed for MEDLINE] 6: Circulation. 2006 Mar 14;113(10):1275-7. Related Articles, Books, LinkOut Comment on: Circulation. 2006 Mar 14;113(10):1311-25. Circulation. 2006 Mar 14;113(10):1326-34. You can't judge a book by its cover. Menasche P. Publication Types: Comment Editorial PMID: 16534026 [PubMed - indexed for MEDLINE] 7: Circulation. 2006 Mar 14;113(10):1295-304. Epub 2006 Mar 6. Related Articles, Books, LinkOut Hemodynamic effects of long-term cardiac resynchronization therapy: analysis by pressure-volume loops. Steendijk P, Tulner SA, Bax JJ, Oemrawsingh PV, Bleeker GB, van Erven L, Putter H, Verwey HF, van der Wall EE, Schalij MJ. Department of Cardiology, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands. p.steendijk at lumc.nl BACKGROUND: Acute hemodynamic effects of cardiac resynchronization therapy (CRT) were reported previously, but detailed invasive studies showing hemodynamic consequences of long-term CRT are not available. METHODS AND RESULTS: We studied 22 patients scheduled for implantation of a CRT device based on conventional criteria (New York Heart Association class III or IV, left ventricular [LV] ejection fraction <35%, left bundle-branch block, and QRS duration >120 ms). During diagnostic catheterization before CRT, we acquired pressure- volume loops using conductance catheters during atrial pacing at 80, 100, 120, and 140 bpm. Studies were repeated during biventricular pacing at the same heart rates after 6 months of CRT. Our data show a significant clinical benefit of CRT (New York Heart Association class change from 3.1+/-0.5 to 2.1+/-0.8; quality-of-life score change from 44+/-12 to 31+/-16; and 6-minute hall-walk distance increased from 260 +/-149 to 396+/-129 m; all P<0.001), improved LV ejection fraction (from 29+/-10% to 40+/-13%, P<0.01), decreased end-diastolic pressure (from 18+/-8 to 13+/-6 mm Hg, P<0.05), and reverse remodeling (end- diastolic volume decreased from 257+/-67 to 205+/-54 mL, P<0.01). Previously reported acute improvements in LV function remained present at 6 months: dP/dtmax increased 18%, -dP/dtmin increased 13%, and stroke work increased 34% (all P<0.01). Effects of increased heart rate were improved toward more physiological responses for LV ejection fraction, cardiac output, and dP/dtmax. Moreover, our study showed improved ventricular-arterial coupling (69% increase, P<0.01) and improved mechanical efficiency (44% increase, P<0.01). CONCLUSIONS: Hemodynamic improvements with CRT, previously shown in acute invasive studies, are maintained chronically. In addition, ventricular-arterial coupling, mechanical efficiency, and chronotropic responses are improved after 6 months of CRT. These findings may help to explain the improved functional status and exercise tolerance in patients treated with CRT. Publication Types: Clinical Trial PMID: 16520415 [PubMed - indexed for MEDLINE] 8: Am J Cardiol. 2006 Mar 15;97(6):899-904. Epub 2006 Feb 3. Related Articles, Books, LinkOut Usefulness of atorvastatin in patients with heart failure due to inflammatory dilated cardiomyopathy and elevated cholesterol levels. Wojnicz R, Wilczek K, Nowalany-Kozielska E, Szygula-Jurkiewicz B, Nowak J, Polonski L, Dyrbus K, Badzinski A, Mercik G, Zembala M, Wodniecki J, Rozek MM. 3rd Department of Cardiology, Silesian Center for Heart Disease, Zabrze, Poland. wojnicz at dom.zab This study evaluated the safety, tolerability, and efficacy of statin therapy in patients with heart failure secondary to inflammatory dilated cardiomyopathy and moderately elevated low-density lipoprotein cholesterol levels. Seventy-four patients were randomized to receive atorvastatin 40 mg/day or conventional treatment for heart failure. After 6 months of therapy, the predefined primary efficacy end point (an increase of >5% in the absolute left ventricular ejection fraction and > or =2 selected criteria by echocardiography and a decrease in New York Heart Association functional class) was significant in the statin-treated patients (p = 0.004). Among secondary efficacy parameters, the quality-of-life index showed a trend suggesting the benefit of statin therapy (p = 0.055). In conclusion, the results of this study demonstrate that treatment with atorvastatin in addition to standard therapy for heart failure may significantly improve clinical outcomes in this cohort of patients. Publication Types: Multicenter Study Randomized Controlled Trial PMID: 16516598 [PubMed - indexed for MEDLINE] 9: Am J Cardiol. 2006 Mar 15;97(6):886-90. Epub 2006 Jan 26. Related Articles, Books, LinkOut Usefulness of a home-based exercise program for overweight and obese patients with advanced heart failure. Evangelista LS, Doering LV, Lennie T, Moser DK, Hamilton MA, Fonarow GC, Dracup K. School of Nursing, University of California, Los Angeles, USA. levangel at ucla.edu Exercise is an important behavior for long-term weight control in overweight and obese patients. However, little evidence exists confirming such findings in patients with advanced heart failure (HF). Using a prospective, experimental design, the effects of 24 weeks of a low-level, home-based walking program on weight loss were studied in overweight and obese (body mass index > or =27 kg/m(2)) patients with advanced HF who were randomized to exercise (n = 48) and control (n = 51) groups. Weight changes between the 2 groups at baseline and 6 months were compared using repeated-measures analysis of variance. Patients were on average aged 53.3 +/- 10.1 years and predominantly male (75%), Caucasian (57%), and married (55%). Most patients were in New York Heart Association class III or IV (67%), with a mean ejection fraction of 25%. Patients in the exercise group showed significant weight reduction from baseline to 6 months compared with those in the control group (-6.37 +/- 11.7 vs -0.33 +/- 9.3 kg, p = 0.002). No significant differences were noted between the 2 groups in 6-minute walk distance or depression, although the changes were in the anticipated direction. Modest weight losses of >5% were associated with cardiopulmonary exercise test-documented workload levels at 6 months (r = 0.331, p = 0.006), as well as decreased depression (r = -0.315, p = 0.01) and hostility (r = -0.355, p = 0.005). The number of hospital admissions was significantly smaller for patients in the exercise group compared with those in the control group (0.63 +/- 0.94 vs 1.07 +/- 0.95, p <0.05). In conclusion, the findings demonstrate the beneficial effects of a low-level, home-based walking program on weight loss in overweight and obese patients with advanced HF. Publication Types: Randomized Controlled Trial PMID: 16516595 [PubMed - indexed for MEDLINE] 10: Am J Cardiol. 2006 Mar 15;97(6):882-5. Epub 2006 Jan 30. Related Articles, Books, LinkOut Proportion of patients followed in a specialized heart failure clinic needing an implantable cardioverter defibrillator as determined by applying different trial eligibility criteria. Toma M, McAlister FA, Ezekowitz J, Kimber S, Gulamhusein S, Pantano A, Sivakumaran S, Cujec B, Paterson I, Armstrong PW. Division of General Internal Medicine, University of Alberta, Edmonton, Canada. Numerous trials have demonstrated survival benefits using implantable cardioverter defibrillators (ICDs) for primary prevention in selected patients with left ventricular (LV) systolic dysfunction. However, eligibility criteria differed across these trials. Without a risk stratification scheme that clearly identifies those who will benefit, there remains debate about which patients with heart failure (HF) should receive ICDs for primary prevention. To explore the implications of applying different eligibility criteria, this study evaluated all patients seen in a specialized HF clinic from August 2003 to January 2004. Of the 309 consecutive patients in the cohort, 46 were excluded because their HF complicated recent myocardial infarcts (n = 3); their LV ejection fractions were not measured (n = 9); or their HF was due to valvular disease, myocarditis, or peripartum cardiomyopathy (n = 34). The Multicenter Automatic Defibrillator Implantation Trial-II criteria were met by 85 patients (32%), and 134 patients (51%) met the Sudden Cardiac Death in Heart Failure Trial criteria. Even allocation decisions based on randomized trial evidence can have vastly different resource implications depending on which trial is chosen. Thus, the development and validation of a risk stratification scheme to identify those patients most likely to benefit from ICDs for primary prophylaxis should be a research priority. PMID: 16516594 [PubMed - indexed for MEDLINE] 11: Am J Cardiol. 2006 Mar 15;97(6):876-81. Epub 2006 Jan 30. Related Articles, Books, LinkOut Relation of response to cardiac resynchronization therapy to left ventricular reverse remodeling. Vidal B, Sitges M, Marigliano A, Diaz-Infante E, Azqueta M, Tamborero D, Macias A, Roig E, Brugada J, Pare C, Mont L. Thorax Clinic Institute, Hospital Clinic, Institut d'Investigacions Biomediques August Pi i Sunyer, University of Barcelona, Spain. mstiges at clinic.ub.es Cardiac resynchronization therapy (CRT) reverses left ventricular (LV) remodeling in patients with congestive heart failure. However, the mechanisms leading to the clinical response to CRT remain unclear. The aim of this study was to analyze whether patients who improve clinically have greater LV reverse remodeling than nonresponders after a 12-month follow-up period. The sample comprised 64 consecutive patients with heart failure, complete left bundle branch block, and LV ejection fractions (EFs) < or =35% who were treated with CRT. Doppler echocardiographic scans were taken just before and immediately after the implantation of the pacemakers and at 6- and 12-month follow-up examinations. LV diameters, volumes, and EFs were compared. Responders were defined as those patients who were alive without cardiac transplantation and with > or =10% improvement in the 6-minute walking test after 1 year of follow-up. There were no clinical differences at baseline between responders and nonresponders. At 6- and 12-month follow-up, LV dimensions decreased significantly in responders but did not change in nonresponders. Furthermore, LVEFs improved only in responders. In conclusion, patients who clinically respond to CRT have greater LV reverse remodeling than nonresponders after 6 and 12 months of follow-up. The effect of CRT on LV remodeling may explain, at least in part, the clinical benefit of this therapy. PMID: 16516593 [PubMed - indexed for MEDLINE] 12: Am J Cardiol. 2006 Mar 15;97(6):872-5. Epub 2006 Jan 25. Related Articles, Books, LinkOut Usefulness of isovolumic and systolic ejection signals by tissue Doppler for the assessment of left ventricular systolic function in ischemic or idiopathic dilated cardiomyopathy. Ruan Q, Nagueh SF. First Affiliated Hospital of Fujian Medical University, Fuzhou, China. Echo cardiography is the imaging modality most frequently used to assess left ventricular ejection fraction (EF). However, the accuracy of the EF can be limited by the technical quality of the examination and observer variability. Recently, tissue Doppler was applied to acquire signals of myocardial systolic function, including systolic ejection velocity (S(a)) and the systolic isovolumic acceleration rate (IVA). In that regard, IVA was reported in animal studies to be the ideal noninvasive index, because it was not affected by preload and afterload and provided a reliable assessment of contractility when examined against invasive gold standards. However, a paucity of data is available about its clinical application. We undertook this investigation to examine S(a) and IVA in 40 normal subjects and 52 patients with depressed EF referred for echocardiographic examination, aiming to identify the signal with the highest reproducibility and the most accurate detection of depressed EF. S(a) had the least inter- and intraobserver variabilities (3 +/- 1.5% and 2.5 +/- 1%, respectively), and IVA had the highest variability (8.1 +/- 2.1% and 6.8 +/- 2%, respectively). Although S(a) and IVA were significantly lower in patients with depressed EF (p <0.05), S(a) had the best correlation with EF (r = 0.65, p <0.03) and S(a) of <7 cm/s was the most accurate (p <0.05 vs IVA) in identifying patients with EF <45% (sensitivity 93%, specificity 87%). In conclusion, S(a) velocity is the most suitable signal for clinical application as a surrogate for left ventricular EF, given its accuracy and reproducibility. PMID: 16516592 [PubMed - indexed for MEDLINE] 13: Am J Cardiol. 2006 Mar 15;97(6):866-71. Epub 2006 Jan 30. Related Articles, Books, LinkOut Comparison of usefulness of echocardiographic Doppler variables to left ventricular end-diastolic pressure in predicting future heart failure events. Liang HY, Cauduro SA, Pellikka PA, Bailey KR, Grossardt BR, Yang EH, Rihal C, Seward JB, Miller FA, Abraham TP. Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA. We sought to determine whether the echocardiographic Doppler parameters of left ventricular diastolic dysfunction predict future heart failure (HF) events and, if so, which parameters best predict HF. We also examined whether the predictive ability of echocardiographic Doppler parameters was related to their prediction of left ventricular end-diastolic pressure (LVEDP). We studied patients who underwent cardiac catheterization and echocardiography performed within a 30-day period. The end point was HF, defined as new-onset or recurrent HF diagnosed by a physician and requiring the initiation or modification of treatment of HF. We identified 289 patients (mean age 63.5 +/- 12.6 years) with a mean follow-up of 10.9 +/- 10.2 months. A total of 24 HF events occurred. LVEDP was a significant predictor of HF univariately and independently in multiple regression models after adjustment for ejection fraction. In Cox models adjusted for age, gender, LVEDP, and ejection fraction, only the left atrial volume index and early mitral inflow to early diastolic tissue velocity (E/e') ratio remained predictive of HF. A multiple regression model, including all echocardiographic variables, showed a persistent, although attenuated, relation of early to late mitral inflow velocity (E/A) ratio and E/e' with LVEDP (p = 0.06 and p = 0.002, respectively). The addition of E/e' or the left atrial volume indexed to body surface area, but not E/A, to the clinical history and left ventricular ejection fraction provided incremental prognostic information. A LVEDP of > or =20 mm Hg, E/e' ratio of > or =15, and left atrial volume index of > or =23 ml/m(2) identified those with a higher risk of HF. In conclusion, invasively determined LVEDP is an independent predictor of future HF events. E/e' and the left atrial volume indexed to body surface area are the best independent predictors of future HF and provide prognostic information incremental to the clinical history and left ventricular ejection fraction. PMID: 16516591 [PubMed - indexed for MEDLINE] 14: Monaldi Arch Chest Dis. 2005 Jun;64(2):148-50. Books, LinkOut [Rehabilitation and models of domiciliary care of patients with chronic heart failure. the Gussago experience] [Article in Italian] Zanelli E. Divisione di Cardiologia Riabilitativa, IRCCS Fondazione Salvatore Maugeri, Istituto Medico di Gussago-Lumezzane. czanelli at fsm.it PMID: 16499309 [PubMed - indexed for MEDLINE] 15: Monaldi Arch Chest Dis. 2005 Jun;64(2):145-7. Books, LinkOut [Domiciliary telemonitoring of vital and cardiorespiratory signs of the HHH project] [Article in Italian] Pinna GD, Maestri R, Capomolla S. IRCCS Fondazione Salvatore Maugeri, Istituto Scientifico di Montescano. gdpinna at fsm.it PMID: 16499307 [PubMed - indexed for MEDLINE] 16: Monaldi Arch Chest Dis. 2005 Jun;64(2):143-5. Books, LinkOut [Rehabilitation and models of domiciliary care of patients with chronic heart failure: preliminary results of the HHH study] [Article in Italian] Mortara A, Pinna GD, Capomolla S, Maestri R, Johnson P, La Rovere MT, Ponikowski P, Tavazzi L, Sleight P; Studio HHH. Divisione di Cardiologia e Unita Scompenso Cardiaco, Policlinico di Monza, Monza. PMID: 16499306 [PubMed - indexed for MEDLINE] 17: Monaldi Arch Chest Dis. 2005 Jun;64(2):140-1. Books, LinkOut [Training of the health personnel: the nurse] [Article in Italian] Martinelli G, Baratti D, Marchina L, Scalvini S, Giordano A. Servizio di Telemedicina, IRCCS Fondazione Salvatore Maugeri, Istituto Scientifico di Gussago/Lumezzane. gmartinelli at e-htn.it PMID: 16499304 [PubMed - indexed for MEDLINE] 18: Monaldi Arch Chest Dis. 2005 Jun;64(2):137-8. Books, LinkOut [Domiciliary care of post-acute patient: experience at the "Umberto I" polyclinic] [Article in Italian] Fedele F. Policlinico Umberto I, Roma. PMID: 16499301 [PubMed - indexed for MEDLINE] 19: Monaldi Arch Chest Dis. 2005 Jun;64(2):135-6. Books, LinkOut [The telemonitoring service] [Article in Italian] Capomolla S, Pinna G, Maestri R, Ferrari M, Ceresa M. IRCCS Fondazione Salvatore Maugeri, Istituto Scientifico Montescano, Montescano PV, Italia. scapomolla at fsm.it PMID: 16499299 [PubMed - indexed for MEDLINE] 20: Monaldi Arch Chest Dis. 2005 Jun;64(2):124-33. Related Articles, Books, LinkOut Anemia in chronic heart failure patients: comparison between invasive and non-invasive prognostic markers. Ceresa M, Capomolla S, Pinna G, Aiolfi E, La Rovere MT, Febo O, Paganini V, Rossi A, Guazzotti G, Caporotondi A, Maestri R, Cobelli F. IRCCS Fondazione Salvatore Maugeri, Istituto Scientifico di Montescano (PV), Italia. BACKGROUND: The prognosis of chronic heart failure (CHF) remains poor despite advances in medical management. Several different variables determine prognosis. Recently anemia has emerged as an independent prognostic variable in the evaluation of CHF. It is therefore important to analyze the role of anemia in patients with mild to severe CHF already well characterized by hemodynamic, echo-Doppler, and cardiopulmonary exercise testing. OBJECTIVE: We performed this study to evaluate, in a large general cohort of CHF patients, the frequency of anemia and its correlation with their clinical profile. We assessed the prognostic value of anemia in relation to other known prognostic variables. METHODS: Two-dimensional echocardiography, right heart catheterization, cardiopulmonary tests and laboratory examinations were performed in a population of 980 consecutive patients with CHF (53 +/- 9.4 years, 85% male, LVEF 25 +/- 8%; 45% with NYHA class III-IV). A hemoglobin (Hb) concentration less than 12 g/dl was used to define anemic patients. The primary end point was cardiac death or urgent heart transplantation. RESULTS: Nineteen percent of patients were anemic. These patients had a lower body mass index (24 +/- 3 vs. 25 +/- 4 Kg/m2 p < 0.0004), a worse functional class (64% were in NYHA class III-IV vs 41% in the non-anemic group, p < 0.0001), poorer exercise capacity (12.4 vs. 14.8 ml/kg/min peak VO2, p < 0.0001) and increased right (7 +/- 5 vs. 5 +/- 4 mmHg, p < . 0004) and left (21 +/- 9 vs. 19 +/- 10 p < 0.007) ventricular filling pressures. During a 3-year follow-up cardiac deaths occurred in 236 (24%) and 52 (5%) of patients received an urgent heart transplant. On univariate regression analysis anemia was significantly correlated with these "hard" cardiac events (39% of anemic patients vs 27% of non-anemic patients). By multivariate logistic regression analysis different prognostic models were identified using non-invasive, with or without peak VO2, or invasive parameters. The prognostic model including anemia (AUC(ROC): 0.720) showed similar accuracy in predicting cardiac events to other prognostic models with peak VO2 (AUC(ROC): 0.719) or invasive variables (AUC(ROC): 0.719). CONCLUSIONS: The present study demonstrates that anemia in CHF patients is associated with prognosis, worse NYHA functional class, exercise capacity and hemodynamic profiles. The relationship between anemia and mortality is independent of other simple non-invasive prognostic factors. Prognostic models with more complex or invasive independent predictors did not increase the accuracy to predict cardiac mortality or the need for urgent transplantation. PMID: 16499298 [PubMed - indexed for MEDLINE] 21: Monaldi Arch Chest Dis. 2005 Jun;64(2):100-4. Related Articles, Books, LinkOut The Left Ventricular Dysfunction Questionnaire: Italian translation and validation. Miani D, Gregori D, Ghidina M, Rozbowsky P, Pilotto L, Albanese MC, Fresco C, Fioretti PM. Department of Cardiopulmonary Sciences, Ospedale S. Maria Della Misericordia, Udine, Italy. Patients affected by heart failure have a compromised quality of life (QOL) and in the last few years "health related quality of life" has become an important outcome indicator for the evaluation of heart failure treatment. Methods: Translation into Italian of the Left Ventricular Dysfunction Questionnaire (LVD-36), a new, 36-item, disease-specific health status instrument for patients with congestive heart failure, and its subsequent validation by administration to 50 consecutive patients in our heart failure outpatient clinic. The Italian LVD-36 was compared to the "The Minnesota Living with Heart Failure Questionnaire" (MLHF). Results: The Italian version of the LVD-36 correlates well with MLHF for ejection fraction (EF), NYHA class I and II, etiology and therapy. Since, however, the LVD-36 has only one domain, it may be able to offer more synthetic information than MLHF about patients' status. Conclusions: The Italian version of the LVD-36 appears to be a reliable instrument for assessing patients' QOL and the degree of limitations imposed on them by the disease. It is short, clear and easy to complete. In patients with heart failure the LVD-36 correlates well with the MLHF and may be considered a new disease- specific instrument to estimate changes in health status, and an useful support in optimizing therapeutic options. Publication Types: Evaluation Studies PMID: 16499294 [PubMed - indexed for MEDLINE] 22: Monaldi Arch Chest Dis. 2005 Jun;64(2):94-9. Related Articles, Books, LinkOut [Favourable effects of cardiovascular rehabilitation on funcional capacity and autonomic balance in elderly patients with heart failure] [Article in Italian] Malfatto G, Branzi G, Bizzi C, Valli P, Facchini M. Divisione di Riabilitazione Cardiologica, Istituto Scientifico Ospedale San Luca, Istituto Auxologico Italiano IRCCS, Milano, Italy. malfi at auxologico.it In 42 patients with chronic heart failure we evaluated left ventricular function, exercise capability and autonomic control before and 3 months after a program of cardiovascular rehabilitation. The results were analyzed separately for younger (Group 1, n=18, age 51 +/- 6 years) and older patients (Group 2, n=24, age 68 +/- 4 years), with comparable clinical characteristics and therapy. Before rehabilitation, compared to younger patients, Group 2 patients showed a lower exercise capability, a comparable left ventricular ejection fraction and similar high sympathetic activity at rest, with no response to regular breathing (= stimulation of cardiopulmonary receptors, i.e. parasympathetic challenge) and active standing (= sympathetic stimulation). After rehabilitation, in both groups a 20% improvement of exercise tolerance and aerobic performance was observed, as well as a slightly increase of left ventricular ejection fraction (about 10%), and a recovery in vagal and sympathetic responsiveness. Thus, in heart failure patients age does not hinder the favorable clinical and autonomic modulation induced by cardiovascular rehabilitation. PMID: 16499293 [PubMed - indexed for MEDLINE] 23: Monaldi Arch Chest Dis. 2005 Jun;64(2):88-93. Related Articles, Books, LinkOut Exercise rehabilitation in heart disease: the real "polypill" for primary and secondary prevention. Piepoli MF. Our society is currently at war against the ominous enemy of chronic disease. Chronic disease presents a heavy burden to society, in terms of both medical costs and human suffering. It is our perception that: 1) much of the medical community underpractises primary prevention as regards appropriate levels of physical activity for health, and 2) much of the research community undervalues the importance of understanding the physiological, genetic and clinical bases of diseases caused by physical inactivity. For many, exercise is viewed solely as a research or diagnostic tool and not as a true weapon against chronic disease. In reality, however, exercise attacks the roots of chronic disease, i.e. physical inactivity. The first step in a common "battle plan" is to convince the medical community that chronic disease is rooted in physical inactivity. In this review, we focus on the biological evidence to date showing how physical inactivity leads to chronic disease. One purpose of this review is to demonstrate that exercise, such as treadmill testing of humans for cardiac dysfunctions, is more than a diagnostic tool but part of disease management itself. Publication Types: Editorial Review PMID: 16499292 [PubMed - indexed for MEDLINE] 24: J Vet Intern Med. 2006 Jan-Feb;20(1):104-10. Related Articles, Books, LinkOut Prognostic indicators for dogs with dilated cardiomyopathy. Borgarelli M, Santilli RA, Chiavegato D, D'Agnolo G, Zanatta R, Mannelli A, Tarducci A. Department Patologia Animale, Faculty Veterinary Medicine, Grugliasco, Italy. michele.borgarelli at unito.it The purpose of this study was to investigate the prognostic value of various clinical, ECG, echocardiographic, and Doppler echocardiographic variables in dogs with dilated cardiomyopathy. The relationship to survival of 11 variables was evaluated in 63 dogs. Studied variables were age at time of diagnosis, class of heart failure (HF), dyspnea, ascites, atrial fibrillation (AF), ejection fraction (EF), E-point septal separation, end-diastolic volume index, end-systolic volume index (ESV-I), and restrictive or nonrestrictive transmitral flow (TMF) pattern. Median survival time was 671 days (lower 95% confidence limit, 350 days). Survival curves showed that severity of HF, ascites, ESV-I greater than 140 mL/m2, EF less than 25%, and restrictive TMF pattern had a significant negative relation to survival time. Thirty-nine dogs with both sinus rhythm and AF presented adequate TMF recordings; in these dogs, after stratification by TMF pattern, the restrictive TMF pattern was the most important negative prognostic indicator. We conclude that in dogs with dilated cardiomyopathy the restrictive TMF pattern appears to represent a useful prognostic indicator. Class of HF, ascites, ESV- I, and EF are also useful indexes if an adequate TMF pattern is not recorded. PMID: 16496929 [PubMed - indexed for MEDLINE] 25: J Vet Intern Med. 2006 Jan-Feb;20(1):97-103. Related Articles, Books, LinkOut Third-degree atrioventricular block in 21 cats (1997-2004). Kellum HB, Stepien RL. Department of Medical Sciences, University of Wisconsin School of Veterinary Medicine, Madison, WI 53706, USA. The effect of 3rd-degree atrioventricular block on long-term outcome in cats is unknown. Clinical findings and long-term outcome of 21 cats with 3rd-degree atrioventricular block were studied retrospectively. Median age of cats studied was 14 years (range 7-19 years). Presenting signs included respiratory distress or collapse, but 6 cats had no clinical signs of disease. Eight cats had congestive heart failure (CHF) at the time that 3rd-degree atrioventricular block was detected. Heart rates ranged from 80 to 140 beats per minute (bpm; median 120 bpm) with no difference in heart rate between cats with and those without CHF. Eleven of 18 cats that had echocardiograms had structural cardiac disease, and 6 cats had cardiac changes consistent with concurrent systemic disease. No atrioventricular nodal lesions were detected by echocardiography. One cat had atrioventricular nodal lesions detected on histologic examination. Median survival of 14 cats that died or were euthanized was 386 days (range 1-2,013 days). Survival did not differ between cats with or without CHF or between cats with or without structural cardiac disease. Thirteen cats with 3rd-degree atrioventricular block survived > 1 year after diagnosis, regardless of presenting signs or underlying cardiac disease. Third-degree heart block in cats is often not immediately life threatening. Survival was not affected by the presence of underlying heart disease or congestive heart failure at the time of presentation. Even cats with collapse might survive > 1 year without pacemaker implantation. PMID: 16496928 [PubMed - indexed for MEDLINE] 26: J Vet Intern Med. 2006 Jan-Feb;20(1):65-77. Related Articles, Books, LinkOut Pulsed tissue Doppler imaging in normal cats and cats with hypertrophic cardiomyopathy. Koffas H, Dukes-McEwan J, Corcoran BM, Moran CM, French A, Sboros V, Simpson K, McDicken WN. Department of Veterinary Clinical Studies, University of Edinburgh, Scotland, UK. h.koffas at rvc.ac.uk Myocardial motion was quantified in normal cats (n = 25) and cats with hypertrophic cardiomyopathy (HCM) (n = 23) using the pulsed tissue Doppler imaging (TDI) technique. A physiologic nonuniformity was documented in the myocardial motion of normal cats, which was detected as higher early diastolic velocities, acceleration, and deceleration in the interventricular septum compared with the left ventricular free wall (LVFW). HCM cats exhibited lower early diastolic velocities, acceleration, and deceleration and also prolonged isovolumic relaxation time compared with normal cats. These differences were detected mainly along the longitudinal axis of the heart. A cutoff value of E' in the LVFW along the longitudinal axis >7.2 cm/s discriminated normal from HCM cats with a sensitivity of 92% and a specificity of 87%. The physiologic nonuniformity of myocardial motion during diastole was lost in affected cats. Systolic impairment (decreased late-systolic velocities in most segments along the longitudinal axis and decreased early systolic acceleration in both mitral annular sites) was evident in HCM cats irrespective of the presence of left ventricular outflow tract obstruction and congestive heart failure. Postsystolic thickening was recorded in the LVFW along the longitudinal axis only in affected cats (n = 6) and was another finding indicative of systolic impairment in the HCM of this species. This study identified both diastolic and systolic impairment in cats with HCM compared with normal cats. The study also documents the normal physiologic nonhomogeneity in myocardial motion in cats and the subsequent loss of this feature in the HCM diseased state. Publication Types: Clinical Trial PMID: 16496925 [PubMed - indexed for MEDLINE] 27: Dev Med Child Neurol. 2006 Mar;48(3):231-5. Related Articles, Books, LinkOut Cardiac monitoring and treatment for children and adolescents with neuromuscular disorders. English KM, Gibbs JL. Department of Congenital Cardiology, Yorkshire Heart Centre, Leeds General Infirmary, Leeds LS1 3EX, UK. kate.english at leedsth.nhs.uk Dilated cardiomyopathy, hypertrophic cardiomyopathy, and cardiac rhythm disturbances are important features of certain neuromuscular disorders in children, adolescents, and young adults. This article summarizes the cardiac features seen in patients with Duchenne muscular dystrophy, Becker muscular dystrophy, myotonic dystrophy, Friedreich's ataxia, and Emery-Dreifuss muscular dystrophy. The optimal management of these cardiac features remains contentious, but increasingly these patients are referred for routine cardiological assessment in the absence of symptoms. This article examines the value of routine screening and drug interventions for cardiac complications in asymptomatic and symptomatic individuals with neuromuscular disorders. We recommend a pragmatic approach, actively looking for cardiac conditions which will benefit from early intervention, but avoiding routine screening for asymptomatic conditions in which there is no evidence of benefit from early intervention. Publication Types: Review PMID: 16483403 [PubMed - indexed for MEDLINE] 28: Dev Med Child Neurol. 2006 Mar;48(3):164. Related Articles, Books, LinkOut Cardiac monitoring and treatment for children and adolescents with neuromuscular disorders. Bourke JP. Freeman Hospital, Newcastle-upon-Tyne, UK. PMID: 16483389 [PubMed - indexed for MEDLINE] 29: Clin Med. 2005 Nov-Dec;5(6):626-9. Related Articles, Books, LinkOut Palliative medicine for the cancer and non-cancer patient. Kite S, Hicks F. The Leeds Teaching Hospitals Trust, Leeds General Infirmary/Cookridge Hospital. Suzanne.kite at leedsth.nhs.uk Publication Types: Review PMID: 16411360 [PubMed - indexed for MEDLINE] 30: Neurology. 2005 Dec 27;65(12):1997; author reply 1997. Related Articles, Books, LinkOut Comment on: Neurology. 2004 Dec 28;63(12 Suppl 6):S28-32. Mitoxantrone treatment of multiple sclerosis: safety considerations. Pratt RG, Boehm GA, Kortepeter CM, Racoosin JA. Publication Types: Comment Letter PMID: 16380636 [PubMed - indexed for MEDLINE] 31: Expert Opin Investig Drugs. 2005 Jun;14(6):659-70. Related Articles, Books, LinkOut An emerging role for calcium sensitisation in the treatment of heart failure. Erhardt L. Lund University, Malmo University Hospital, 205 02 Malmo, Sweden. Leif.Erhardt at medforsk.mas.lUSe Heart failure occurs in 2 - 3% of the adult population in the developed world. With decompensation of cardiac function, haemodynamic stability can be achieved by using intravenous vasodilators, diuretics and inotropes. Unlike traditional inotropes, Ca2+ sensitisers enhance cardiac function without significantly increasing cardiac oxygen consumption, promoting arrhythmia or impairing lusitropy. The most promising drug in this new class is levosimendan, which has a unique dual mechanism; it enhances cardiac output through a Ca(2+)-dependent stabilisation of cardiac myofilaments and exhibits vasodilatory effects by opening ATP- dependent K(+) channels. Clinical trials have demonstrated the beneficial haemodynamic effects of levosimendan, and prospective trials are currently underway to confirm its potential benefits on long-term prognosis. Updated guidelines from the European Society of Cardiology advise on how to incorporate levosimendan into care for patients who have acute heart failure. Publication Types: Review PMID: 16004594 [PubMed - indexed for MEDLINE] 32: Ann Hum Genet. 2005 Jul;69(Pt 4):382-8. Related Articles, Books, LinkOut HLA-DQA1, -DQB1 polymorphism and genetic susceptibility to idiopathic dilated cardiomyopathy in Hans of northern China. Liu W, Li WM, Sun NL. Department of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin 150001, China. doctor_liuwei at yahoo.com.cm Autoimmune mechanisms are likely to participate in the pathogenesis of at least a subgroup of idiopathic dilated cardiomyopathy (IDC), and components of the major histocompatibility complex (MHC) may serve as markers for the propensity to develop immune-mediated myocardial damage. Human leukocyte antigen (HLA) class II genes, especially HLA-DQ genes, which are highly polymorphic, play an important role in the activation of immune responses and thus control the predisposition to, or protection from, IDC. This study was conducted to investigate the association of HLA-DQA1, -DQB1 allele polymorphisms with an autoantibody against the myocardial mitochondria ADP/ATP carrier, and to explore susceptibility to idiopathic dilated cardiomyopathy (IDC) among the Han ethnic group in northern China and the immunological mechanisms and hereditary susceptibility to IDC. Polymerase chain reaction sequence-specific primer (PCR-SSP) techniques were used to analyze polymorphisms of the second exon of HLA-DQA1 and -DQB1 alleles among 68 unrelated IDC patients, 4 probands of IDC pedigrees, and 100 healthy controls, all of Han nationality and having lived in northern China for a long time. Following echocardiography examination the IDC subjects were stratified according to ejection fraction (EF) values. Those with EF values higher than 50% were placed in subgroup 1, subgroup 2 included the patients with an EF value of 15-35%, and subgroup 3 consisted of those whose EF values were less than 15%. An autoantibody against the myocardial mitochondria ADP/ATP carrier was examined using immunoblot analysis. The frequencies of HLA-DQA1*0501 and HLA-DQB1*0303 were 0.3889 and 0.1806 in the IDC group, significantly higher than those of the healthy controls (0.0900 and 0.0364 respectively, both P < 0.05). The OR was 5.20 (95% CI: 3.60-8.50) and 4.85 (95% CI: 2.56-9.39) respectively. Further analysis of the three subgroups showed a higher frequency of HLA-DQA1*0501 among patients whose EF was less than 15% than those whose EF values were > or =15%. Conversely, the frequencies of HLA-DQA1*0201 and -DQB1*0502, *0504 were significantly lower in the IDC group (0.0139, 0.0139 and 0.0417 respectively) than in the control group (0.2000, 0.0727 and 0.1091 respectively) (P < 0.05). The frequency of the HLA-DQA1*0501 allele was significantly higher in IDC patients whose autoantibody is positive in contrast with those whose autoantibody is negative (18.57% vs. 5.86%, P < 0.05); the relative risk (RR) was 4.32. The other frequencies of HLA-DQA1 and -DQB1 alleles showed no significant difference in the antibody positive and negative groups of IDC patients. The alleles of HLA-DQA1*0501 and HLA-DQB1*0303 were closely associated with poor EF values in the IDC group, and may be involved in susceptibility to the disease. The DQA1*0201 and DQB1*0502, *0504 alleles may confer protection to IDC among individuals of northern Chinese Han nationality. The SER(57) residue in the second exon of DQB1*0502 and *0504 may confer resistance to IDC, and defects or substitution of this amino acid residue at position 57 of the DQbeta chain may be associated with IDC susceptibility. HLA-DQ allele polymorphisms may serve as genetic markers for IDC and be involved in the regulation of the immune specific response to auto or exterior anti-myocardium antibodies. PMID: 15996167 [PubMed - indexed for MEDLINE] 33: Expert Opin Investig Drugs. 2005 May;14(5):687-91. Related Articles, Books, LinkOut The therapeutic potential of vasopressin receptor antagonists in congestive heart failure. Salam AM. Department of Cardiology and Cardiovascular Surgery, Hamad Medical Corporation, PO Box 3050, Doha, Qatar. amaramin at yahoo.com Hospitalisation of patients presenting with deteriorating congestive heart failure is occurring with increasing frequency and is associated with significant morbidity and mortality. Diuretic use, the mainstay therapy for congestion, is associated with electrolyte abnormalities and deteriorating renal function. In a recent randomised study, tolvaptan, a novel vasopressin antagonist, in addition to standard therapy including diuretics, increased net fluid loss resulting in decreased body weight more effectively than standard therapy alone in patients hospitalised for heart failure. This desirable effect was achieved without adversely affecting blood pressure, heart rate, electrolyte levels, or renal function. Although tolvaptan did not reduce the rate of deteriorating heart failure after discharge, post hoc analysis suggested that mortality might be reduced in high-risk patients treated with tolvaptan. These results make an important contribution to heart failure research, and offer an insight into the future role of vasopressin antagonism in the treatment of congestive heart failure. PMID: 15926874 [PubMed - indexed for MEDLINE] 34: Expert Opin Investig Drugs. 2005 May;14(5):593-600. Related Articles, Books, LinkOut Vasopressin receptor antagonists in the management of acute heart failure. Tang WH, Bhavnani S, Francis GS. Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA. tangw at ccf.org Vasopressin is a potent vasoconstrictor and plays a significant role in the regulation of volume homeostasis. Several non-peptide vasopressin receptor antagonists (vaptans) have emerged as promising drugs in the management of acute heart failure. Results of early trials with tolvaptan (selective vasopressin subtype 2 receptor antagonist) and conivaptan (dual vasopressin subtypes 1a and 2 receptor antagonist) have demonstrated improvement in the fluid status, osmotic balance and haemodynamic profile in patients with heart failure presenting with signs and symptoms of decompensation. Nevertheless, their comparative long-term safety and efficacy remains to be determined in large-scale clinical trials. Publication Types: Review PMID: 15926866 [PubMed - indexed for MEDLINE] 35: Expert Opin Investig Drugs. 2005 May;14(5):567-77. Related Articles, Books, LinkOut Depression in chronic heart failure: novel pathophysiological mechanisms and therapeutic approaches. Parissis JT, Fountoulaki K, Paraskevaidis I, Kremastinos D. Attikon University Hospital Heart Failure Clinic, Aftocratoros Irakliou 17, 15122, Maroussi, Athens, Greece. jparissis at yahoo.com Depression is four to five times as common in chronic heart failure (CHF) patients as in the general population, may confer a higher risk of developing CHF in susceptible populations, and is significantly related to higher hospital readmission rates and increased mortality in established CHF. This effect may be mediated via the pathophysiological mechanisms that are shared between CHF and depression, including increased hypothalamic-pituitary-adrenal function, sympathoadrenal hyperactivity, diminished heart-rate variability and excessive pro-inflammatory cytokine activation. Each of these pathways of linkage represents a potential therapeutic target to improve outcome in CHF. This paper reviews the recent investigational observations that clarify the direct effects of antidepressants on immune functions, as well as the indirect effects of anticytokine pharmacological agents on depressive symptoms in CHF. With recent evidence suggesting that selective serotonin re-uptake inhibitors improve survival after myocardial infarction in patients with depression, diagnosis and treatment of this comorbidity may beneficially affect the functional capacity and prognosis of CHF patients. Publication Types: Review PMID: 15926864 [PubMed - indexed for MEDLINE] 36: Expert Opin Investig Drugs. 2005 May;14(5):557-66. Related Articles, Books, LinkOut Agents targeting inflammation in heart failure. Gullestad L, Kjekshus J, Damas JK , Ueland T, Yndestad A, Aukrust P. Department of Cardiology, University of Oslo, N-0027 Oslo, Norway. lars.gullestad at medisin.uio.no Evidence from both experimental and clinical trials indicates that inflammatory mediators are important in the pathogenesis of chronic heart failure (HF), contributing to cardiac remodelling and peripheral vascular disturbances. Several studies have shown raised levels of inflammatory cytokines such as TNF-alpha, IL-1beta and -6 in HF patients in plasma, circulating leukocytes, atherosclerotic lesions, and in the failing myocardium itself. Importantly, this rise in inflammatory mediators does not seem to be accompanied by a corresponding increase in anti-inflammatory cytokines such as IL-10 and transforming growth factor-beta; thus resulting in an inflammatory imbalance in the cytokine network. Traditional cardiovascular drugs have little influence on the cytokine network in HF patients. Results from randomised, placebo-controlled anti-TNF studies suggest lack of effect of such therapy. Although somewhat disappointing, these negative results do not necessarily argue against the 'cytokine hypothesis'; these studies just underscore the challenges in understanding the complex cytokine network in order to develop effective treatment modalities in HF patients. More general immunmodulating treatments, such as pentoxyfylline, intravenous immunoglobulin, thalidomide and statins, have shown promising results in smaller studies, which need to be confirmed in larger studies with hospitalisations and death as the end points. In addition, further research in this area will have to be more precise in identifying the most important 'actors' in the immunopathogenesis of chronic HF. Publication Types: Review PMID: 15926863 [PubMed - indexed for MEDLINE] -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 07:08:36 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 07:08:36 -0300 Subject: [HF-FORUM] 59S RE: Resynchronization or transplantion. Dr. Freire Message-ID: <9901E1A6-EC3A-4449-B126-4C537460A822@hf-symposium.org> Dear colleague, According to the information available and my modest experience, my opinion is: 1. The ideal candidates for resynchronization and not for transplantation are those in class III and who show elements of desynchronization. 2. For patients in class IV, the age and the general state are important: if the patient is elderly, I prefer resynchronization, and if the patient is young or under 60 years old, I prefer transplantation. I hope these comments are useful. Dr. Diego Freire Montevideo-Uruguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 07:31:14 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 07:31:14 -0300 Subject: [HF-FORUM] 61E RE: Restrictive cardiomyopathy in pediatrics. Dr. Towbin Message-ID: Children with RCM have a 50% 2-yr survival with sudden death as the cause of death. We typically list these children for transplantation at the time of diagnosis. No evidence exists that beta blocker, calcium channel blocker or any other medical therapy is efficacious. See the papers by Rivenes et al and Denfield et al for details. Jeff Towbin, MD. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 07:42:58 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 07:42:58 -0300 Subject: [HF-FORUM] 62C About pharmaceutical treatment of HF. Ning Zhu Message-ID: <14F197BD-9943-46FC-94EC-5572F0F76D72@hf-symposium.org> Pharmaceutical therapy is still a cost-effective alternative in HF treatment, especially in some poor areas in China. Diuretic could rapidly relieve the symptoms, and the nitroglycerine could function well for the patients with severe heart failure. Even the sudden dyspnea could be alleviated with acute administration of sublingual nitroglycerine. After half month discussion in HF forum, nothing was mentioned on these 2 kinds of drugs. Could our experts comment on it? Ning Zhu Dalian Medical University -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 07:43:45 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 07:43:45 -0300 Subject: [HF-FORUM] 60E DCM in obese patient with risk factors. Dr. Safer Message-ID: <7370D9B5-00F3-4F9C-9B4D-F4563F452A25@hf-symposium.org> Dear Dr. Garcia, In this case as the patient is morbidly obese (BMI 46) you should consider weight reduction by bariatric surgery (gastric banding) as a primary approach. At least the long lasting diabetes plus HBP let me think of a very high risk of next MI, and also stroke. Thus, weight reduction is the primary approach, and it will only work by surgery plus change in diet. Condition is that your patient is compliant and collaborative. As the weight reduces, she will also be able to move a little more, and starting a mild physical exercise program would help her improve the CV as well as diabetes status. This usually als results in an improvement of EF. The administration of Digitalis (or Beta-Methyldigoxin) may improve the cardiac output function, but in this case a careful titration starting with a low daily dose (0.25 mg) should be recommended; Holter monitoring mandatory. The QS time of currently 140 ms should be reduced by Digitalis to possibly approx. 110 ms, which should help improve the EF signicantly. Anyway, this would suppose that the previous MIs have not destroyed too much tissue. In case that stress ECG and/or Holter monitoring reveals complex ectopes (which I would assume), an ICD implantation should be considered. Dr. Anton Safer from Germany ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 16:23:26 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 16:23:26 -0300 Subject: [HF-FORUM] 64C. RE: Echocardiographic variables. Dr.Wu Message-ID: Subject: [HF-FORUM] 64C. Echocardiographic variables. Dr.Wu > > Thank you very much to everyone who made this great event possible. > I would like to ask the distinguished specialists, what role do > echocardiographic indexes of ventricular performance, different > from ejection fraction, for instance derived from pulsed Doppler > (dP/dT, Tei), of pulsed tissue Doppler of the ring, strain, and so > on, have. > Do you use some of these to establish a prognosis or to make > therapeutic choices? > Regards from Chile > Mario Zapata, mzapatam at manquehue.net Answer? In clinical practice, ejection fraction is usually used to assess systolic function, dp/dt can be used to assess both systolic and diastolic function. In contrast, there are fewer indices to assess diastolic function. There are impaired relaxation and decreased diastolic compliance with left ventricular diastolic dysfunction. It can be measured by echocardiography indices of diastolic filling. The approaches which are most useful are the measurement of transmitral or pulmonary venous flow velocity by pulsed doppler echocardiography (PDE) and mitral annual velocity by tissue doppler imaging(TDI). The peak of early diastolic mitral flow velocity (E) by PDE is directly related to transmitral pressure gradient and left atrial pressure and is therefore markedly load-dependent. But the peak of early diastolic mitral annual velocity by TDI is less load-dependent and more related to the rate of left ventricular relaxation. Tei = (isovolumeric contraction time + isovolumeric relaxation time)/ ejection period [(IVCT+IVRT)/EP]. It can be measured by both pulsed doppler echocardiography or tissue doppler imaging. So far both dp/dt and Tei indices are usually just used in clinical research work, but not in clinical practice. Prof. Xuesi Wu, MD. Dept. of Cardiology. Beijing Anzhen Hospital, China -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 17:04:20 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 17:04:20 -0300 Subject: [HF-FORUM] 65C RE: Levosimendan. Dr. Lu Message-ID: Subject: 46S RE: Levosimendan. Dr. Reyes > First, I would like to congratulate the people in charge of this > Symposium for the great opportunity of being able to exchange our > experience and for the good organization of this event. > I do not doubt about the advantages of Levosimendan in acute > myocardial infarction, complicated with heart failure, but Dr. > Yongxin Lu from China, in her review on this topic, and quoting > Sonntag, S et al, from Germany, says that the latter reported about > a clinical trial in which 24 patients with acute coronary syndrome > underwent angioplasty, followed by a randomized and double-blind > treatment with levosimendan or placebo. The number of hypokinetic > segments decreased with levosimendan and the elasticity by beat > increased with levosimendan. My question is: how could we know > whether this is due to Levosimendan and not to opening the vessel > responsible by Angioplasty? > > Dr Raul Reyes. > > Cuba. Thanks for your question. My personal view is that PCIs were performed in both groups, effect of levosimendan on cardiac function was compared with that of placebo under similar background. Additional benefit was related with levosimendan. I don?t doubt that opening the coronary artery is good for cardiac function. At least, the combination of levosimendan with PCI is better than that of placebo with PCI. Dr. Yongxin Lu -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 17:35:19 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 17:35:19 -0300 Subject: [HF-FORUM] 66C About restrictive cardiomyopathy. Dr. Lin Zhu Message-ID: <59374A11-13E4-4EEF-8543-132C973AED2D@hf-symposium.org> Subject: About restrictive cardiomyopathy A Case for Discussion: A 36-year-old female, who was found having heart murmur at age 6 and was suspected having ?ventricular septal defect?. Angiography was performed and she was diagnosed ?small size VSD? based on angiographic results and physical examination. No surgery or other treatment was performed due to the ?small? nature of the defect. The patient had no symptoms until she was 18-year-old when she experienced an episode of syncope after having diarrhea. ECG recording showed atypical ST-T changes that simulated hypertrophic cardiomyopathy. Echocardiography demonstrated: IVS 18mm, LVPW 19mm, LA 41mm, LV 32mm. Twenty days after, the patient showed left ventricular failure and proxismal AF. At age 24, the patient developed right ventricualar failure and diuretics were used periodically. At age 28, her AF became persistent. Echocardiography was again performed, and two equivocal diagnosis was proposed: hypertrophic cardiomyopathy or restrictive cardiomyopathy. She was given regular treatment with digoxin and diuretics. At age 34, the patient developed severe ascetics. Monthly abdominal drainage was needed in the recent half year to alleviate the symptoms. The drainage was ~2,000mL/time with 7 times per month. The patient suffered from hypoalbuminemia. The liver and renal function was within the normal range. Most cardiologists think that she had restrictive cardiomyopathy rather than hypertrophic cardiomyopathy based on a latest echocardiographic results: IVS 11.4mm ?LVPW 11.0 mm?LA 62 MM?LV 37.2mm? RV 20.3mm. MRI results also support the diagnosis of restrictive cardiomyopathy, but CT scan suggested hypertrophic cardiomyopathy. I would appreciate any comments on the diagonosis and further treatment regimen from everybody. Thanks. Lin Zhu, MD -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 17:56:10 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 17:56:10 -0300 Subject: [HF-FORUM] 68E RE: CMD in obese patient with risk factors. Dr. Levine Message-ID: <9EB1D838-C035-4059-81D4-67F9C35E7810@hf-symposium.org> Dr. Jose Angel Valdes Garcia presented the case of a 62-year-old female patient, morbid obesity. Her height is 1.55 m and her weight is 110 kg. She has been a diabetic with a 10-year evolution [glibenclamide-metformin], HBP with a 15-year evolution [candesartan- hydrochlorothiazide], hypothyroid [normal values of T3, T4, TSH], old anteroseptal and inferior myocardial infarction [2 vessels, it seems], QRS 140 ms. Dilated cardiomyopathy [probably ischemic]. EF 30%. NYHA Class III. She is also treated with 25 mg of atenolol, spironolactone 50 mg and furosemide 80 mg a day. She came to Mexico DF to visit relatives and presented an episode of Acute Pulmonary Edema. After 10 days of hospitalization, she went to her home. Currently in Class II. Dr. Valdes Garcia then asks what would be the best management choice? Continuing with the medical management or using devices? Dear Dr. Valdes Garcia, This patient has significant congestive heart failure but based on the summary, she responded very well using a relatively standard and indeed, simple, regimen. It would be premature to recommend device implantation. Once, she returns to the care of her primary physician, she should be referred to a cardiologist who could pursue a further evaluation. With the diabetes, hypertension and an ECG that suggests ischemic heart disease, I would evaluate her for active ischemia with an exercise stress test using some an imaging modality in addition to the ECG (thallium, echo....). If there is evidence of active reversible ischemia (since diabetics are more likely to have silent ischemia), I would strongly consider revascularization (bypass or PTCA with or without stents depending on the anatomy and resource availability). I would also consider the addition of an ACE inhibitor (or resume the ARB if this had been stopped) to the beta blocker and diuretics that had already been started. Further, if her diabetes and hypertension have not been in good control, a more intensive effort to control both of these conditions would be warranted along with a statin even if her cholesterol level was technically normal (see Heart Protection Study from a couple of years ago). My initial approach to this patient would be intensive medical management before recommending an implanted device, either ICD or CRT system. I have suggested a number of steps - these should be pursued one at a time observing her response to each new drug or other intervention before moving on to the next. With respect to an ICD, if she has reversible ischemia and can be revascularized, her EF may improve taking her out of the MADIT II group (post MI, EF less than or equal to 30%) and based on the CABG- Patch trial, an ICD would not be warranted. Her EF may also improve simply with optimal pharmacologic therapy if this is sufficient to control any active ischemia although for me to not recommend an intervention, I would require some clearly identifiable ischemic symptoms so that her response to therapy could be appropriately monitored. With ACE inhibitors and intensive medical therapy, her EF may also improve and if she stays in NYHA Functional Class II status, a biventricular (CRT) stimulation system would not be warranted even presuming a wide QRS. Paul A. Levine, MD, FHRS, FACC Vice President, Medical Director St. Jude Medical, CRMD 15900 Valley View Ct. #980, Sylmar, CA 91342 818-493-2900 / Fax: 818-362-2242 Clinical Professor of Medicine Loma Linda University School of Medicine -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 18:45:02 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 18:45:02 -0300 Subject: [HF-FORUM] 70E RE: Chagasic cardiomyopathy. Dr. Perez Riera Message-ID: <6AE57B20-CB7F-4064-A53F-5AD299694389@hf-symposium.org> First question: The evolution is the same as cardiomyopathies with another etiology? Answer: No In early-stage Chagas' heart disease without HF Vitori et al studied a group of 856 patients with 3 positive anti-Trypanosoma cruzi test results. Patients were divided into 3 clinical groups: Group I: without heart disease; Group II: with heart disease but without left ventricular enlargement; Group III: with LV enlargement but without HF. The endpoint was progression to a more severe clinical stage or death due to cardiovascular disease. A Cox regression model was used to derive a clinical risk score from clinical, electrocardiographic and echocardiographic variables. Patients' mean age was 43.7 years. Mean follow up: 8 years. The following were predictors of heart disease progression: 1) Age at entry; 2) Left ventricular systolic diameter; 3) Intraventricular conduction abnormalities ; 4) Sustained VT. The devised clinical risk score was effective in stratifying the likelihood of cardiopathy progression. The author conclude that specific clinical indicators and a derived clinical risk score can be used to predict the progression of chronic chagasic myocarditis in patients without HF. Patients with chronic Chagas' heart disease have a clinical course worse than that of patients with nonchagasic dilated cardiomyopathy. This fact may be ascribed to the electrocardiographic and morphological peculiarities usually found in chronic Chagas' heart disease (1). Among patients with cardiomyopathies of different etiologies, those with Chagas' heart disease had the lowest cumulative probability of nonoccurrence of life- threatening ventricular arrhythmias, confirming its unfavorable prognosis and the importance of preventive measures against SD in this disease(2). Only in Chagas entity is observed reactivation of infection with immunosuppression protocols after heart transplantation for advanced chagasic cardiomyopathy(3). The left ventricular mass index is greater in patients with hypertensive cardiomyopathy, with idiopathic dilated cardiomyopathy and with cardiomyopathies of other etiologies than in patients with chagasic or ischemic cardiomyopathy(4). In man, plasma Atrial natriuretic factor ANF could be a sensitive marker capable of detecting gradual impairments in cardiac function and poor survival in CHF patients and of myocardiopathy development in the asymptomatic state(5). Second question: The medical treatment should be the same? Answer: No or sometime (only the ICD inplantation.) 1) In chagasic patients without HF treatment with benznidazole reduced the risk of progression(6); 2) Only in Chagas disease we use Allopurinol, Benznidazol y Nifurtimox, for the parasitemia, specific serology and evolution of the clinic manifestations(7); 3) In Chagas disease a new therapeutic approach is suggested using one or more agents that prevent or inhibit the adherence of mycoplasma to host cell membranes by removing sialic acid residues and preventing oxidation of the cells. The use of a neuraminidase enzyme, particularly the T. cruzi trans-sialidase enzyme, associated with treatment using anti-oxidating agents was proposed. Preliminary experimental animal and laboratory tests showed good results. The proposal that trans-sialidase from T. cruzi is efficient in combating co-infection of mycoplasma and chlamydia is based, at least in part, on the observation that chagasic patients suffering from T. cruzi infection present less mycoplasma and chlamydia infection in their tissues. Co-infection with mycoplasma and chlamydia may induce oxidation of the host cells. Anti-oxidants such as those present in plant extracts may also be used in the treatment. Other diseases such as chronic hepatitis, glomerulonephritis, Multiple Sclerosis, Alzheimer's Syndrome and idiopathic encephalitis are other examples of chronic diseases where mycoplasma and chlamydia might be present, as they have the characteristics of unknown etiology, persistent chronic inflammation and fibrosis(8); 4) Patients with Chagas' disease, compared with coronary artery disease patients, have similar clinical characteristics leading to ICD implantation(11) Third question: someone has experience on the use of resynchronizers and/or ICD, can they tell about it? Answer: 1) In patients with chagasic cardiomyopathy and sustained VT, EPS can predict long-term efficacy of Class III antiarrhythmic drugs. This may help in the selection of patients for ICD therapy(9); 2) The ICD-LABOR study: Latin American experience in the secondary prevention of SCD, by means of an ongoing registry involving seven Latin American countries and 770 patients. Every individual within the registry presented with antecedents of aborted SCD or cardiac arrest due to VT/ VF. Patients included have fulfilled the Class I indication for ICD. The primary end point was death from all causes. Secondary end points were SCD and death due to CHF. Despite the differences in terms of pathologies between the ICD-LABOR (Latin American bioelectronic ongoing registry) and randomized ICD trials, a parallel evolution in all cause mortality and cardiac mortality was observed. Independent risk factors for mortality included age > 70 years, male gender, NYHA III/IV, and EF <0.30. The etiology of > heart > disease (Chagas vs Coronary Disease) was not found to be a risk factor (10); 3) Patients with Chagas' disease, compared with coronary artery disease patients, have similar clinical characteristics leading to ICD implantation (11). In reference to cardiac resynchronization therapy (CRT) in Chagas disease there is only one manuscript that used RV bifocal pacing, in Chagasic population who developed both severe dilated cardiomyopathy and chronic AF. The study included 30 patients with a mean age of 52 +/- 6 years (16 male), who had AV at functional class II or IV (NYHA). Patients underwent endocardial dual-chamber pacemaker implantation with two RV leads-one placed near the RVOT and the other in the apex. Patients were examined by echocardiography, 24-hour Holter, and NYHA class determination before and 3, 6, 12, 18, 24, and 36 months after CRT. Compared to the baseline, the LVEF increased in the first month of CRT, the LV end diastolic diameter decreased, all patients were downgraded to NYHA class I or II, and the incidence of ventricular arrhythmias decreased. However, these could not be maintained and worsened after 6 months CRT. There was a mortality rate of 43.3% during the first year, and only 23.3% of patients remained alive after 3 years. They underwent an EPS, which revealed complex arrhythmias justifying ICD in six out of seven patients. The favorable effects of RV bifocal pacing could not be maintained beyond the first 6 months, likely due to the VT. Therefore, CRT combined with ICD from the outset may be recommended for this patient group (12). References 1) Bestetti RB, Muccillo G. Clinical course of Chagas' heart disease: a comparison with dilated cardiomyopathy. Int J Cardiol. 1997;60:187-193. 2) Martinelli Filho M, De Siqueira SF, Moreira H, Fagundes A, Pedrosa A, Nishioka SD, et alProbability of occurrence of life-threatening ventricular arrhythmias in Chagas' disease versus non-Chagas' disease. Pacing Clin Electrophysiol. 2000; 23:1944-1946. 3) Bacal F, Silva CP, Bocchi EA, Pires PV, Moreira LF, Issa VS, et al. Mychophenolate mofetil increased chagas disease reactivation in heart transplanted patients: comparison between two different protocols. Am J Transplant. 2005;5:2017-2021. 4) Markus MR, Freitas HF, Chizzola PR, Silva GT, Lima AC, et. al. Left ventricular mass in patients with heart failure. Arq Bras Cardiol. 2004;83:232-236. 5) Puyo AM, Scaglione J, Auger S, Cavallero S, Postan M, Fernandez BE. Natriuretic peptides as prognostic and diagnostic markers in Chagas' disease. Regul Pept. 2005;128:203-210. 6) Viotti R, Vigliano C, Lococo B, Petti M, Bertocchi G, Alvarez MG, et al. Clinical predictors of chronic chagasic myocarditis progression Rev Esp Cardiol. 2005;58:1037-1044. Rev Fac Cien Med Univ Nac Cordoba. 2000;57:135-162. 7) Gallerano RR, Sosa RR. Interventional study in the natural evolution of Chagas disease. Evaluation of specific antiparasitic treatment. Retrospective-prospective study of antiparasitic therapy Rev Fac Cien Med Univ Nac Cordoba. 2000;57:135-162. 8) de Lourdes Higuchi M. Trypanosoma cruzi trans-sialidase as a new therapeutic tool in the treatment of chronic inflammatory diseases: possible action against mycoplasma and chlamydia. Med Hypotheses. 2004; 63:616-623. 9) Leite LR, Fenelon G, Simoes A Jr, Silva GG, Friedman PA, de Paola AA. Clinical usefulness of electrophysiologic testing in patients with ventricular tachycardia and chronic chagasic cardiomyopathy treated with amiodarone or sotalol. J Cardiovasc Electrophysiol. 2003;14:567-573. 10) Dubner S, Valero E, Pesce R, Zuelgaray JG, Mateos JC, Filho SG, Reyes W, Garillo R. A Latin American registry of implantable cardioverter defibrillators: the ICD-LABOR study. Ann Noninvasive Electrocardiol. 2005;10:420-428. 11) Muratore C, Rabinovich R, Iglesias R, Gonzalez M, Daru V, Liprandi AS. Implantable cardioverter defibrillators in patients with Chagas' disease: are they different from patients with coronary disease? Pacing Clin Electrophysiol. 1997;20:194-197. 12) da Silva Menezes A. Outcome of right ventricular bifocal pacing in patients with permanent atrial fibrillation and severe dilated cardiomiopathy due to Chagas disease: three years of follow-up. J Interv Card Electrophysiol. 2004; 11:193-198. All the best Andr?s Ricardo P?rez Riera -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 19:00:35 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 19:00:35 -0300 Subject: [HF-FORUM] 71E RE: Resynchronization therapy and cardiac transplantation. Dr. Moss Message-ID: <415F2A14-94AF-4383-B2A0-12B16A48D507@hf-symposium.org> Here is my reply to the resynchronization question by Dr. Serra: Regarding patients with advanced heart failure who are on the wait list for cardiac transplantation, cardiac resynchronization therapy (CRT) has provided dramatic improvement in functional class and ejection fraction in approximately 40% of the patients on whom it has been utilized, with many of these patients temporarily coming off the transplant wait list. In view of this experience, it is reasonable to first utilize CRT before putting a patient on the transplant list. For those who improve, they can be followed and added to the transplant list when and if they deteriorate. Those who don't get improvement with CRT can be placed directly on the transplant wait list. Of course, those who are too old for transplant consideration should be aggressively treated with CRT when they are optimal medical therapy. There should not be a competition between resynchronization and transplant experts caring for patients with advanced heart failure. Rather, it should be a joint effort since most patients will require sequential therapy. ...Arthur J. Moss, MD -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 19:04:13 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 19:04:13 -0300 Subject: [HF-FORUM] 63R: RE: Dry weight. Dr. Ivanov Message-ID: <8661F574-8D1A-4A34-ABC5-CA73EC0ADC09@hf-symposium.org> Since the mid 90s, the method of bioimpedanciometry has proved to be better than other technologies proposed for the evaluation of the content of body tissues. The concept of evaluation of body content, was developed and widely accepted, and not just by anthropometric indexes, but also with methods based on the biophysical properties of different tissues. Since 1985, many papers were published showing the method of bioimpedanciometry for the evaluation of fat and non-fat lean body weight, using weight under water, densitometry (for bone tissue), the method of indicator dilution (for extra and intracellular liquid) and the Fick method (to evaluate basal metabolism). Within the biological object, the substrates of active resistance (R) are liquid (extra and intracellular), which have ion mechanism of conduction. The substrates of reactive resistance Xc (the component of impedance) are cell membranes. With active resistance, the total content of water (TCW) is estimated in the organism. The resistance of fat tissue is approximately 20 times greater than the rest of the body tissues, which make up the non-fat lean body weight (LBW). The accuracy of the evaluation of regressive variables is 0.9-1.8 Kg for TCW and 2.5% for LBW. By using the reactive component of impedance, basal metabolism and the active cellular mass are estimated (mass of muscles and internal organs). There are several methods of bioimpedance, which are classified according to: frequency (uni, bi and polyfrequent) and location (local, regional, integral, polysegmentary). There are many more possibilities for the study of patients with heart failure in the analyzers of bioimpedance with different frequencies (5-1000kHz). It is important to emphasize that the method of spectral bioimpedanciometry requires meeting in detail the anthropometric measurements and an exact location of electrodes. In obese patients, it is important to achieve a proper contact between hip, arms and trunk surfaces. Segmentary analysis may reflect more accurately the changes in extra and intracellular volumes, making a comparison of the impedance of the whole body, mostly in cases of patients with severe hydric balance disorders and in the presence of ascites, anasarca, massive hyperhydration, with the TCW and LBW. The analysis of body content of patients with a lower degree of heart failure is not so difficult. According to our data, the formulas are properly used only for the limbs, since they present a homogenous electrical field, and a cylindrical form of the segment. For the improvement of the techniques of bioimpedance in patients with heart failure, it is important to better understand the connection between body content and the electrical properties of each segment. The resistances of extra and intracellular liquids vary because of the difference in redistributing the electrical field, which is affected by the differences in geometrical volumes. To calibrate the values of the resistances of segments (since there is no "gold standard"), the estimation of the resistances of each segment has been proposed, additionally. Prof.Dr.Ivanov G.G. Russia, Moscow -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 22:12:33 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 22:12:33 -0300 Subject: [HF-FORUM] 72C Appreciation to Dr Yongxin Lu. Dr. Deng Message-ID: I appreciate Dr Yongxin Lu's detail reply very much, especially under her that busy schedule. It gives us very good direction in our clinical work. Thanks again. Dr. Yaolian Deng -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 18 22:25:23 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 18 Apr 2006 22:25:23 -0300 Subject: [HF-FORUM] 67S RE: Chagasic cardiomyopathy. Dr. Arabia Message-ID: Dear Dr. Juri, The topic of generalization about the etiology of dilated heart disease and the different results has always been a reason for controversy (ischemic vs. non ischemic), but in the case of Chagas disease, this reaches its peak. According to our experience with patients with chronic chagasic heart disease, with EF >30% and syncopal sustained ventricular tachycardia, refractory to antiarrhythmic agents, we use in 3 cases ICD + CRT, and the improvement of functional capacity was remarkable; moreover, there were no ICD shocks delivered since the implantation (although follow-up time is not so long: 10, 6 and 4 months). All these patients live in rural areas in the province of Santiago del Estero (Argentina), endemic area of Chagas, and progressively they could go back to develop their daily activities. Although the number is insignificantly low, we estimate that it is an excellent alternative to be considered, but the other great problem is the availability for the patients, who mostly lack economic resources, to a therapy so expensive currently, such as CRT, and since nearly all of them present malignant ventricular arrhythmias, the addition of ICD is the rule, making the device even more expensive. Congratulations for the excellent level and organization of the Symposium. Dr. Luis Arabia C?rdoba. Rep?blica Argentina. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 19 08:44:49 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 19 Apr 2006 08:44:49 -0300 Subject: [HF-FORUM] 74C RE: Chagasic cardiomyopathy. Dr. Li Zhang Message-ID: Dear Dr. Schapachnik: I think Dr. Juan Carlos Juri has raised several very practical questions. Along this line, may I ask you, the well-known Chagas cardiomyopathy expert, how many people in South and Central America suffer from heart failure caused by Chagas cardiomyopathy? Previously you indicated that bundle branch blocks are very common in HF patients with Chagas cardiomyopathy. I suppose many of them are suitable for CRT. What percentage of those HF patients, though, cannot afford bi-ventricular pacing +ICD? In China, over 10 million people suffer from HF. Unfortunately, the vast majority of patients who are suitable for CRT cannot afford this over priced little life saving device. Many patients in US also cannot afford it, which is true in many other countries. Thank you, Li Zhang LDS Hospital Salt Lake city, UT -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 19 10:41:33 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 19 Apr 2006 10:41:33 -0300 Subject: [HF-FORUM] 76E Non-responders to CRT. Dr. Wang Message-ID: <9F97821E-775D-4ED0-9743-014DFA63B267@hf-symposium.org> May I ask the panel experts, preferably Dr Arthur Moss to comment on how to identify the non-responders to CRT. I too see about 35% of patients who were on transplantation list had significant improvement in NYHA functional class after receiving CRT, some even refused to consider the surgical option after experiencing symptomatic improvement, which was pleasing. However, there are still a proportion of patients in whom CRT did make not much difference in clinical symptoms or LVEF. There are many countries or regions where CRT remains an expensive option. Therefore, identification of non-responders is an important issue worthy of further discussion, Cheers Lexin Wang, MD, PhD Charles Sturt University Australia -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 19 13:38:20 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 19 Apr 2006 13:38:20 -0300 Subject: [HF-FORUM] 73S RE: Beta blockers. Dr. Gorini Message-ID: Due to its pharmacodynamics and by the "evidence" gathered, in patients with asthma or bronchial hyperreactivity, I would rather choose and try first Bisoprolol (CIBIS). Regards, N?stor Gorini -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 19 19:44:45 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 19 Apr 2006 19:44:45 -0300 Subject: [HF-FORUM] 75E BNP and diastolic dysfunction. Dr. Wang Message-ID: May I ask the symposium participants that how many of us are currently using BNP to detect diastolic left ventricular dysfunction, and how useful do you think this test is. I found that given the recent clinical evidence that the test appears relatively sensitive and specific for diastolic heart failure, the actual clinical applications of the test have been patchy. Regards Lexin Wang, MD, PhD Charles Sturt University Australia -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 19 20:33:39 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 19 Apr 2006 20:33:39 -0300 Subject: [HF-FORUM] 77S Heart failure in children. Dr. Petrozzi Message-ID: <8E7CC51B-4864-483C-828F-F0EFCC2D7D89@hf-symposium.org> In my country there are numerous cases of heart failure secondary to congenital heart diseases that have not been treated surgically (1 or 2 years) by a lack of resources, or surgeons, or other reasons. The medical treatment is made almost invariably with furosemide, spironolactone, captopril and digoxin, until the patient may be operated (1 or 2 years). Is there any evidence about the use of digoxin, captopril or spironolactone in children with heart failure by this cause? Is the use of medication in CHF justified in children with no growth delay and no poor weight gain? Thank you very much, Dra Petrozzi Pediatra- Peru -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 19 20:47:58 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 19 Apr 2006 20:47:58 -0300 Subject: [HF-FORUM] 78C About restrictive cardiomyopathy. Dr. Perez Riera Message-ID: <3F326E16-A9D8-463F-8D21-4E2798BF42D8@hf-symposium.org> Dear Lin Zhun: Both entities to day are considered belonging to the same group: They are sarcomeric cardiomyopathies or ?force of generation diseases?. Please see below the new proposal of classification of cardiomyopathies: NEW PROPOSAL OF CLASSIFICATION OF CARDIOMYOPATIES 1) CYTOSKELETAL CARDIOMYOPATHY: "force transmission" disease: Dilated cardiomyopathy (DCM); 2) SARCOMERIC CARDIOMYOPATHY: Hypertrophic cardiomyopathy (HCM) and Restrictive cardiomyopathy (RCM ) "force generation diseases"; 3) CELL JUNCTION CARDIOMYOPATHY: Desmosomal: cell junction disease: Arrhythmogenic Right Ventricular Dysplasia; 4) ION CHANNEL (CHANNELOPATHIES) CARDIOMYOPATHIES: If we consider also cardiomyopathy as ion channel disease (LQTS, SQTS, Brugada Syndrome, and CPVT), because they are diseases of the myocardium associated with electrical dysfunction. I think that is not easy to say if RCM or HCM Why? Because in some forms of HCM have not and outflow gradient of the LVOT and diffuse hypertrophy. Dear friend for me is very important to see the ECG. In RCM the most characteristic ECG feature is diffusely diminished voltage. On the other hand in HCM the voltage of QRS complex are augmented. Sometimes this centenary method is the clue for the diagnosis. Both entities could have diastolic rather than sistolic dysfunction with impaired ventricular filling and end-diastolic pressure, markedly increased left ventricular mass. HCM is a relatively common primary cardiac disorder (with an incidence of 1 in 500 and prevalence of 0.2%. ) defined as the presence of disproportionate hypertrophied LV in the absence of any other diagnosed etiology. HCM is the most common cause of SCD in young people (especially in athletes) which often occurs without precedent symptoms. RCM is an uncommon heart muscle disorder characterized by impairment of ventricular filling during diastole with reduced volume and preserved systolic function (Normal or near normal LV size and function and atrial enlargement). Its principal abnormality is diastolic dysfunction. (Restrictive filling pattern). It is least- common type in the United States and most other industrial nations. The muscles of the ventricles become excessively rigid, and the filling of the ventricles with blood between heartbeats is impaired. This form of cardiomyopathy may be idiopathic or associated with other systemic disease, which occurs elsewhere in the body but is most often idiopathic. Inside the myocardial noninfiltrative forms we have the idiopathic, familiar, scleroderma pseudoxanthoma elasticum, diabetic cardiomyopathy and the hypertrophic cardiomyopathy. The last one the differential diagnosis with the HCM is not easy sometimes. Neonates born to maternal insulin-dependent diabetes mellitus frequently have association with congenital heart disease: patent ductus arteriosus, patent foramen ovale ASD, small muscular VSD, MVP, and PS. HCM was observed. Severe forms of congenital heart disease: encountered were D-transposition of great arteries, tetralogy of Fallot, and hypoplastic left heart syndrome. Overall incidence of congenital heart disease was 15% after excluding patent ductus arteriosus and HCM. Maternal insulin-dependent diabetes mellitus is a significant risk factor for congenital heart disease. Careful evaluation and early diagnosis of CHD in this high-risk group are highly indicated. There is a need for development of prenatal screening programs for CHD in our population. (Abu-Sulaiman RM, Subaih B. Congenital heart disease in infants of diabetic mothers: echocardiographic study. Pediatr Cardiol. 2004;25:137-140.). The treatment is dependent of cause and stage of the disease. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andre - Sao Paulo - Brazil. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 19 22:56:32 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 19 Apr 2006 22:56:32 -0300 Subject: [HF-FORUM] 82C Bifascicular block in HF patients with Chagas cardiomyopathy. Dr. Li Zhang Message-ID: <6E74165C-2574-49B1-835E-B61CD9480462@hf-symposium.org> Dear Dr. Perez Riera: HF patients with Chagas cardiomyopathy often display various cardiac conduction abnormalities. Since many of our curso-ecgvcg.com.ar online classmates are also participating in this HF-forum, may I take this opportunity to ask you, the world ECG master, how to differentiate right bundle branch block plus left anterior fascicular block (RBBB+LAFB) from LAFB+left septal fascicular block LSFB? For the example you provided in the ECG class (see attached***), the right bundle branch block pattern seems evident addition to LAFB. Could it be considered as RBBB+LAFB instead of LAFB+LSFB that you indicated? I?m sorry that most of us still do not have enough knowledge about LSFB. Another purpose of such differentiation is to get a sense as whether the disease has resulted in the left or both left and right ventricular conduction delay in this case. Would you please advice? Thank you very much, Li Zhang LDS Hospital Salt Lake city, UT SEE THE ECG http://www.hf-symposium.org/files/Li_ECG.pdf -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 20 06:59:40 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 20 Apr 2006 06:59:40 -0300 Subject: [HF-FORUM] 80S RE: Chagasic cardiomyopathy. Dra Valero Message-ID: <3F5C55AB-1D69-4417-9C53-DE96002C1A56@hf-symposium.org> Dear Juri, I'm glad you sent the data from the LABOR Registry, which has currently 1050 patients incorporated, out of which 24% are chagasic. I can add to the mentioned papers, that to this date we have not seen in the evolution of the patients with ICD by secondary indication, a difference about the mortality regarding the patients with idiopathic dilated cardiomyopathy. About the experience regarding the treatment with resynchronizers (biventricular pacing), I think there is none. We have started 4 months ago an open registry called CARLA (CArdiac Resyncronization in Latin America), and we have added 16 patients between Argentina and Brazil, but none of them has chagasic cardiomyopathy. We hope to add patients with this pathology to be able to draw conclusions. It is possible that poverty may be one of the factors because we don't have implantations in chagasic patients; in countries with wider possibilities due to their economy, they luckily don't have Chagas disease between the native population. Elina Valero -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 20 07:01:19 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 20 Apr 2006 07:01:19 -0300 Subject: [HF-FORUM] 79S RE: DCM in obese patient with risk factors. Dr. Rodriguez Artuza Message-ID: <12DD82FF-6CE6-4EC5-B941-CA97E267FEC8@hf-symposium.org> We agree with Dr. Levine, but there is a controversial issue in this patient: is atenolol a drug equivalent to carvedilol, bisoprolol or metoprolol in dilated patients. In this setting I lean toward the drugs I mentioned above, unless there is some important study with atenolol in this type of patients. Carlos R. Rodriguez Artuza -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 20 07:49:23 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 20 Apr 2006 07:49:23 -0300 Subject: [HF-FORUM] 81S RE: DCM in obese patient with risk factors. Dr. Encinas Message-ID: Dr. Valdez Garcia asked which would be the best treatment choice. Continuing with the medical treatment or using devices? About this patient, I would like to contribute the following additional aspects besides those presented by Dr. Levine. 1) Control of risk factors. She has a body mass index over 40, and is a candidate to bariatric surgery, as it has already been mentioned, and due to her FC the ring would be advisable, though not the best choice, cause it is a minor procedure in comparison to gastric reduction. 2) Surely due to the time of evolution of diabetes > 10 years, the response to hypoglycemiant agents should be poor, and for this reason I would implement a scheme with insulin, trying as much as possible, to reach the current goals of glycemia control (preprandial glucose between 80 and 120 mg/dl, capillary glycemia before going to bed, between 100 and 140 and Hb glycosylated < to 7). 3) This patient is in high risk and is in the group of secondary prevention (DM and prior infarction), and for this reason, as mentioned by Dr. Levine, she requires a treatment with statins (goal: LDL 70). 4) She should be taking aspirin between 100 and 325 mg per day. 5) I suppose that she is taking candesartan because she could not tolerate ACEI. It is important to remember that if possible, and if the conditions of the patient allow it, the doses reached in papers should be reached. Renal function and kalemia should be monitored, due to the use of ACEI, furosemide and spironolactone. The levels of creatinine are not mentioned, but my attention was drawn to the dose of furosemide 80 mg per day. I suppose that this was at the moment of the decompensation, or the patient has renal impairment secondary to the DM? If so, the use of thiazide agents is not justified, since as you may remember, it has no effect with Cr >2, except in the cases where we attempt to strengthen the effect of loop diuretics. In such case, it should be administered 30 minutes before furosemide. In general, the lowest possible dose of diuretics should be used, to reach a proper hydric balance, which in general varies from patient to patient. If there is pulmonary congestion, a good option is to associate nitrates. If possible, excessive diuresis should be prevented in the morning, because this is the time when the effective circulating volume is lowest, due to the increased diuresis when the patient is lying down. The use of diuretics at this time would yield fatigue during the day and symptoms of orthostatic hypotension that will lead to reflex neurohormonal activation and a greater requirement of diuretics during the afternoon. Using them 5 to 6 hours before going to sleep may prevent these symptoms. 6) Undoubtedly, it should be ruled out that the pulmonary congestion is not secondary to myocardial ischemia. For this some ischemia evoking test should be performed, or if there is some electrocardiographic evidence, I would make her undergo catheterization. 7) I was surprised by the fact she is taking atenolol and not a B- blocker such as carvedilol/bisoprolol/metoprolol to treat her HF, since these are the medications that have proved to be effective in HF management, remembering that its behavior is better in ischemic patients. 8) QRS is increased. Does she have any block or is it the translation of a severe myocardial involvement? Dr. Javier Encinas Landivar Cardi?logo - M?dico Internista. Area M?dica Santa Cruz - Bolivia -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 20 09:58:09 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 20 Apr 2006 09:58:09 -0300 Subject: [HF-FORUM] 83E RE: Chagasic cardiomyophaty. Dr. Hamilton Message-ID: Hello Li Another issue with Chagasic cadiomyopathy is that the WHO has put their resources essentially only into primary prevention through eradication of the vector, rather than any investment into understanding the basic mechanisms or treatments of the disease. Bob Hamilton, Toronto -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 20 10:06:48 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 20 Apr 2006 10:06:48 -0300 Subject: [HF-FORUM] 85R Heart failure in Russia. Dr. Vorotniak Message-ID: <17A39CC9-1865-4D54-AD3D-73E9577D35F9@hf-symposium.org> Dear Russian colleagues, Everybody knows the old traditions of the independent Russian medicine. However, the typical risk factors for the Russian society are also known, which result in the development of high blood pressure, diabetes, which in turn influence on an important incidence of heart failure (the numbers mentioned in the great interview with Dr. Mareev). My question is the following: what percentage of patients in Russia, with advanced heart failure and indication for CRT or ICD, has access to this treatment? Does the Russian state help in the purchase of these devices? Thank you, Dr. Andriy Vorotniak Buenos Aires, Argentina -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 20 15:58:08 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 20 Apr 2006 15:58:08 -0300 Subject: [HF-FORUM] 86S RE: Beta blockers and asthma. Dr. Guerra Orozco Message-ID: <33AD1035-8676-4FD0-95E0-86F9720B3AA6@hf-symposium.org> Greetings. First I would like to congratulate you for such excellent Symposium and the great contribution that implies improving the quality of the care we provide to our patients. I would like to make the following comment and ask a question. I'm working with an institution where I have a 72-year-old patient with CHF, Class II-III, EF 40%, HBP for more than 20 years, diabetes type 2 treated with glibenclamide and metformin, currently stable, asthmatic and treated with salbutamol inhalers, beclomethasone and ipratropium bromure, prostate cancer treated with cyproterone. He receives treatment with ACEI+diuretics, BB carvedilol, which was added by the clinician maybe by mistake since he is asthmatic and it would be contraindicated, and approximately 20 days ago Digoxin was added, and thus the quality of life of the patient has improved and now he is stabilized in class II. Is the management appropriate? According to EBM the patient is stable. Do I have to withdraw the BB in spite of the evidence of improvement? Thank you, LUIS GUERRA OROZCO MD Barranquilla _ Colombia -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 20 16:00:56 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 20 Apr 2006 16:00:56 -0300 Subject: [HF-FORUM] 89S RE: Chagasic cardiomyopathy. Dr. Dubner Message-ID: <8CC5DC93-F4F1-44E0-98FB-9B17A67D8F2F@hf-symposium.org> Dear Dr. Juri, The evolution and treatment of chagasic cardiomyopathy has been published in several journal and articles in books about the specialty previously, but not so the topic of the devices about which you ask. In this sense, in Latin-America a registry of ICD has been carried out, the ICD-LABOR, which included to this date more than 1000 patients from 7 countries and 94 centers. It was an observational registry, not randomized, which included patients with a background of malignant ventricular arrhythmia or aborted sudden cardiac death, and who received an ICD. Within this group, 27% had chagasic cardiomyopathy as etiology. The comparison between these patients and those with ischemic heart disease differed as to population composition (female sex 45.5% vs. 11.9%, Chagas vs. ischemic heart disease, p<0.0001) and ejection fraction (37.4% vs. 32.5%, Chagas vs. ischemic heart disease, p<0.0035); however, mortality was similar (15.4% vs. 15.3% p: ns). In summary, different population features but similar mortality, from where we conclude that these results DO NOT support automatic transference of indications used for ICD implantation in patients with ischemic heart disease to those with Chagas disease. Scientific Societies have now the challenge of defining the future indications of ICD in Chagas. Dr. Sergio Dubner and the researchers from ICD-Labor * Dubner et al: A Latin American Registry of Implantable Cardioverter Defibrillators: The ICD-Labor Study. ANE 2005, 10:420-28 * Garillo et al: Cardiodesfibrilador implantable como prevenci?n secundaria en la Enfermedad de Chagas. Los resultados del Estudio Latinoamericano ICD-LABOR Rebrampa 2004,17:169-177 -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 20 16:22:11 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 20 Apr 2006 16:22:11 -0300 Subject: [HF-FORUM] 90E Heart failure in chidren. Dr. Towbin Message-ID: Children with CHF should be treated with ACE Inhibition and Beta blockers with or without diuretics (depending on fluid status). No groth or other delays occur due to the medication. Dosing, of course varies by weight. Jeff Towbin, MD Professor and Chief Pediatric Cardiology Director, Cardiomyopathy/Heart Failure Texas Children's Hospital Baylor College of Medicine Houston, Texas ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 20 20:40:33 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 20 Apr 2006 20:40:33 -0300 Subject: [HF-FORUM] 88E RE: Bifascicular block. Chagas. Dr. Perez Riera Message-ID: Dear Dr Li Zhang: my best virtual pupil of Forum of 1st Advanced Virtual Course on Normal and Pathologic Electrocardiogram and Vectorcardiogram through the Internet. RBBB + LAFB (Bifascicular block) is the hallmark of ECG/VCG in chronic Chagas cardiomyopathy. The diagnosis of association: RBBB + LAFB + LSFB (a rare trifascicular block) has some particularities: both BDAM and BRD manifest in the horizontal plane. The BRD modifies the ECG additionally in the frontal plane, being responsible for broad S waves in DI and aVL and final broad R wave in aVR. An outstanding element of this trifascicular block is the delay in the initial 20 ms in the left middle-septal and antero-superior regions, dependent from the respective fascicles or divisions: LSF and ASF, now blocked. In this case, we may divide the ventricular activation sequence in three moments: 1) Vector of initial 20 ms; 2) Vector from 30 to 60 ms; 3) Vector from 60 ms to 120 ms. 1) Vector of initial 20 ms: it represents the activation of the subendocardium of the postero-inferior region, which is not affected. As the antero-superior and antero-medial regions are blocked, an initial vector is originated, which depends on the posterior division (called vector 1PI), and which heads backward and to the left. This explains the small initial q wave in V1, V2 or V3 (1). The absence of the vector dependent on the middle-septal fascicle (vector 1AM dependent on the middle fasicle), which would normally head to the front and the right, explains the lack of initial q wave in the left leads V5, V6 and DI. 2) Vector from 30 to 60 ms: it represents the activation of the antero-superior and antero-medial regions, which is processed by the septal Purkinje arborizations and the free wall, which causes an important anterior shift, mildly to the left, of forces. The activation of this area is translated by prominent and spikey R waves, with a broadening in the descending ramp in V2 and/or V3, R of V2 > V3 and QRS loop shift in the HP to the front and the left with clockwise rotation: Prominent Anterior Forces (PAF). It is very important to take into account that the diagnosis of this association should obligatorily be clinical and electrocardiographic; i.e. in absence of causes for right ventricular enlargement, dorsal electrically inactive area or other less common causes of PAF (3). Additionally, the diagnosis is reinforced and unequivocal if the phenomenon manifests intermittently or sequentially (4). 3) Vector from 60 ms to 120 ms: it represents RV activation by the vectors of transeptal jumping wave (5). A shift to the right and the front of the QRS loop in the HP is observed, with significant end delay located in the right anterior quadrant, with the classical "glove-finger" image, typical of RBBB. In ECG it is responsible by broad S wave in the left leads DI, aVL, V5 and V6, by broad R' in aVR and V1. It is important to emphasize that as a consequence of the competition between the LSFB forces to the left and the slow right end forces of RBBB, the S waves in V5 and V6 are wider than they would be in isolated RBBB. References 1) Moffa PJ, Del Nero E, Tobias NM, Serro Azul LG, Pileggi F, Decourt LV.: The left anterior septal block in Chagas? disease. Jap Heart J. 1982; 23:163-5 2) Vichi FL, Romero LC, Arevalo JR. The prevalence of branch and left fascicular blocks in the bundle of His in Chagas' cardiomyopathy. Arq Bras Cardiol 1982;39:87- 88. 3) P?rez Riera AR ?Electrocardiographic and Vectorcardiographic Sequencial Demonstration of Unknown Left Trifascicular Intraventricular Conduction Block: Right Bundle Branch Block, Left Posterior Fascicular Block and Left Septal Fascicular Block: Anterior Conduction Delay? 1rs Virtual Congress of Cardiology. October, 1999 to March, 2000 on Internet. 4) Dhala A, Gonzalez Zuelgaray J, Deshapande S, et. al.: Unmasking the trifascicular left intraventricular conduction system by ablation of the right bundle block. Am J Cardiol 1996; 77: 706-712. 5) Sanches PCR, Moffa PJ, Sosa E, et al. ELECTRICAL ENDOCARDIAL MAPPING OF FIVE PATIENTS WITH TYPICAL ECG OF LEFT-MIDDLE(SEPTAL) FASCICULAR BLOCK. In Proceeeding of The XXVIII International Congress on Electrocardiology Guaruj? SP Brazil. 2001 pp89-95. All the best Andr?s Ricardo P?rez Riera. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 20 21:33:04 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 20 Apr 2006 21:33:04 -0300 Subject: [HF-FORUM] 91S DCM in obese patient with risk factors. Dr. Larrateguy Message-ID: Dear colleagues, In this case, I agree with everything that was expressed, although I think it would be a good practice to assess the symptoms of sleep apnea syndrome (there should be some) and in this case conduct a night polysomnography and titrate the pressure necessary for CPAP. In these cases, the benefit of this treatment to improve her heart disease while waiting for bariatric surgery and the response to cardiological medication have been proven. I attach a review on the topic. Kind regards, Bibliographical references: 1. K?hnlein T, Welte T, Tan LB, Elliot MW.. Central sleep apnoea syndrome in patients with chronic heart disease: a critical review of the current literature. Thorax 2002;57:547-54. [Medline] [Descargar cita] 2. Yan AT, Bradley TD, Liu PP.. The role of continuous positive airway pressure in the treatment of congestive heart failure. Chest 2001;120:1675-85. [Medline] [Descargar cita] 3. Leung RS, Bradley TD.. Sleep apnea and cardiovascular disease. Am J Respir Crit Care Med 2001;164:2147-65. [Medline] [Descargar cita] 4. Roux F, D'Ambrosio C, Mohsenin V.. Sleep-related breathing disorders and cardiovascular disease. Am J Med 2000;108:396-402. [Medline] [Descargar cita] 5. Ho KK, Anderson KM, Kannel W, Grossman W, Levy D.. Congestive heart failure/myocardial response/valvular heart disease: survival after the onset of congestive heart failure in Framingham heart study subjets. Circulation 1993;88:107-15. [Medline] [Descargar cita] 6. Javaheri S, Parker TJ, Liming JD, Corbett WS, Nishiyama H, Wexler L, et al.. Sleep apnea in 81 ambulatory male patients with stable heart failure: types and their prevalences, consequences and presentations. Circulation 1998;97;2154-9. [Medline] [Descargar cita] 7. Sin D, Fitzgerald F, Parker JD, Newton G, Floras JS, Douglas T.. Risk factors for central and obstructive sleep apnea in 450 men and woman with congestive heart failure. Am J Respir Crit Care Med 1999;160:1101-6. [Medline] [Descargar cita] 8. Solin P, Bergin P, Richardson M, Kaye DM, Maydn WE, Naughton HT.. Influence of pulmonary capillary wedge pressure on central apnea in heart failure. Circulation 1999;99:1574-9. [Medline] [Descargar cita] 9. Hanly PJ, Zuberi-Khokhar NS.. Increased mortality associated with Cheyne-stokes respiration in patients with congestive heart failure. Am J Respir Crit Care Med 1996;153:272-6. [Medline] [Descargar cita] 10. Sin D, Logan A, Fitzgerald F, Liu P, Bradley TD.. Effects of continuous positive airway pressure on cardiovascular outcomes in heart failure patients with and without Cheyne-stokes respiration. Circulation 2000;102:61-6. [Medline] [Descargar cita] 11. Shahar E, Whitney CW, Redline S, Lee ST, Newman AB, Nieto FJ, et al, for Sleep Heart Health Study Research Group.. Sleep-disordered breathing and cardiovascular disease. Am J Respir Crit Care Med 2001;163:19-25. [Medline] [Descargar cita] 12. Naughton MT.. Pathophysiology and treatment of Cheyne-stokes respiration. Thorax 1998; 53:514-8. [Medline] [Descargar cita] 13. Walsh JT, Andrews R, Srarling R, Cowely AJ, Johnston ID, Kinnear WJ.. Efeccts of captopril and oxygen on sleep apnoea in patients with mild to moderate congestive cardiac failure. Br Heart J 1995;73:273-41. 14. Tremel F, P?pin L, Veale D, Wuyam B, Sich? P, Maillion JM, et al.. High prevalence and persistence of sleep apnoea in patients referred for acute left ventricular failure and medically for over 2 months. Eur Heart J 1999;20:1201-9. [Medline] [Descargar cita] 15. Takasaki Y, Orr D, Popkin J, Rutherford R, Liu P, Bradley TD.. Effect of nasal continuous positive airway pressure on sleep apnea in congestive heart failure. Am Rev Respir Dis 1989;140:1578-84. [Medline] [Descargar cita] Luis Dar?o Larrateguy Jefe del Servicio de Neumonolog?a Hospital San Mart?n. Director del Centro Privado de Medicina Respiratoria de Paran?. Presidente de la Asociaci?n de Neumonolog?a de Entre R?os. Urdinarrain 120 (3100) Paran?. Entre R?os. Argentina. TE/FAX: 54-343-4319919 www.RespirarParana.com.ar -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 20 21:50:06 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 20 Apr 2006 21:50:06 -0300 Subject: [HF-FORUM] EXPERTS ASK, EXPERTS ANSWER 2 Message-ID: <4AA1C90C-338B-48E0-89C9-1D2163A7F7B2@hf-symposium.org> Dr. Luis Castro Diaz from Panama asks - Is there a definite indication for the anticoagulation in patients with heart failure, sinus rhythm and a very low ejection fraction? Drs. Yongxin Lu and Gao Runlin from China answer - No, the usefulness of anticoagulation is not well established in patients with heart failure, sinus rhythm and a very low ejection fraction. Although, patients with heart failure are at increased risk of thromboembolic events due to stasis of blood in dilated hypodynamic cardiac chamber and in peripheral blood vessels and increased activity of procoagulation factors, the rate of thromboembolism in clinically stable patients has been very low, about 1-3%. In the absence of definitive trials, it is not clear how anticoagulants should be prescribed in patients with heart failure. Anticoagulation with warfarin is reasonable in patients with atrial fibrillation who have experienced a previous embolic event or who have paroxysmal or persistent atrial fibrillation. Anticoagulation should be considered in patients with underlying disorders such as amyloidosis or noncompaction of left ventricle and so on that may be associated with increased risk, and in patients with familial dilated cardiomyopathy and a history of thromboembolism in first-degree relatives. In CHF patients with acute illness, upon hospital admission or bed confinement with additional risk factors (such as active cancer, prior VTE, sepsis, acute neurologic disease, or inflammatory bowel disease), low molecular weight heparin is recommended to prevent venous thromboembolism, according to ACCP Evidence-Based Clinical Practice Guideline on Antithrombotic and Thrombolytic Therapy. Yongxin Lu MD and Gao Runlin, MD China -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 21 15:17:35 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 21 Apr 2006 15:17:35 -0300 Subject: [HF-FORUM] 84S RE: Patients who don't respond to CRT. Dr. Schapachnik Message-ID: <9E054B65-AFBF-4A39-B9E2-F10ADCA33568@hf-symposium.org> Dear Dr. Wang, At the Lecture Hall of the Symposium, the presentation by Drs. Johnson Francis, Sunil Roy and Roy John is available, with the title "Prediction of response to cardiac resynchronization therapy," which widely responds your question. You may have access from: http://www.hf-symposium.org/lectures.php Cordially, Edgardo -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 21 17:29:50 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 21 Apr 2006 17:29:50 -0300 Subject: [HF-FORUM] 92S RE: DCM in obese patient with risk factors. Dr. Valdes Garcia Message-ID: <224B03E3-2CE6-422A-9EEC-BF72163052FC@hf-symposium.org> Greetings! Thank you very much for all your comments. The patient will come back to Los Angeles, where her other children live. Dr. Valdes Garcia -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 21 18:03:40 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 21 Apr 2006 18:03:40 -0300 Subject: [HF-FORUM] 93P RE: Chagasic cardiomyopathy. Dr. Perez Riera Message-ID: Dear Li, There is a great number of studies in evidence-based medicine that are aimed at the efficacy, the improvement of quality of life (MUSTIC-MIRACLE) and increase of survival (COMPANION, CARE) and safety of cardiac resynchronization therapy (CRT) in treating heart failure in those patients with systolic dysfunction that remain in NYHA functional class III or IV in spite of optimal pharmacological treatment and ejection fraction = or < 35% with QRS duration > 120 ms, mainly left bundle branch block. This dromotropic disorder causes asynchronous contraction of the left ventricle between the septum and the posterior wall, increasing the fall in EF and dysfunction worsening. In spite of this advancement, approximately 25% to 30% of the cases do not respond, even following these indication criteria subsequent to the independence existing between electrical and mechanical asynchrony. The delay in LV free wall activation in LBBB is considered to be one of the main causes of contraction asynchrony, and it should be expected that contraction asynchrony should not occur in RBBB, since LV contraction in this dromotropic disorder is not altered (1). In Chagas disease the presence of LBBB is an exceptional fact that leads to think that this may be the main cause not to indicate CRT in this entity. Additionally, the presence of LBBB is one of the predictors of low EF (2). RBBB, polymorphic PVCs and LAFB are the commonest cardiac arrhythmias among the chagasic patients, and each of these types of arrhythmia (alone or with other types of arrythmia) is more frequent in the chagasic patients than the non-chagasic. The incidence of RBBB among the arrhythmic varied significantly with age in the non-chagasic patients (increasing with age among both the males and females) but not among the chagasic subjects. When the frequencies of each type of arrythmia and each combination of types were compared, the co- occurrence of RBBB and another type of arrhythmia was almost indicative of American trypanosomiasis (occurring in 30.6% of the chagasic subjects but only 2.6% of the non-chagasic). Similarly, only 0.4% of the non-chagasic patients but 7.4% of the chagasic had RBBB, PVCs and LAFB concurrently. However, the frequencies of RBBB in isolation (i.e. with no other, concurrent, electrocardiographic abnormality), PVCs in isolation, or LAHB in isolation were not significantly different in the chagasic and non-chagasic patients (3). Clinical trials of CRT have not included many patients with RBBB. Egoavil et al (4)pooled data from two randomized controlled trials of CRT MIRACLE and Contak CD in order to assess outcomes of patients with RBBB. A total of 61 patients with RBBB were identified, 34 of whom were randomized to the CRT group and 27 to the control group. Baseline demographics were not different between the two groups (mean age 65.5 +/- 11.3 years vs 69.5 +/- 9.6 years; male gender 91% vs 85%; patients with coronary disease 76.5% vs 88%; QRS duration 167 ms vs 164 ms; all P = NS). Outcome variables NYHA class, 6-minute hall walk distance, peak oxygen consumption (VO2), Minnesota Living with HF quality-of-life scores, LVFE, and norepinephrine levels were analyzed at randomization, 3 months, and 6 months. Conclusions: 1) With the exception of NYHA class, patients with RBBB as the qualifying wide QRS did not derive significant benefit from CRT in any of the other parameters studied at 3 or 6 months; 2) RBBB patients who received CRT showed significant improvements in NYHA class by 6 months and trends toward improvement in 6-minute walk distance, quality-of-life scores, and norepinephrine levels. However, control patients also showed significant improvement in NYHA class by 6 months but showed no improvement in objective measurements VO2, 6-minute walk distance, LVFE, and norepinephrine levels, consistent with a placebo effect. 3) Analysis of a larger cohort of patients with RBBB undergoing CRT may demonstrate significant benefit, but the current analysis does not support the use of CRT in patients with RBBB. References 1) Khand A, Gemmel I, Clark AL, Cleland JG. Is the prognosis of heart failure improving?J Am Coll Cardiol. 2000;36:2284-6. 2) Garzon SA, Lorga AM, Nicolau JC. Electrocardiography in Chagas' heart disease. Sao Paulo Med J. 1995;113:802-813. 3) Jorge MT, Macedo TA, Janones RS, Carizzi DP, Heredia RA, Acha RE. Types of arrhythmia among cases of American trypanosomiasis, compared with those in other cardiology patients. Ann Trop Med Parasitol. 2003;97:139-148. 4) Egoavil CA, Ho RT, Greenspon AJ, Pavri BB.Cardiac resynchronization therapy in patients with right bundle branch block: analysis of pooled data from the MIRACLE and Contak CD trials. Heart Rhythm. 2005;2:616-618. Best for all Andr?s Ricardo P?rez Riera -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 21 18:08:36 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 21 Apr 2006 18:08:36 -0300 Subject: [HF-FORUM] 94S RE: Chagasic cardiomyopathy. Dr. Pellizon Message-ID: <65E249BA-A17D-422A-8E4A-404100DA4404@hf-symposium.org> Chagasic cardiomyopathy has always generated debates, discussions and controversies about the treatment of complications, particularly CHF and ventricular arrhythmias. This is due, as far as I know, to the fact that a randomized trial has never been made as with other diseases, such as the ischemic. The ICD-Labor is offering us some interesting data, but of course, it is just a registry and only less than a third of the implantations is due to Chagas disease, thus showing that it is the second cause for implantations in Latin-America. Undoubtedly, the AVID is missing in Chagas. Until we have this trial, I think that most electrophysiologists will have to extrapolate class I indications from the ACC/AHA/HRS. According to Dr. Dubner, taking into account the characteristics of these patients, he concludes that the results obtained from ICD-Labor DO NOT support the automatic transference of indications used for ICD implantation in patients with ischemic heart disease into those with Chagas disease. According to your criteria, today, what patients with chronic chagasic cardiomyopathy should receive an ICD? Excellent symposium and interesting questions and debate. Dr. Oscar A. Pellizz?n. Rosario. Argentina -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 21 19:04:49 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 21 Apr 2006 19:04:49 -0300 Subject: [HF-FORUM] 98E RE: Non-responders to CRT. Dr. Moss Message-ID: <2C3549B4-9653-42C0-9B18-FEAB0801F333@hf-symposium.org> Dear Dr. Wang, At the present time, there is no reliable way of determining who will and will not achieve a favorable response from CRT. A number of groups are working on this problem with tissue doppler, echo- determined regional wall motion dysfunction, etc., but none of the currently available techniques have sufficient sensitivity and specificity to reliably include or exclude patients from CRT. Yes, CRT is an expensive option, but it is much less expensive than cardiac transplant. Regards, ...Dr. Moss ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 21 19:19:39 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 21 Apr 2006 19:19:39 -0300 Subject: [HF-FORUM] 99E RE: DCM in obese patient with risk factors. Dr. Levine Message-ID: Dr. Encinas Landivar raised the same question with respect to beta blockers. I have also not seen any major studies evaluating the use of atenolol as a treatment for CHF. Dr. Valdez Garcia acquired this patient when she was admitted with pulmonary edema and then when she had been stabilized, discharged her and she returned home to another city or country under the care of another physician. In that atenolol is an inexpensive medication, particularly in comparison to carvedilol, and that she appeared to respond well to the therapy, I would also have continued that agent rather than starting her on some medications that she may or may not be able to obtain (or afford) when she returned home. If I was the physician who would then be following this patient, I would have switched her to carvedilol but if I was returning the patient to the care of another physician at a far distance such that I would no longer be involved in that patient's care, I would have continued the simplest regimen possible. It is nice to be highly academic and all of Dr. Encinas Landivar's points are very valid and appropriate, one also needs to also keep in mind the practicalities of available resources, both medical and financial. With that said, Dr. Encinas Landivar makes some excellent points, however presumptions are made that are not justified. Dr. Valdez Garcia did not comment on the width of the QRS - I also presumed that it was likely to be wide with respect to his question as to whether we should proceed with drugs or turn to an implanted device. With respect to a > 10 year history of diabetes in an obese patient, we can not > automatically assume her response to oral hypoglycemics will be inadequate. It may be that she was non-compliant or because she appeared to be clinical stable, her local physician was not insistent about adherence to a weight reduction diabetic diet, taking her medications on a regular basis and monitoring both blood sugars and her glycosylated hemoglobin level. In view of the problems that she encountered requiring acute hospitalization, multiple factors might have to be addressed almost simultaneously but the important point is to now make every effort to assure that the diabetes is under control, her HBP is under control, her cholesterol level is as low as possible..... She will not lose weight overnight, her diabetes - if out of control will not come under control instantly but if everything is going in the right direction, she should probably do well. The very cryptic description of the clinical case for which advice was sought, based on many of the very appropriate responses and suggestions, also point out the need for a comprehensive history of what had been tried in the past with a full knowledge of the patient's socio-economic state and available medical resources with respect to where ever she lived. All of us treat patients - that is far more complex than treating a disease. Prevention is wonderful. However, we do not know the patient's level of compliance with any recommended medical regimen prior to this patient's acute decompensation or whether the physician who was caring for her before this episode was very aggressive in an effort to control her DM, HBP, etc. All too often, all of us meet patients in the hospital environment for the first time who, if we had earlier control of the patient, might have approached that patient differently in the hope of preventing this very problem. Having said that, I am sure that we have all had patients (at least I know that I have had patients) who despite my best efforts to get them to stop smoking, to take a statin because of either high risk or their cholesterol was too high, take a beta blocker, meticulously control their diabetes .... had one excuse after the next for why they were not compliant. In the United States with all the sub-specialization, In my current very focused practice, I see patients for follow-up with their pacemaker who also have diabetes or hypertension or elevated cholesterol and while I check their BP as part of my follow-up evaluation, I defer management of their diabetes and cholesterol to another physician (usually their primary care physician) and while I check the BP, if it high, and talk to the patient about the need to control these disease, I do not specifically prescribe medications for it. Rather, I mention this in my letter to the referring physician relying on that physician to follow-up those other conditions. Sometimes the physician is not aggressive. Other times, the patient is non-compliant. Even in the relatively "wealthy" United States, I have had patients who could not afford their medications or who would have to decide between purchasing the prescribed medications or buying food so that they could eat. Food always wins, particularly when the problem being treated is relatively silent (HBP, elevated cholesterol) until an adverse clinical consequence (pulmonary edema, acute myocardial infarction....) occurs. This becomes a very powerful incentive to get control of various medical conditions. Paul A. Levine, MD, FHRS, FACC Vice President, Medical Director St. Jude Medical, CRMD 15900 Valley View Ct. #980, Sylmar, CA 91342 818-493-2900 / Fax: 818-362-2242 ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 21 19:21:14 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 21 Apr 2006 19:21:14 -0300 Subject: [HF-FORUM] 95E RE: BNP and diastolic dysfunction. Dr. De Bold-Dr. Stanton Message-ID: The following answer was provided by Dr. Eric Stanton. Dr. Eric Stanton, of Hamilton, Ontario, Canada, is Associate Professor of Medicine at McMaster University in Hamilton. He is former Head, Division of Cardiology, at St. Joseph's Hospital. He has been extensively involved in projects using BNP as a biomarker. Here is his answer: Clearly there is mounting evidence (I can supply some references if required) that BNP/NTproBNP are very sensitive markers for diastolic dysfunction and are more specific than other non invasive tests such as echocardiography. In patients who present with Shortness of Breath or with signs and symptoms of left ventricular failure with normal systolic function and a norml heart size on the Chest X-ray (these are usually patients with left ventricular hypertrophy (LVH) from a hypertrophic cardiomyopathy or significant LVH from uncontrolled hypertension) I believe that these will prove to be valuable markers in guiding the clinician to a correct diagnosis. As to how many clinicians are familiar with this concept and are at present using the markers in this way is difficult to say. As clinicians in general become more aware and familiar with the attributes and clinical utility of these important markers through diverse events I believe we will see increased use of these markers in t he evaluation of patients suspected of having diastolic dysfunction. Adolfo J. de Bold, OC, Ph.D., FRSC Professor of Pathology and Laboratory Medicine Cardiovascular Endocrinology Laboratory University of Ottawa Heart Institute 40 Ruskin St. Ottawa, Ontario K1Y 4W7 Canada Tel.: +1(613) 761 4265 Fax: +1(613) 761 1597 adebold at ottawaheart.ca ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 21 20:07:33 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 21 Apr 2006 20:07:33 -0300 Subject: [HF-FORUM] 101E Sleep apnea. Miss Tink Long Message-ID: The following was written by Luis Dar?o Larrateguy: "In this case, I agree with everything that was expressed, although I think it would be a good practice to assess the symptoms of sleep apnea syndrome." For what it might be worth... The above text was a reminder of sleep apnea reported by at least 4 patients with ARVD. Two of the patients noted increased and problematic arrhythmias in the early morning hours (i.e. those threatening VT; male patient approx. mid 30s, female patient approx. late 50s.) The other two were noted to have breathing difficulties during the night (male patient approx. late 30s, male patient approx. late 50s.) All 4 were evaluated for sleep apnea. All were found with it and treated by CPAP. After CPAP treatment, the two patients who had experienced early morning arrhythmias reported being relieved of them. The other two have had their nighttime breathing difficulties alleviated. Micheline "Tink" Long Email: tink2000 at antelecom.net ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 21 22:29:11 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 21 Apr 2006 22:29:11 -0300 Subject: [HF-FORUM] 97S Sleep apnea. Dra. Perez Leon Message-ID: Dear Professors, Something else about sleep apnea: It is associated with arrhythmias, hypertension, myocardial infarction and stroke by the recurrent intermittent hypoxia of sleep respiratory disorders and overstimulation of systemic sympathetic tone. This is reflected in the increase of nocturnal death. Could send bibliography about this? Thank you very much and kind regards, Dra. Mariblanca P?rez Le?n. Cuba. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 21 22:37:02 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 21 Apr 2006 22:37:02 -0300 Subject: [HF-FORUM] 96S Cardiac tumors. Dr. Perez Leon Message-ID: <3E240ACF-E349-4C40-BAC7-72E8941FFD80@hf-symposium.org> Dear colleagues, What are the current news about primary cardiac tumors? Kind regards, Dra. Mariblanca P?rez Le?n. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 21 23:10:19 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 21 Apr 2006 23:10:19 -0300 Subject: [HF-FORUM] 103E RE: Bifascicular block. Chagas. Dr. Li Zhang Message-ID: Thank you so much Dr. Perez Riera for the magnificent explanation. May I ask you one more question: The P-R interval is about 230-240 ms in this case. Is it reasonable to consider the possibility of complete RBBB+LAFB+LSFB and first degree incomplete left posterior fascicle block (LPFB)? In other words, the AV-His-Purkinje system has been significantly affected in this case due to Chagasic cardiomyopathy. Because HF patients with conduction blocks often with poor prognosis, but some of them can be benefited from CRT. Thus it may be necessary to learn and recognize various bundle/fascicular blocks. SEE THE ECG http://www.hf-symposium.org/files/Li_ECG.pdf Sincerely, Li Zhang, MD LDS Hospital Salt Lake City, UT ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 22 08:57:16 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 22 Apr 2006 08:57:16 -0300 Subject: [HF-FORUM] 104E RE: Non-responders to CRT. Dr. Perez Riera De Message-ID: Dear Prof. Dr. Arthur Moss: indeed a three-dimensional echocardiography and Tissue Doppler imaging (TDI) are relatively new tools for de evaluation the systole delay. Delays = or > 34,4ms identify the patients that CRT will be effective. CRT is a no pharmacological treatment option in patients with HF and LBBB but response rates are still disappointing. Extent of mechanical LV asynchrony as detected by TDI has emerged as an independent predictor of outcome to CRT. In addition, long-term therapy delivery may be further improved through optimized lead positioning and pacing programming. TDI should be included in the evaluation of potential CRT candidates but standardized evaluation criteria have not yet been provided (1). The extent of the LV base displaying delayed longitudinal contraction, as detected by TDI before pacemaker implantation, predicted long-term efficacy of CRT. The QRSd failed to predict resynchronization efficacy (2). The improvement in the interventricular mechanical delay after CRT is significantly correlated with the decrease in LV end-systolic volume. CRT reduces LV volumes in patients with advanced HF, CLBBB and detailed documentation of ventricular asynchrony prior to therapeutic pacing. Broadly applicable Doppler echocardiography measures may increase the specificity of the long-term response to CRT in terms of LV performance (3). For the detection of regional longitudinal LV contraction asynchrony in patients with severe HF, supplementary methods to the surface ECG, such as Color Doppler tissue velocity imaging, are strongly recommended(4). References 1) Sogaard P, Hassager C. Tissue Doppler imaging as a guide to resynchronization therapy in patients with congestive heart failure. Curr Opin Cardiol. 2004 ; 19:447-451. 2) Sogaard P, Egeblad H, Kim WY, Jensen HK, Pedersen AK, Kristensen BO et al. Tissue Doppler imaging predicts improved systolic performance and reversed left ventricular remodeling during long-term cardiac resynchronization therapy. J Am Coll Cardiol. 2002;40:723-730. 3) Barbieri A, Bursi F, Bonatti S, Coppi F, Zanasi V, Reggianini L, et al.Evidence of reverse remodeling after long-term biventricular stimulation for resynchronization in patients with wide QRS selected on the basis of echocardiographic electromechanical delays. 4) Schuster P, Faerestrand S, Ohm OJ. Color Doppler tissue velocity imaging can disclose systolic left ventricular asynchrony independent of the QRS morphology in patients with severe heart failure. Pacing Clin Electrophysiol. 2004; 27:460-467. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 22 09:17:32 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 22 Apr 2006 09:17:32 -0300 Subject: [HF-FORUM] 105E Dobutamine. Dr. La Rovere Message-ID: Is it possible to administer dobutamine to a patient with chronic heart failure under beta-blocker treatment when he becomes clinically unstable? Dr. Maria Teresa La Rovere Italy -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 22 09:36:56 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 22 Apr 2006 09:36:56 -0300 Subject: [HF-FORUM] 100R CRT in children. Dr. Macarov Message-ID: <2AD60A1D-128F-4A80-A3CA-D61FE3D4F9EB@hf-symposium.org> I would like to ask a question to the participants of the Symposium: There is no significant experience on CRT in pediatrics, or clear indications about it. To this date, in Russia CRT was never used in pediatric patients. According to my knowledge, in the St. Luis Hospital (USA), among the hemodynamic indications, only EF <50% is included. Really, is this the only indication? What is the significance of LV end diastolic diameter and other indicators? We would like to know the opinion of the specialists who may have this experience, since currently, we have the CRT available in our institution. Institute of Pediatrics and Pediatric Surgery (Moscow, Russia) Dr. Macarov L.M. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 22 10:09:44 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 22 Apr 2006 10:09:44 -0300 Subject: [HF-FORUM] 107R Digoxina and carvedilol. Dr. Yabluchansky Message-ID: I would like to know which doses do you use for digoxin and carvedilol? Thank Myckola Yabluchansky, Kharkov, Ukraine -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 22 11:56:26 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 22 Apr 2006 11:56:26 -0300 Subject: [HF-FORUM] 102S RE: Resynchronization or transplantation. Dr. Montes de Oca Message-ID: <27BA116A-9CD6-4212-B620-3B538550D114@hf-symposium.org> Dear colleague, I think when there is indication for resynchronization, we have to apply it, since there is strong evidence that it improves functional class and decreases mortality. Therefore, I don't use it as an alternative method for cardiac treatment. Dr. Omar Montes De Oca Montevideo-Uruguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 22 15:32:18 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 22 Apr 2006 15:32:18 -0300 Subject: [HF-FORUM] 110E RE: Non-responders to CRT. Dr. Saksena Message-ID: This is an interesting discussion. This year we will be presenting data on the use of intracardiac echocardiography for patient selection and optimizing programming of CRT devices. This has reduced the number of non-responders very substantially. The pilot clinical data will be presented at a symposium at the upcoming Heart Rhythm Society meetings. Sanjeev Saksena Sanjeev Saksena MD FACC FESC FHRS FAHA Professor of Medicine, UMDNJ-Robert Wood Johnson Medical School Medical Director, Electrophysiology Research Foundation Editor in Chief, Journal of Interventional Cardiac Electrophysiology Past President, Heart Rhythm Society ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 22 15:51:31 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 22 Apr 2006 15:51:31 -0300 Subject: [HF-FORUM] 106S RE: DCM in obese patient with risk factors. Dr. Ortiz Message-ID: <129D2C80-4925-4B84-AC3F-821E7C089E62@hf-symposium.org> Dear colleague, About your patient, in my opinion, since this is a woman with multiple positive coronary risk factors, history of previous AMI with possible involvement of 2 vessels, as you told us, and having recently presented acute pulmonary edema, I would perform a coronary angiography first, to rule out coronary injuries that could be revascularized, and thus prevent a greater impairment of heart performance. I send my regards to everyone, and I would like to thank especially the organizers of this excellent symposium for the chance to exchange such enriching opinions with colleagues from all over the world. Dra. Patricia Ortiz- Buenos Aires-Argentina -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 22 19:16:03 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 22 Apr 2006 19:16:03 -0300 Subject: [HF-FORUM] 108S Chagasic cardiomyopathy. ECG. Dr. Viano Message-ID: Tracing of a 65-year-old male patient, from Santiago del Estero, Argentina (a highly endemic province for Chagas disease) and carrier of Chagasic cardiomyopathy. Francisco Viano See the tracing at: http://www.hf-symposium.org/files/Viano_ECG.jpg -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 22 22:59:34 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 22 Apr 2006 22:59:34 -0300 Subject: [HF-FORUM] 109E RE: Cardiac tumors. Dr. Chachques Message-ID: Dear colleagues, We have developed a surgical approach for the reconstruction of the ventricles following tumor resection. This approach avoids heart transplantation. You can find enclosed the Abstract and the PDF version of this article****. Best regards, JC Chachques J Thorac Cardiovasc Surg. 2002 May;123(5):889-94. Cardiomyoplasty: ventricular reconstruction after tumor resection. Chachques JC, Argyriadis PG, Latremouille C, D'Attellis N, Fornes P, Bruneval P, Couetil JP, Carpentier AF. Department of Cardiovascular Surgery, Broussais and Pompidou Hospitals, Paris, France. j.chachques at brs.ap-hop-paris.fr OBJECTIVE: Although cardiac transplantation has been performed for complete removal of ventricular tumors, complete surgical resection with ventricular reconstruction is desirable. Thus patients with benign tumors would probably be cured, and those with malignant tumors would have a better prognosis. In this study extensive and complete surgical resection of ventricular tumors is followed by anatomic and functional ventricular reconstruction with a dynamic cardiomyoplasty procedure. METHODS: Seven patients (mean age, 32.7 years) underwent complete resection of ventricular tumors. Histologic types were distributed as follows: fibroma in 2 patients and sarcoma, lymphosarcoma, hemangioma, lipoma, and metastatic angiosarcoma, respectively, in the remaining 5 patients. Six of the patients were considered candidates for heart transplantation because of the extent of tumor invasion. Surgery consisted of 4 steps: (1) tumor resection; (2) coronary artery resection (when invaded by th e tumor) and coronary artery bypass grafting; (3) valvular reconstruction (when possible) or replacement; and (4) ventricular wall reconstruction with a pericardial patch for closure of the ventricular defect (neoendocardium) covered by the electrostimulated latissimus dorsi muscle flap (neomyocardium). RESULTS: All patients survived surgical intervention, but 2 late postoperative deaths are reported. Among the surviving patients, early complications played a major role in their postoperative course and consisted of arrhythmias, atrioventricular block necessitating a dual-chamber pulse generator, respiratory insufficiency, and heart failure. Two patients were assisted postoperatively with an intra-aortic balloon pump. On postoperative follow-up (mean, 72.4 +/- 8.5 months), an improvement in the patients' functional status was observed. Patients moved from a mean New York Heart Association functional class of 2.8 to a mean functional class of 1.2. CONCLUSIONS: The excellent lo ng-term evolution without recurrence, ventricular dysfunction, and/or thromboembolic complications implies that cardiomyoplasty could be recommended as an alternative to heart transplantation for the therapy of large ventricular tumors. **** SEE THE FILE AT http://www.hf-symposium.org/files/Chachques.pdf -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 22 23:37:10 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 22 Apr 2006 23:37:10 -0300 Subject: [HF-FORUM] 111S RE: DCM in obese patient with risk factors. Dr. Valdes Garcia Message-ID: <56665298-D862-4FB3-B914-FA8209567243@hf-symposium.org> I agree with Dr. Levine. The patient was also taking 200 mg of metoprolol and on top of that, she had ventricular rhythm with a mean ventricular rate 40-44, which made her management a bit more difficult. Nevertheless, heart rate improved 36 hours after the management with beta-blockers antagonist (dopamine). She had been taking 200 mg of metoprolol for six months, being diabetic. About other studies, azoates were initially high with 2.4 creatinine; she was discharged with 1.2 after being treated with hydration, dopamine and intravenous loop diuretics; glycose out of control with 282 mg/dl and at discharge with 136 mg/dl. The rest of azoates also decreased, they were only slightly high. The Holter study showed 40 isolated ventricular beats of 2 morphologies (class II B of Myerburg), maximal 7 in one hour. About supraventricular activity, she displayed 1 run of 4 beats at a rate of 104 bpm, 4 couplets and 122 isolated ones of a total of 92,346 beats analyzed. Maximal HR 86, minimal 50, and in average 64 (one week after dopamine was suspended), and with a 25 mg dose of atenolol, several pauses by sinus block, the greatest one 1.8 sec, inverted T wave several times, NNSD 94.20 ms, SSDA 69.54 ms, NNDrms 84.25 ms, total RR50 12,50%. Total beat 92259 beat, NNA 936.29 ms, SASD 40.07 ms. QRS remained between 130-140 ms; QT between 440 and 460 ms. Abdominal ultrasound: kidneys with initial loss of cortex-medullar ratio, congestive liver, with liver steatosis without precise details of nodules, not free of liquid, chest roentgenogram, moderate biventricular cardiomegaly with bibasal inflammatory injuries and slight left pleural effusion. Tests of liver performance were normal. Total cholesterol 198, triglycerides 195. She was discharged with the medication explained in this presentation. Waiting for control by echo. Dr. Valdes Garcia -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 23 14:04:16 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 23 Apr 2006 14:04:16 -0300 Subject: [HF-FORUM] 112S RE: Chagasic cardiomyopathy. Dr. Schapachnik Message-ID: Dear Li, It is a pleasure to answer the question you asked about chagasic heart disease, and twice as nice since it comes from a colleague from China and living in USA, two countries where this disease is not native regarding the possibility of vectorial transmission, since the vector insect of Trypanosoma Cruzi (the causative agent) is a heritage just from the American continent, especially from the south of USA to Argentine Patagonia; although the colleagues living in other countries should know about it, considering the so-called "globalization" has brought about other social phenomena such as massive migrations, which from the point of view of this disease has originated the relative growth of two other forms of transmission: one by transfusion and the other congenital by vertical transmission from mother to child; a phenomenon that has already determined the appearance of cases in USA, Europe and Japan, where Latin immigration is very important. On the other hand and inversely, our Latin countries are receiving a great immigration quota (for instance in our case, there is a numerous Chinese and Korean community living in Argentina, just to mention two communities that over the last 20 years have decided to join our society). This determines that these populations of immigrants are exposed to the same epidemiological risks as native inhabitants: they receive transfusions, transplantation of organs, etc., which makes them potential hosts of pathologies such as Chagas Disease. This should be a reason for reflection for authorities and medical institutions of the countries of origin and it is a reason to praise the concern and the question by our friend, Li Zhang. The first part of the question is about the epidemiological impact of this parasitosis, and especially the impact of heart failure attributable to this etiology. I regret having to disappoint the colleague, since I have to tell her that the poverty in our countries, besides economically and socially, is also expressed in the poverty and the lack of accurate data about the real prevalence of this disease and many others. The WHO estimates that in all the continent there are 120 millions of people exposed to contracting this disease vectorially, and that there are 16 millions who are already parasited. Now, not all of them will develop a dilated cardiomyopathy that would lead to heart failure and death. Traditionally, it has been accepted that 70% of the parasited patients are in the so-called indeterminate phase, in which there are no manifestations of organ involvement, and in which the diagnosis can only be established by the presence of circulating antibodies. The remaining 30% will develop some degree of heart disease. But if you pay careful attention to my words, you will see that I mention "some degree of heart disease" and not the final stage of Dilated Cardiomyopathy. This is because from this initial 30% of patients with heart disease, the great majority (more than 80% of them), only present ECG alterations as conduction disorders or ventricular arrhythmias, but with no manifestations of heart failure. This syndrome, which is the one causing this Symposium we are developing, is present only in the initial 5% of the whole parasited population. That is to say, if all these approximate figures the WHO has are correct, we would be talking about 800,000 patients approximately, in the American continent, who are carriers of the most severe forms of this disease. For instance, in our country Argentina, it is estimated that there are around 2 million parasited patients. A 70% of them, i.e. 1.4 million do not present any type of manifestations of heart involvement. There are 600,000 patients that make up the population of those "with some degree of cardiac involvement," and approximately 500,000 among them only present ECG alterations of variable severity; and the remaining 100,000 present varied dilated cardiomyopathies and heart failures. The second part of the question is about how many of these patients would be candidates and may afford CRT therapy and/or ICD implantation. We answer quickly that the great majority of the affected patients cannot afford such indications. Maybe it is difficult for colleagues from other countries to understand that our main concern -I repeat, MAIN- is not how many biventricular pacing devices we may indicate in these patients, but instead how to solve problems more pressing, such as the possibility of having a decent house or getting a job to support their families. Or what is more related to our work as cardiologists, how to guarantee that these patients have access to a continuing pharmacological treatment when indicated. In the pure field of contraction synchrony mechanics, as my friend Andres Perez Riera explained, these patients present as prevalent conduction disorder the association of complete right bundle branch block and left anterior fascicular block (or as they are more commonly known, although such nomenclature is not appropriate as Andres teaches, left anterior hemiblock), and therefore, would not be an indication for CRT therapy. It is a different matter with ICDs, since all the colleagues who take care of chagasic patients that are carriers of severe ventricular arrhythmias, know that this device has extended the life and recovered many of the more than 250 patients included in the LABOR study. I hope, dear Li, to have answered your question, and the possibility it gave me to explain why I insist on the idea that in the 21st century with the so-called globalization, all the cardiologists of the world should know about this disease, and for this reason Latin physicians have the obligation of transmitting our modest experience, as well as the responsibility of asking the Chinese colleagues to teach us about Keshan disease, by lack of selenium, and the cardiomyopathy associated with it. Warm regards, Edgardo -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 23 14:19:16 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 23 Apr 2006 14:19:16 -0300 Subject: [HF-FORUM] 114S Stem cells. Dr. Pereira Message-ID: Is there some ongoing study to prove the efficacy of procedures with stem cells, differentiating the different etiologies of heart failure? Luciano Pereira Paraguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 23 14:27:47 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 23 Apr 2006 14:27:47 -0300 Subject: [HF-FORUM] 115S Peripartum cardiomyopathy. Dr. Pereira Message-ID: <4298562E-C001-4684-AAC4-D97BE0641BBB@hf-symposium.org> Peripartum cardiomyopathy is an entity that has been intriguing for a long time for cardiologists all over the world. Is there any identified risk factor or biomarker for the study of this disease that is a cause of heart failure? Dr. Luciano Pereira Paraguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 23 15:08:14 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 23 Apr 2006 15:08:14 -0300 Subject: [HF-FORUM] EXPERTS ASK, EXPERTS ANSWER 3 Message-ID: <96FBBBB4-23A8-4275-A317-EF29E09226F9@hf-symposium.org> Dr. Alfedo Piombo from Argentina asks - Must Angiotensin II Receptor Antagonists be indicated in patients with congestive heart insufficiency already treated with angiotensin converter enzyme inhibitors? Dr. Marco Stramba-Badiale from Italy asks - IShould we use the combination of an ACE inhibitor and an ATII antagonist in all heart failure patients? Dr. Bertram Pitt from U.S.A. answers Thank you. The role of angiotensin receptor blockers (ARBs) in patients with heart failure due to systolic dysfunction treated with an ACE- inhibitor (ACE-I) remains controversial in view of the conflicting results in Val-heft, in which adding an ARB to an ACE-I had no effect on survival but reduced hospitalization for HF. However, the benefit in regard to hospitalization for HF was diminished in those on target doses (i.e. the dose shown to be effective in reducing mortality in a major randomized trial) of their ACE-I. In contrast the Charm added trial showed a benefit of adding an ARB to an ACE-I on both CV mortality and hospitalization for HF. These benefits did not appear to diminish in patients on recommended doses of their ACE-Is. My own view is that before considering adding an ARB to an ACE-I one should attempt to achieve the target dose of the patients on ACE-I and BB. In patients with mild-moderate HF, who remain symptomatic despite being on the target dose of their ACE-I and a BB, it would be reasonable to add an ARB. In patients with severe HF who are symptomatic despite being on target doses of their ACE-I and a BB, my preference is to add an aldosterone blocker based upon the results of RALES demonstrating a reduction in total mortality. Regardless of whether one adds an ARB or an aldosterone blocker to an ACE-I and a BB, one should carefully monitor serum potassium. If serum potassium increases to > 5.5 meq/l I would halve the dose of the ARB or aldo blocker, and if it reaches 6.0 I would discontinue the ARB or aldoblocker. In patients who show signs or symptoms of progressive HF despite the use of an ACE-I, BB and an ARB I would consider adding an aldoblocker. However there is only limited experience with all 4 of these agents. Conversely, if the patient was on an ACE-I, BB, and an aldoblocker but still had signs of progressive HF, I would consider adding an ARB. However if serum potassium was > 5.0 meq/l I would not add an aldo blocker to an ACE-I and an ARB, or conversely would be hesitant to add an ARB to a patient on an ACE-I and an aldo blocker if the serum potassium was > 5.0. If all 4 agents are used serum potassium should be closely monitored (at 1 week and then monthly for at least a year and any time the patient has a situation altering serum electrolytes such as vomiting or diarrhea). There are no large-scale trials comparing an ARB to an aldoblocker in patients on optimal doses of an ACE-I and a BB, so that you will find that some clinicians will prefer to add an ARB to an ACE-I and a BB while others, such as myself, would prefer an aldo blocker. Sincerely, Bertram Pitt MD -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 23 17:00:48 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 23 Apr 2006 17:00:48 -0300 Subject: [HF-FORUM] EXPERTS ASK, EXPERTS ANSWER 4 Message-ID: <60D9C6E4-02C7-4648-A590-7D36AF36A2FF@hf-symposium.org> Dr. Elzbieta Katarzyna Wlodarska from Poland asks - Complications after heart transplantation in patients with arrhythmogenic right ventricular cardiomyopathy Dr. Mariell Jessup from USA answers - Since the right ventricle and the outflow tract of the right ventricle are replaced completely at the time of heart transplant, there is no particular reason why patients with arrhythmogenic right ventricular cardiomyopathy have any different outcome than other patients. Indeed, since they often do not have other medical problems, such as diabetes or vascular disease, they are frequently overall better candidates than the majority of patients who currently come to transplant. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 23 17:17:38 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 23 Apr 2006 17:17:38 -0300 Subject: [HF-FORUM] 121S RE: Stem cells. Dr. Kingenheben Message-ID: <5FA3FDC9-255F-42BA-9504-64F5FE9727D8@hf-symposium.org> One Group in Germany, of Prof. Andreas Zeiher, J.W. Goethe University Frankfurt, Frankfurt Germany, is doing clinical studies in patients with heart failure, and there is one protocol including patients with non-ischemic dilated cardiomyopathy, as well. Regards Thomas Klingenheben, Bonn, Germany Thomas Klingenheben, M.D. Assistant Professor of Medicine (Univ. of Frankfurt) Cardiology Practice Alfred-Bucherer-Str. 6 DE-53115 Bonn Germany phone: +49-228-623324 fax: +49-228-616881 Klingenheben at aol.com www.bonn-kardiologie.de ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 23 21:09:03 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 23 Apr 2006 21:09:03 -0300 Subject: [HF-FORUM] 123E RE: Peripartum cardiomyopathy. Dr. Perez Riera Message-ID: <0AF1EF1E-BE4F-4718-AB67-FCD9F5974030@hf-symposium.org> Dear Dr. Luciano Pereira from Paraguay: Peripartum cardiomyopathy (PPCM) is an important cause for idiopathic HF associated with pregnancy. It is observed during late pregnancy or the early puerperium. PPCM is relatively rare and serious disorder ( because is associated with high rates of mortality) which affects women within one month antepartum to five months after delivery with the typical signs of acute cardiac HF in the absence of any other signs or history of heart disease. About 3% to 4% of these patients present before delivery (1). Risk factors for peripartum cardiomyopathy include (2): 1) Advanced maternal age; 2) Multiparity; 3) African descent; 4) Twinning and 5) Long-term tocolysis. To date, its etiology is unknown, although several theories are under investigation in an effort to provide more information regarding available treatment options. Viral myocarditis, maladaptive response to the hemodynamic stresses of pregnancy, prolonged tocolysis and abnormal immune response to pregnancy,(autoimmune), causes may contribute. Several compelling sets of data support the view that PPCM is a form of autoimmune IDCM. However, PPCM differs from autoimmune IDCM in that 1) it is associated with unique sets of autoantibodies and autoantigens; 2) it has a relatively rapid onset, and 3) it exclusively affects pregnant women. Furthermore, the etiology of PPCM is dependent on the interaction of pregnancy associated factors, e.g. increased hemodynamic stress, vasoactive hormones and fetal microchimerism, that co-operate in the context of essential immune and genetic environments for disease progression(3). The incidences vary from 1 in 1300 to 4000 pregnancies. The estimated incidence in the USA is 1 case per 3000 to 4000 live births (4). The ratio of PPCM deaths for the 5-year period in the USA is 0.62 per 100,000 births. The mortality rates in the acute phases and subacute phases range from 25 to 50 %. The prognosis is especially poor in patients with cardiomegaly persisting > 6 months and in patients with low LVEF. A comprehensive understanding of the physiology of pregnancy and the pathophysiology of maternal cardiac disease is of great importance for anesthesiologists, gynecologists and cardiologists involved in peripartum care. A high occurrence of PPCM in central Haiti (1 case per 300 live births) provided the unique opportunity to study the relationship of immune activation and dendritic cell maturation to the etiology of this disorder. Plasma samples from two groups (n = 12) of age- and parity-matched Haitian women with or without evidence of PPCM were tested for levels of biomarkers of cardiac tissue remodeling and immune activation. Significantly elevated levels of the human granulocyte macrophage colony-stimulating factor (GM-CSF), endothelin-1, N-terminal-pro- brain natriuretic peptide and CRP and decreased levels of TGF-beta were measured in PPCM subjects relative to controls. Yet despite these findings, in vitro maturation of normal human cord blood derived progenitor dendritic cells (CBDCs) was significantly reduced (p < 0.001) in the presence of plasma from PPCM patients relative to plasma from post-partum control subjects as determined by expression of CD80, CD86, CD83, CCR7, MHC class II and the ability of these matured CBDCs to induce allo-responses in PBMCs. These results represent the first findings linking inhibition of DC maturation to the dysregulation of normal physiologic cardiac tissue remodeling during pregnancy and the pathogenesis of PPCM(5). B-type natriuretic peptide is secreted mainly in the left ventricle in response to elevated wall tension. Plasma levels of the peptide correlate positively with cardiac filling pressures, making it an excellent marker for the presence of left ventricular dysfunction. Because peripartum cardiomyopathy is diagnosed by exclusion, other causes of HF should first be ruled out. The subsequent preconceptional advice will depend on the recovery of cardiac function. Women with residual myocardial dysfunction run a severe risk of aggravated HF and should be strongly advised against becoming pregnant again (6). A multidisciplinary review of PPCM held by the National Heart, Lung, and Blood Institute, in conjunction with the Office of Rare Disease of the National Institutes of Health, in April 1997 reviewed the current knowledge and developed recommendations for areas of further research and education about PPCM. Peripartum cardiomyopathy is a rare lethal disease about which little is known. Clinically, PPCM shows pulmonary symptoms such as dyspnea, tachypnea and coughing. Diagnosis is confined to a narrow period and requires echocardiographic evidence of LV systolic dysfunction. Echocardiography is central to diagnosis. Early diagnosis and initiation of treatment are essential to optimize pregnancy outcome. Intensivists and anesthesiologists should be consulted to assist with management in complicated cases. Management of PPCM is essentially supportive. Symptomatic patients should receive standard therapy for HF, managed by a multidisciplinary team (cardiologist, anesthesiologists, gynecologists, obstetricians, perinatologists, maternal-fetal specialists, family practitioners, intensivists) in a perinatal center with consequent follow-up of the patients for risk stratification including echocardiography. If subsequent pregnancies occur, they should be managed in collaboration with a high-risk perinatal center. The mainstays of medical therapy are digoxin, beta- blokers, loop diuretics, sodium restriction and afterload reducing agents (hydralazine and nitrates). Due to a high risk for venous and arterial thrombosis, anticoagulation with heparin should be instituted. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers should be avoided during pregnancy because of severe adverse neonatal effects (7). But only 3% to 4% of these patients present before delivery. Caution is advised in recommending subsequent pregnancy, especially if LV dysfunction is persistent. Systematic data collection is required to answer important questions about incidence, treatment, and prognosis (8). Future pregnancies should be avoided with at least 50 % risk of recurrence (9). Patients with PPCM have a higher mortality rate and a poorer return of normal ventricular function. Cardiac transplant is improving prognosis and should be considered when conventional therapy fails. Immunosuppressant therapy has been used successfully in only a small number of patients who were unimproved after 2 weeks of standard therapy. The utility of immunosuppressive therapy remains ambiguous. References 1) Lee W. Clinical management of gravid women with peripartum cardiomyopathy. Obstet Gynecol Clin North Am. 1991; 18:257-271. 2) Al-Shamiri MQ, Al-Nozha MM. Peripartum cardiomyopathy searching for a better understanding. Saudi Med J. 2003; 24:1048-1051. 3) Sundstrom JB, Fett JD, Carraway RD, Ansari AA. Is peripartum cardiomyopathy an organ-specific autoimmune disease? Autoimmun Rev. 2002; 1:73-77. 4) Fett JD, Christie LG, Carraway RD, Murphy JG.Five-year prospective study of the incidence and prognosis of peripartum cardiomyopathy at a single institution. Mayo Clin Proc. 2005;80:1602-1606. 5) Ellis JE, Ansari AA, Fett JD, Carraway RD, Randall HW, Mosunjac MI, et al. Inhibition of progenitor dendritic cell maturation by plasma from patients with peripartum cardiomyopathy: role in pregnancy-associated heart disease. Clin Dev Immunol. 2005; 12:265-273. 6) Boxmeer JC, Balk AH, Steegers EA, Visser W. Two pregnant women with shortness of breath due to peripartum cardiomyopathy Ned Tijdschr Geneeskd. 2006; 150:255-258. 7) Ferrero S, Colombo BM, Fenini F, Abbamonte LH, Arena E. Peripartum cardiomyopathy. A review. Minerva Ginecol. 2003;55:139-51. 8) Pearson GD, Veille JC, Rahimtoola S, Hsia J, Oakley CM, Hosenpud JD, et al. Peripartum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendations and review. JAMA. 2000; 283:1183-1188. 9) Bruck VA, Butterwegge M, Cadenbach A, Treese N Peripartum cardiomyopathy--Obstetric emergency for mother and child. Z Geburtshilfe Neonatol. 2002; 206:98-101. All the best Andr?s Ricardo P?rez Riera ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 23 21:09:51 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 23 Apr 2006 21:09:51 -0300 Subject: [HF-FORUM] 124E Digoxina and carvedilol. Dr. de Sousa Message-ID: <1457FD88-8D44-44B0-9305-CB41BBED5F4C@hf-symposium.org> Congratulations to all for the symposium! The dosis of carvedilol in my opinion is the maximum tolerated until 50 mg/day or 75 mg/day in patients above 70 kg of body weight. I'd like to discuss digoxin dosis. Rathore SS, et al. showed in post-hoc analysis of DIG trial that at levels above 1.2 ng/ml, there is increased mortality. At levels as low as 0.5 ng/ml, there was benefit in terms of reduced hospitalizations and death. So I prefer to start with 0.125 mg of digoxin dosis. I would like to know the opinion of other participants because these are post-hoc conclusions. Ref.: Rathore SS, et al. Association of serum digoxin concentration and outcomes in patients with heart failure.JAMA. 2003;289(7):871-8. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med.1997;336(8):525-33. Rathore SS, et al. Sex-based differences in the effect of digoxin for the treatment of heart failure. N Engl J Med. 2002;347(18):1403-11. Thank you, Marcos Roberto de Sousa Cardiology Service of Mater Dei Hospital and Hospital das Cl?nicas da UFMG. Phone number + 55 31 3295-0257 Address: Rua Juiz de Fora, 273 sala 1003 Bairro Barro Preto ZIP CODE 30.180-060 Belo Horizonte - Minas Gerais - Brasil mrsousa at ufmg.br mrsousa at cardiol.br marcos.sousa at ipsemg.mg.gov.br mrsousa at hc.ufmg.br ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 23 21:16:49 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 23 Apr 2006 21:16:49 -0300 Subject: [HF-FORUM] 113E RE: Bifascicular block. Chagas. Dr. Perez Riera Message-ID: Dear Li: Please see in attachment the ECG/VCG correlation on Horizontal Plane of this case (HP)****. We can see: 1) The 10 to 20ms vector is directed to back and leftward because the initial ventricular activation is exclusively dependent of Left Posterior Septal Fascicle( LPSF): Initial embryonic q wave from V1 to V3 with absence of initial q wave in left leads V5-V6: Absence of 1AM vector( There is not the initial vector of septal fascicle or antero-medial division of left bundle); 2) QRS loop (see in attachment ) is located predominantly on left anterior quadrant: Prominent Anterior forces (PAF) typical of Left Septal Fascicular Block(LSFB). There are not diagnosis of CRBBB because the morphology of QRS loop on HP in cases of RBBB the afferent limb of QRS loop does not return to the point of origin but continues in a rightward and predominantly anterior direction to inscribe a terminal, fingerlike appendage, whose average orientation is along the +120 degree on HP( on right anterior quadrant); 3) R waves are "in crescendo" from V1 to V3 and decreased from V4 to V6: Typical of LSFB; 4) R V1 > 5mm and RV2 > 15mm: Typical of LSFB; 5) I agree with you that PR interval in V1, V2 and V2 = 230 ms or more: First degree AV block. But in V5 and V6 is = or < 200ms. Intermittent claudicating of LPFB??? . Conclusion: bifascicular block: left anterior fascicular block (Frontal plane with extreme left axis deviation) + Left Septal Fascicular Block or ?ntero-medial block. It is possible the presence of incomplete intermitente LPFB: In this case trifascicular block; LAFB+ LSFB+ LPFB. This is a new form of Incomplete LBBB. Others denominations of LSFB are: 1) Focal septal block 1 - septal focal block 2. 2) left septal fascicular block 3-4-5. 3) left anterior fascicular block 6. 4) left anterior septal block 7. 5) septal fascicular conduction disorders of the left branch 8. 6) left septal Purkinje network block 9-10. 7) left septal subdivision block of the left bundle branch 11. 8) anterior conduction delay 12-13. 9) left median hemiblock 14-15-16-17-18-19-20-21-22. 10) left medial subdivision block of the left bundle branch 23. 11) middle fascicle block 24. 12) block of the antero-medial division of the left bundle branch of His 25-26 or antero-medial divisional block (AMDB) 27-28-29-30. **** SEE THE ECG/VCG http://www.hf-symposium.org/files/Riera_ECG.pdf Refer?nces 1) Athanassopoulos CB. Transient focal septal block. Chest 1979 Jun;75(6):728-730. 2) Gambetta M, Childers RW, - Rate-dependente right precordial Q waves: "Septal focal block". Am J Cardiol 1973;32:196- 3) Nakaya Y, Hiasa Y, Murayama Y, Ueda S, Nagao T, Niki T, Mori H, Takashima Y. Prominent anterior QRS force as a manifestation of left septal fascicular block J Electrocardiol 1978 Jan;11(1):39-46. 4) Nakaya Y, Murayama Y, Mori H.: Left septal fascicular block as a new type of divisional block of the left bundle. In Moderm Electrocardiology. Excerpta Medica, Amsterdam, 1978; :435-439. 5) Mori H, Kobayashi S, Mohri S.[Electrocardiographic criteria for the diagnosis of the left septal fascicular block and its frequency among primarily elderly hospitalized patients]. Nippon Ronen Igakkai Zasshi 1992 ; (4):293-297. 6) Sakai T.[Left anterior fascicular block, left posterior fascicular block, left septal fascicular block]. Ryoikibetsu Shokogun Shirizu 1996;(12):282-284. 7) Moffa PJ, Del Nero E, Tobias NM, et al. - The left anterior septal block in Chagas disease. Jap Heart J 1982; 23:163-165. 8) Magnacca M, Valesano G, Rizzo G, Trotti F, Pagetto A, Boverio R. [Diagnostic value of electrocardiogram in septal fascicular conduction disorders of the left branch in diabetics] Minerva Cardioangiol 1988; 36 (7-8):361- 363. 9) Iwamura N, Kodama I, Shimizu T, Hirata Y, Toyama J, Yamada K. Functional properties of the left septal Purkinje network in premature activation of the ventricular conduction system. Am Heart J 1978; 95(1):60-9. 10) Nakaya Y, Inoue H, Hiasa Y, et al. Functional importance of the left septal Purkinje network in the left ventricular conduction system. Jpn Heart J 1981;(3):363-76. 11) Nakaya Y, Hiraga T. - Reassessment of the Subdivision Block of the Left Bundle Branch. Jpn Circ J 1981; 45:503-516. 12) Hoffman I, Mahter L, Hilzenrath J, Hamby RI, - Anterior conduction delay: A possible cause for prominent anterior QRS forces. J Electrocardiol 1976; 9:15-21. 13) Reiffel JA, Bigger J T,: Pure anterior conduction delay: A variant "fascicular" defect. J Electrocardiol 1978; 11:315-7. 14) DeMoulin JC, Kulbertus HE, - Histopathological examination of concept of left hemiblock. Br Heart J 1972; 34:807-814. 15) Demoulin JC, Kulbertus HE, - Left hemiblocks revisited from the histopathological view point. Am Heart J 1973; 86(5):712-3. 16) De P?dua F, Reis DD, Lopes VM, et al. - Left median hemiblock - a chimera? In: Rijlant P; Kornreich F, eds. 3rs Int. Congr. Electrocardiology. ( 17th Int. Symp. Vectorcardiography). Brussels, 1976. 17) De P?dua F, Lopes VM, Reis DD, et al. - O hemibloqueio esquerdo mediano - Uma entidade discut?vel. Bol Soc Port Cardiol 1976. 18) De P?dua F: Bloqueios fasciculares - Os hemibloqueios em quest?o. Rev Port Clin Terap?utica 1977; 3: 199. 19) De P?dua F. Intraventricular conductions defects - What future? In de P?dua F, MacFarlane P, W. eds. News Frontiers of Electrocardiology. Chichester: Research Studies Press 1981; 181-185. 20) Kulbertus HE, - Concept of left hemiblocks revisited: a histopathological and experimental study. Advances in Cardiology 1975; 14,126-32. 21) Kulbertus HE, Demoulin J: Pathological basis of concept of left hemiblock. In Wellens HJJ, Lie KI, Janse MJ, editors: The conduction system of the heart, Philadelphia, 1976, Lea&Febiger. 22) Kulbertus HE, de-Leval-Rutten F, Casters P - Vectorcardiographic study of aberrant conduction. Anterior displacement of QRS: another form of intraventricular block. Br Heart J 1976; 38:549-557. 23) Inoue H, Nakaya Y, Niki T, Mori H, Hiasa Y. Vectorcardiographic and epicardial activation studies on experimentally -induced subdivision block of the left bundle branch. Jpn Circ J 1983;47(10):1179-89. 24) Alboni P, Malacarne C, Baggioni G, Masoni A. Left bifascicular block with normally conducting middle fascicle. J Electrocardiol 1977;10 (4):401- 404. 25) Tranchesi J, Moffa PJ, Pastore CA, et al. Block of the antero- medial division of the left bundle branch of His in coronary diseases. Vectorcardiographic characterization]. Arq Bras Cardiol 1979;32(6):355-60. 26) Cesar LAM, Carvalho VB, Moffa PJ, et al. - Bloqueio da divis?o ?ntero-medial do feixe de His e obstru??o da art?ria coron?ria descendente anterior. Correla??o eletro-cinecoronariogr?fica. Rev Latina de Cardiol 1980; 1:57-63. 27) Moffa PJ, em Jo?o Tranchesi. ELECTROCARDIOGRAMA NORMAL E PATOL?GICO. No??es de vectorcardiograf?a. Sexta edi??o, Cap?tulo XVI pag: 294-347 Atheneu. Editora S?o Paulo Ltda. 1983. 28) Pileggi F, Moffa PJ, Sosa E, Cardiologia. Ign?cio Ch?vez Rivera. Editora M?dica Panamericana, S.A. de C. V. ; Volumen 1 Cap?tulo 7, pg.: 332, 1993. 29) Moffa PJ, Sanches PCR, em Jo?o Tranchesi. ELECTROCARDIOGRAMA NORMAL E PATOL?GICO. No??es de vectorcardiograf?a. S?tima edi??o, Cap?tulo XVI pg.: 413-461. 1a Edi??o pela Editora ROCA Ltda. S?o Paulo 2001. 30) Moffa PJ, Ferreira BM, Sanches PC, et al.: [Intermittent antero-medial divisional block in patients with coronary disease]. Arq Bras Cardiol 1997; 68(4):293-296. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 23 22:31:37 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 23 Apr 2006 22:31:37 -0300 Subject: [HF-FORUM] 116E RE: Dobutamine. Dr. Orzech Message-ID: You're asking if there're any indications for dobutamine treatment in a patient on a b-blocker. In my opinion it depends on the reason of clinical instability. Say, the exacerbation is mainly due to b-blocker overdose the drug of choice would rather be glucagone and then if no response dopamine or dobutamine. Dobutamine antagonizes the b-blocker's action at its receptor, competing and in proper doses taking over the receptor. Thus any further indication for the use of dobutamine emerges from its beta-stimulating potential. If the pt develops pulmonary edema with low SBP (<70 mmHg) there are no doubts that his LV pump went on a fritz and that he needs strong stimuli to overcome the vicious circle that had led to deterioration of his condition. Dobutamine would be the drug of choice and if no proper response was observed I'd go for IABP + DB and NA. Janusz Orzech, MD Univ. Hosp. Angiol. Dept., Poland ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 13:56:21 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 13:56:21 -0300 Subject: [HF-FORUM] 117P Complete left bundle branch block. Dr. Perez Riera Message-ID: Conditioning factors of prognosis in patients carriers of CLBBB From a cohort in Manitoba, 3983 patients were examined, who developed CLBBB with no evidence of coronary insufficiency or valve disease. Before the appearance of CLBBB, ECG was normal o had associated LVE less frequently. The appearance of CLBBB caused a mild deviation of SAQRS to the left, and the most frequent clinical event observed in a 5-year follow-up was sudden cardiac death, which presented a 10-fold greater incidence in men with CLBBB than those without the dromotropic disorder1. The new onset of CLBBB was studied in an 18-year follow-up in 55 patients from the Framingham study. The age average of the registry for the appearance of CLBBB was 62 years. The underlying cause was systemic hypertension, cardiomyopathy, coronary insufficiency, or their association. In a 10-year follow-up of the patients with CLBBB, 50% had died of cardiovascular disease. In men, the appearance of CLBBB is an independent factor of increased risk of cardiovascular mortality. The presence of CLBBB of new onset indicates with a greater frequency hypertensive or coronary disease, more advanced or both2. Literature mentions eight factors that influence the prognosis in the presence of CLBBB: 1) patient's age when the dromotropic disorder appears; 2) gender; 3) QRS duration (QRSd); 4) SAQRS; 5) Heart magnitude; 6) underlying disease; 7) constancy of the block; 8) duration of HV interval. 1) Age of appearance of dromotropic disorder: directly proportional. The younger the patient was, the greater the survival. When CLBBB appears at an age > 44, it indicates a worse prognosis and less life expectation3. 2) Gender: greater survival in women. 3) QRSd: in general, narrow CLBBB (120 ms) presents a greater survival, except two coronary patients. In patients carriers of idiopathic dilated cardiomyopathies, QRSd is a predictive factor of mortality4. Approximately, 50% of the patients with CLBBB and QRSd <160 ms present normal heart area, while only 5% of the patients with QRSd = or >160 ms have a normal heart size. A QRSd of 150 ms or > indicates prescription of cardiac resynchronization therapy (CRT) in the presence of class III or IV of CHF not responsive to drugs, being a marker of better acute response of systolic performance as response to this therapy5. The presence of CLBBB is a marker of bad prognosis in patients with CHF. This negative effect is independent of age, CHF severity and type of drugs used. This data makes the indication of multisite resynchronizing ventricular pacemaker rational in patients with CHF and CLBBB6. CRT constitutes a therapeutic option for patients with severe CHF class III or IV (NYHA), EF of LV <35%, CLBBB and QRSd >120 ms and CLBBB however, approximately 20% to 30% of the patients do not respond to CRT. Thus, patients with CHF of coronary etiology may respond less favorably than those with idiopathic dilated cardiomyopathy. This concept of different responses according to etiology was not confirmed in some recent papers, where a similar response is shown in CHF by unknown causes7. QRSd in values = or > 170 ms in the presence of CLBBB constitutes a significant marker of ventricular dysfunction. The presence of extreme left shift of SAQRS in the presence of CLBBB does not indicate a future worsening in ejection fraction8. CRT improves contractility, decreases the area with dysynchrony, and improves functional capacity and quality of life. Additionally, it causes the same in 50% of the control group only as placebo effect. The different trials show heterogeneous responses with a significant percentage of absence of benefits, which suggests that what is important is detecting the presence and precise location of the mechanical dysynchronization, to properly locate the position of the device9. The hemodynamic improvement proven by CRT and invasive studies is chronically sustained and ventricular-arterial coupling with mechanical efficiency and the chronotropic response are better after 6 months of CRT. These data may help us to understand the functional improvement and the increase of tolerance to exercise in patients treated with CRT10. Baseline QRSd is not a predictor of clinical response to CRT and the presence of a narrow QRS complex after the procedure, is not related to clinical and hemodynamic improvement. Mechanical dysynchrony is better shown by the tissue Doppler echo technique, which is in a standardization process11. 4) SAQRS: patients carriers of CLBBB with non-shifted SAQRS (between -300 and +600) have a greater survival than those with extreme shift of SAQRS, whether to the left (between -300 and -900)12 or to the right. In both cases there is a greater incidence of involvement in left ventricular performance; consequently they present a greater rate of cardiovascular mortality. Thompson (1979) proved that in the presence of CLBBB, SAQRS to the left from -300 in patients carriers of aortic stenosis or post- operative of aortic stenosis correction, causes a greater incidence of delayed left ventricular failure or death. 5) Heart size: it is directly related to survival; thus, the patient with CLBBB and normal cardiac size has a greater survival than those with increased cardiac area. 6) Underlying disease: it is directly related to survival; thus, the patients with CLBBB with no apparent cause present a greater survival than those the cause of which is isolated systemic hypertension, who in turn present a greater survival than the patients with coronary insufficiency as underlying cause. Among 933 hypertensive patients (548 women) studied by Li et al, with echocardiogram and ECG and average age of 66 years old +/- 7 and essential systemic hypertension. CLBBB defined by the Minnesota code 7.1 was present in 47 and absent in 886. The patients with and without CLBBB were similar in regard to age, gender, body mass index, prevalence of diabetes and history of infarction, and have a similar wall thickness and mass estimation. Those with CLBBB identified subjects with a worse global and regional ventricular performance and worse LV compliance, i.e. less relaxation capacity13. Recently, a case of an elderly man (75 years old) with ischemic heart disease and intermittent CLBBB was reported. The angina episode was preceded by intermittent CLBBB, rise in pulmonary capillary pressure and concomitant increase of mitral and tricuspid valve regurgitation observed in Doppler echocardiogram. After the implantation of biventricular pacemaker, the patient did not present any more dyspnea or angina and intermittent LBBB14. Left sclerosis of the cardiac skeleton associated to LBBB is nearly always benign; while idiopathic sclerosis of the His conduction system (Lenegre disease) has a variable prognostic behavior. This is a genetic entity that affects the SCN5A gene and is allelic to Brugada disease. In spite of the cause, the simple presence of CLBBB in a patient with CHF constitutes an independent predictor of death, but not the presence of CRBBB15. The presence of CLBBB in chagasic patients, considered a rare dromotropic disorder in this entity, is a parameter for a negative prognosis. 7) Constancy of the block: patients carriers of intermittent CLBBB have a less severe disease and a better prognosis than patients with permanent CLBBB. Maybe the intermittence translates the disease in its initial stages. 8) HV interval: the progression to complete AV block occurs more frequently when the HV interval of the electrogram is >100 ms and the PM implantation does not improve the prognosis in these cases due to the co-existence of severe basal disease16;17;18. "Bening" CLBBB These are usually asymptomatic patients, with no underlying disease that would justify a block. The finding of block is by chance, in patients nearly always with less than 50 years, with SAQRS with no extreme shifts (to the left from -300 or to the right from +900), normal cardiac area in chest roentgenogram, ventricular performance and septum and wall thickness preserved in echocardiographic study, and ventricular coronary angiography was normal. Which is the cause of benign CLBBB? Replies: the following possible etiologies have been proposed: 1) congenitally short truncus of the left coronary artery (less than 6 mm); 2) sequel of viral myocarditis with left branch involvement; 3) initial phase of Lev and Lenegre diseases. In 23 asymptomatic patients with CLBBB who underwent stress test with thallium 201, the uptake was abnormal in all of them; however, nine had cardiomyopathy and only two coronary diseases. Thallium is hardly valuable in patients with CLBBB19. Patients with CLBBB, frequently display a false positive pattern for ischemia in the interventricular septum, when the rest/stress myocardial perfusion scintigraphy with thallium 201 (201TI) is used. The study with 99mTc-MIBI is more specific than 201TI to identify coronary insufficiency in the presence of CLBBB20. Dipyridamole stress echocardiography (DSE) has at least a similar accuracy to dipyridamole sestamibi scintigraphy to predict coronary artery disease in patients with CLBBB and tends to be more specific in those patients with LV dilatation21. Single photon emission computed tomography (SPECT) or stress-rest SPECT using the compounds from technetium and using only stress when enough or associating dipyridamole if the strain was not enough, proved to be an accurate method to locate the infarcted area in patients with CLBBB and with addition of stress and dipyridamole, it has a high positive predictive value and specificity for coronary obstruction22. Body surface mapping improves diagnostic sensitivity in comparison to 12-lead ECG in the early diagnosis of acute infarction and precordial pain23. References 1) Rabkin SW, Mathewson FA, Tate RB. Natural history of left bundle-branch block. Br Heart J. 1980; 43:164-169. 2) Schneider JF, Thomas HE Jr, Kreger BE, McNamara PM, Kannel WB.Newly acquired left bundle-branch block: the Framingham study. Ann Intern Med. 1979; 90:303-310. 3) Deharo JC. Left bundle branch block. Electrocardiographic and prognostic aspects Arch Mal Coeur Vaiss. 2000; 93:31-37. 4) Unverferth DV, Majorien RD, Moeschberger MI, et al. Factors influencing the one-year mortality of dilated cardiomiopaty, Am J Cardiol 1984; 54:147-152. 5) Auricchio A, Stelbrink C, Block M, et al. Effect of pacing chamber and atrioventricular delay on acute systolic function of paced patients with congestive heasrt failure. The pacing therapies for congestive heaart failure group. The guidant congestive heart failure research group Circulation 1999; 99: 2293-3001. 6) Baldasseroni S, Opasich C, Gorini M, et al. Italian Network on Congestive Heart Failure Investigators. Left bundle-branch block is associated with increased 1-year sudden and total mortality rate in 5517 outpatients with congestive heart failure: a report from the Italian network on congestive heart failure. Am Heart J 2002; 143:398-405. 7) Molhoek SG, Bax JJ, van Erven L, Bootsma M, Boersma E, Steendijk P, van der Wall EE, Schalij MJ.Comparison of benefits from cardiac resynchronization therapy in patients with ischemic cardiomyopathy versus idiopathic dilated cardiomyopathy. Am J Cardiol. 2004; 93:860-863. 8) Das MK, Cheriparambil K, Bedi A, Kassotis J, D ES, Reddy CV, Makan M, Dunbar CC, Saul B. Prolonged QRS duration (QRS >/=170 ms) and left axis deviation in the presence of left bundle branch block: A marker of poor left ventricular systolic function? Am Heart J. 2001; 142:756-759. 9) Mehra MR, Greenberg BH. Cardiac resynchronization therapy: caveat medicus! J Am Coll Cardiol. 2004; 43:1145-1148. 10) Steendijk P, Tulner SA, Bax JJ, Oemrawsingh PV, Bleeker GB, van Erven L,et al. Hemodynamic effects of long-term cardiac resynchronization therapy: analysis by pressure-volume loops. Circulation. 2006;113:1295-304. 11) Kashani A, Barold SS. Significance of QRS complex duration in patients with heart failure. J Am Coll Cardiol. 2005; 46:2183-2192. 12) Parharidis G, Nouskas J, Efthimiadis G, Styliadis J, Gemitzis K, Hatzimiltiadis S, Karoulas T, Tsifodimos D. Complete left bundle branch block with left QRS axis deviation: defining its clinical importance. Acta Cardiol. 1997; 52:295-303. 13) Li ZB, Wachtell K, Okin PM, Gerdts E, Liu JE, Nieminen MS, Jern S, Dahlof B, Devereux RB.Association of left bundle branch block with left ventricular structure and function in hypertensive patients with left ventricular hypertrophy: the LIFE study.J Hum Hypertens. 2004 J Hum Hypertens. 2004;18:397-402.. 14) Yonekura T, Toda G, Furudono S, Minami T, Kawano H, Koide Y, Yano K.The hemodynamic benefit of biventricular pacing therapy on mitral regurgitation as demonstrated in a patient with ischemic cardiomyopathy and intermittent left bundle branch block. Intern Med. 2003; 42:1107-1111. 15) Baldasseroni S, Gentile A, Gorini M, Marchionni N, Marini M, Masotti G, Porcu M, Maggioni AP; Italian Network on Congestive Heart Failure Investigators.Intraventricular conduction defects in patients with congestive heart failure: left but not right bundle branch block is an independent predictor of prognosis. A report from the Italian Network on Congestive Heart Failure (IN-CHF database). Ital Heart J. 2003; 4:607-6013. 16) Narula OS, Javier RP, Samet P, Maramba LC.Significance of His and left bundle recordings from the left heart in man. Circulation. 1970; 42:385-396. 17) Trevino AJ, Beller BM. Conduction disturbances of the left bundle branch system and their relationship to complete heart block. II. A review of differential diagnosis, pathology and clinical significance. Am J Med. 1971; 51:374-382. 18) Rahimtoola SH, McAnulty JH.'High-risk' bundle branch block. Hosp Pract (Off Ed). 1981; 16:73-80, 85-7, 91-92. 19) Ollivier JP, Gaillard JF, Seigneuric A, Brion R, Droniou J.Etiological study of 23 cases of complete block of the left branch of the bundle of His, in the absence of myocardial infarction Ann Med Interne (Paris). 1985; 136:378-381. 20) Ellmann A, van Heerden PD, van Heerden BB, Klopper JF. 99mTc-MIBI stress-rest myocardial perfusion scintigraphy in patients with complete left bundle branch block. Cardiovasc J S Afr. 2001; 12:252-256. 21) Vigna C, Stanislao M, De Rito V, Russo A, Natali R, Santoro T, Loperfido F. Dipyridamole stress echocardiography vs dipyridamole sestamibi scintigraphy for diagnosing coronary artery disease in left bundle- branch block. Chest. 2001; 120:1534-1539. 22) Candell-Riera J, Oller-Martinez G, Pereztol-Valdes O, Castell- Conesa J, Aguade-Bruix S, Soler-Peter M, Simo M, Santana-Boado C, Soler- Soler J. Usefulness of myocardial perfusion SPECT in patients with left bundle branch block and previous myocardial infarction. Heart. 2003; 89:1039-1042. 23) Maynard SJ, Menown IB, Manoharan G, Allen J, McC Anderson J, Adgey AA. Body surface mapping improves early diagnosis of acute myocardial infarction in patients with chest pain and left bundle branch block. Heart. 2003; 89:998-1002. Best regards Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 15:26:24 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 15:26:24 -0300 Subject: [HF-FORUM] 128C Left ventricular pacing and the individualized pacing site. Dr. Li Zhang Message-ID: <2474C60A-C3F1-45E4-B53F-EB809DD1AADF@hf-symposium.org> Dear Dr. Levine: Based on the recent study (Jia P, et al. Heart Rhythm 2006;3(3): 296-310), the efficacy of CRT is depended strongly on patient- specific electrophysiologic substrate. For patients with left ventricular ischemic cardiomyopathy, left ventricular (LV) pacing, although it increases QRS duration and dispersion, may do as good as bi-ventricular pacing in improving the mechanical uniformity. Another issue is the LV pacing site. As we know there are multiple factors involved in the cardiac remodeling process in the failing hearts, such as depressed myocardial excitability, changes in the extracellular matrix due to scar tissue or diffused fibrosis and decreased gap junction functions, etc (Akar FG, et al Trens Cardiovasc Med 2005;15(7):259-64). Those factors may have contributed to the outcome as non-responders to CRT. The non- invasive ECG imaging (ECGI) developed by Dr. Rudy's group, as well as the advanced MRI techniques (Helm Pa, et al Cir Res 2006;98(1): 125-32) may not only help predict the non-responders in some degree, but also help identify the optimal pacing site. I wonder if you would be willing to make comments about the ideas of LV pacing and the individualized pacing site. Thank you very much, Li Zhang, MD -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 15:41:48 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 15:41:48 -0300 Subject: [HF-FORUM] 130E RE: Digoxina and carvedilol. Dr. Marcus Message-ID: <6012775E-CA56-4D03-B2CD-9CB9B49DD26C@hf-symposium.org> I agree with the starting dose suggested by Dr. Roberto de Sousa. It is advisable to check the serum levels of digoxin after one week. Be sure to withdraw blood for this test at least six hours and preferably 12 hours after the last dose or steady state levels will not be obtained. Frank Marcus -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 15:45:34 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 15:45:34 -0300 Subject: [HF-FORUM] 129E Heart transplantation in ARVD. Dr. Marcus Message-ID: I agree with Dr. Jessup. The experience with heart transplantation in ARVD has bee excellent both at our institution as well as in others. Frank Marcus ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 18:10:44 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 18:10:44 -0300 Subject: [HF-FORUM] 131R RE: Digoxina and carvedilol. Dr. Yabluchansky Message-ID: <2B4CB39E-5C6F-4087-8114-127ABF29F173@hf-symposium.org> From my point of view it is not necessary and even not right to mount to maximum endurable dose of carvedilol. Criterion for dose should be achievement of desirable clinical effect. What about digoxin, I think, that this one should be used in a small doses at which it infuences nondirect inotropic action. Mykola Yabluchansky ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 18:39:10 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 18:39:10 -0300 Subject: [HF-FORUM] 132E RE: Dobutamine. Dr. Lu Message-ID: <13904A91-49ED-4D3E-87AA-1B5166E333FA@hf-symposium.org> > Is it possible to administer dobutamine to a patient with chronic > heart failure under beta-blocker treatment when he becomes clinically > unstable? > > Dr. Maria Teresa La Rovere > Italy Hi, Dr. Maria Thanks for your question. Dobutamine is a beta-adrenergic agonist, cannot be effectively used in the presence of high levels of beta-blocker. It is not good for patients with HF and received beta- blockertreatment. . You could choose the other drug, such as levosimendan, or phosphodiesterase inhibitors. Yongxin Lu China -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 19:44:51 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 19:44:51 -0300 Subject: [HF-FORUM] 118S RE: Sleep apnea. Dr. Larrateguy Message-ID: <546DD7DF-6CF9-4201-80DB-BFD43DAE5133@hf-symposium.org> Dear Dr. Perez Leon, I send you the bibliography related to sleep apnea. You may find more information in my page: www.RespirarParana.com.ar Regards, Dr. Luis Larrateguy Bibliography Mathis J. The history of sleep research in the 20th century. Schweiz Rundsch Med Prax. 1995 Dec 12;84(50):1479-85. Guilleminault C, Van Den Hoed J, Mitler M: Clinical overview of sleep apnea syndrome. In Guilleminault C, Dement W (ed): Sleep Apnea Syndromes. New York: Alan R. Liss, 1978. Dur?n-Cantolla Joaquin et al. Consenso Nacional sobre el s?ndrome de apneas-hipopneas del sue?o. Arch Bronconeumol. 2005; 41 Supl 4:12-29. Sala H, Nigro C, Rabec C, Guardia A, Smurra M et al. Consenso Argentino de Trastornos Respiratorios Vinculados al Sue?o. Medicina (Buenos Aires) 2001; 61: 351-363. American Academy of Sleep Medicine. International classification of sleep disorders, revised: Diagnostic and coding manual. Chicago, Illinois: American Academy of Sleep Medicine, 2001. American Academy of Sleep Medicine Task Force. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. Sleep 1999;22:667?689. Lugaresi E, Cirignotta F, Montagna P, Zucconi M. Snoring: pathophysiology and clinical consequences. Semin Respir Med 1988; 9:577-85. Stoohs R, Guilleminault C. Snoring during NREM sleep: respiratory timing, esophageal pressure and EEG arousal. Respir Physiol 1991; 85: 151-67. Young T, Palta M, Dempsey J, et al. The occurrence of Sleep disorders breathing among middle aged adults. N Engl J Med 1993;328:1230-1236. Duran J, Esnaola S, Rubio R, Iztueta. Obstructive sleep apnea- hypopnea and related clinical features in a population-based sample of subjects aged 30 to 70 yr. A Am J Respir Crit Care Med. 2001 Mar; 163(3 Pt 1):685-9 Nieto FK, Young TB, Lind BK, Sahar E, Samet JM, Redline S, D?gostino RB, Newman AB, Lebowith MD, Pickering TG. Association of sleep- disordered breathing, sleep apnea, and hypertension in a large community-based study. JAMA 2000;283:1829-1836. Lavie P, Herer P., Hofstein V. Obstructive Sleep Apnea syndrome as a risk factor for hypertension: population study. BMJ 2000;320:479-482. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. New Eng J Med 2000;342:1378-1384. Newman AB, Nieto J, Guirdry U, Lind BK, Redline S, Sharar E, Pickering TG, Quant SF. Relation of sleep-disordered breathing to cardiovascular risk factors. The Sleep Hearth Healt Study. Am J Epidemiol 2001;154:50-59. Baseti C and Aldrich MS. Sleep apnea in acute cerebrovascular disease: final report in 128 patients. Sleep 1999;22:217-223. Parra O, Arboix A, Bechich S, Garc?a-Eroles L, Montserrat JM, Lopez JA, Ballester E, Guerra JM, Sope?a JJ. Time course of sleep-related breathing disorders in first-ever stroke or transient ischemic attack. Am J Respir Crit Care Med 2000;161:375-380. Ter?n-Santos J, Jim?nez-G?mez A, Cordero-Guevara J, and the Cooperative Group Burgos?Santander. The association between sleep apnea and the risk of traffic accidents. N Engl J Med 1999;340:847?851. Barb? F, Peric?s J, Mu?oz A, Findley L, Ant? JM, Agust? AGN. Automobile accidents in patients with sleep apnea syndrome. An epidemiological and mechanistic study. Am J Respir Crit Care Med 1998;158:18?22. He J, Kriger MH, Zorick FJ, Conway W. Mortality and apnea index in obstructive sleep apnea. Chest 1988;94:9-14. Baldwin CM, Griffith KA, Nieto FJ, O?Connor GT, Walsleben JA, Redline S. The association of sep-disordered breathing and sleep symptoms with quality of life in the Sleep Heart Healt Study. Sleep 2001;24:96-105. Guilleminault C: Clinical features and evaluation of obstruvtive sleep apnea. En: Kryger, M.H., Roth, T. and Dement, W.C., Editors. Principles and practice of sleep medicine (2da. Edici?n), Philadelphia: W B Saunders, 1994: 667-677. Peraita Adrados R et al, Trastornos respiratorios durante el sue?o. Vigilia-Sue?o,2000, 12 (1) (Supl): pp S3-S111. Larrateguy, L; Rosselli, R; Hern?ndez Rosales, A; Salas, N;Boero I; Rossa S. S?ndrome de apneas S?ndrome de apneas-hipopneas obstructivas del sue?o. Nuestra Experiencia. Presentado en el 30? Congreso Argentino de Medicina Respiratoria. C?rdoba. 2003 (revista en que se public?) Larrateguy L; Wustten S; Rosselli R; Hern?ndez Rosales A. S?ndrome de Crouz?n y apneas durante el sue?o. Centro de Medicina Respiratoria de Paran?. Laboratorio del Sue?o del Litoral. Presentado en el 32 Congreso Argentino de Medicina Respiratoria 2004. Buenos Aires. (revista en que se public?) 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Blankfield RP, Tapolyai AA, Zyzanski SJ.Left ventricular dysfunction, pulmonary hypertension, obesity, and sleep apnea. Sleep Breath 2001 Jun;5(2):57-62. Lee AG, Golnik K, Kardon R, Wall M, Eggenberger E, Yedavally S.Sleep apnea and intracranial hypertension in men. Ophthalmology 2002 Mar;109 (3):482-5. Marcus DM, Costarides AP, Gokhale P, Papastergiou G, Miller JJ, Johnson MH, Chaudhary BA. Sleep disorders: a risk factor for normal- tension glaucoma? J Glaucoma. 2001 Jun;10(3):177-83. Mojon DS, Hess CW, Goldblum D, Boehnke M, Koerner F, Gugger M, Bassetti C, Mathis J. Normal-tension glaucoma is associated with sleep apnea syndrome. Ophthalmologica. 2002 May-Jun;216(3):180-4. Onen SH, Mouriaux F, Berramdane L, Dascotte JC, Kulik JF, Rouland JF. High prevalence of sleep-disordered breathing in patients with primary open-angle glaucoma. Acta Ophthalmol Scand. 2000 Dec;78(6): 638-41. Gus M, Silva DN, Fernandes J, Cunha CP, Sant'Anna GD. 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Wang Y, Teschler T, Weinreich G, Hess S, Wessendorf TE, Teschler H. Validation of microMESAM as screening device for sleep disordered breathing. Pneumologie 2003;57:734-740. Dur?n J, Amilibia J, Barb? F, Capote F, Gonzalez-Mangado N, Jimenez A, Mar?n JM, Masa JF, Montserrat JM, Ter?n J. Disponibilidad de recursos t?cnicos para el diagn?stico y el tratamiento del s?ndrome de apneas obstructivas durante el sue?o en los hospitales de la red p?blica del Estado. Arch Bronconeumol 1995;31:9:463-469. Ter?n Santos J, Fern?ndez-Garc?a C, Cordero-Guevara J. Situaci?n en Espa?a de los recursos diagn?sticos y de los tratamientos con CPAP en el s?ndrome de apneas-hipopneas obstructivas del sue?o. Arch Bronconeumol 2000;36:494-499. Dur?n J, Esnaola S, Rubio R, De la Torre G. Obstructive sleep apnoea- hypopnoea in the elderly. A population-based study in the general population aged 71-100. Annual Meeting of ERS. Madrid. Eur Respir J. 2000;16 Suppl 31:S167. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289:2560-72. Masa Jim?nez JF, Rubio Gonz?lez M, Findley LJ, Riesco Miranda JA, Sojo Gonz?lez A, Disdier Vicente C. Sleepy drivers have a high frequency of traffic accidents related to respiratory effort-related arousals. Arch Bronconeumol. 2003;39:153-8. Luis Dar?o Larrateguy Jefe del Servicio de Neumonolog?a Hospital San Mart?n. Director del Centro Privado de Medicina Respiratoria de Paran?. Presidente de la Asociaci?n de Neumonolog?a de Entre R?os. Urdinarrain 120 (3100) Paran?. Entre R?os. Argentina. TE/FAX: 54-343-4319919 www.RespirarParana.com.ar -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 19:55:18 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 19:55:18 -0300 Subject: [HF-FORUM] 122S RE: Chagasic cardiomyopathy. Dr. Dubner Message-ID: The results of the ICD-Labor registry show that chagasic patients with implanted ICD due to secondary prevention, are different from the patients with ischemic heart disease (greater incidence in women and less ejection fraction among groups) and this cannot be extrapolated to which patients should receive an ICD. I think scientific societies should make up a "task force" to define such an important topic rather than a personal opinion about this. The presidents/directors of societies or committees on arrhythmias should speak now. Warm regards, Sergio Dubner -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 20:08:50 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 20:08:50 -0300 Subject: [HF-FORUM] 125E Sino atrial block. Dr. Xiuling Tan Message-ID: Respectable Professors Really glad to have chance to ask questions during HF-FORUM. Now there is a female patient whose age is 59, and she is diagnosed as SAB, ???degree, type 1. Her mother and elder brother died in sleeping some years ago, not clearly of the disease history of them. And recently she felt dizzy or suffocating sometimes. It's quite difficult to persuade her to implant pacemaker. The question is: is it ok of using drugs to cure her? what drugs have assured effect? is there any heredity factors of this disease? Thanks in advance for your replies. Dr. Xiuling Tan China -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 20:15:19 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 20:15:19 -0300 Subject: [HF-FORUM] 119S RE: Peripartum Cardiomyopathy. Dr. Rondon Message-ID: Dr. Luciano Pereira, Interesting question and there may be even a few replies for this. We do know, at least in our small country, some facts that lead us to think on Peripartum Cardiomyopathy: 1- Multigestation 2- Multiple pregnancies 3- Age of first pregnancy (the greater the age, the greater the risk) 4- Family history with similar symptoms 5- Risk factors such as Diabetes Mellitus and obesity 6- More sensibility in women who had immunological diseases of the LES type, antiphospholipid syndrome. Regarding prevention, I think not very much has been developed unless regarding classical clinics, but no prognostic biomarkers for the disease. I wonder the same and I have had to place resynchronizers in patients because of peripartum cardiomyopathy twice, and even though the response is quite good, we couldn't stop the rapid evolution of heart muscle impairment, with a relatively short response of the device, with regular programming and frequent treatment adjustments to improve the evolution of these patients. Regards and congratulations for the organizers of this symposium for such excellent quality of questions and comments. Mauricio Rond?n MD Hospital Universitario de Caracas Unidad de Electrofisiolog?a y Marcapasos -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 22:41:00 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 22:41:00 -0300 Subject: [HF-FORUM] 127S CHF in oncological patients. Dr. Acuna Message-ID: I would like to know the opinion of the colleagues about HF and LVEF impairment in hemato-oncological patients who undergo chemotherapy; generally young people who receive anthracyclic agents. Thank you, Dr. Jos? Acu?a Uruguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Mon Apr 24 23:37:52 2006 From: info at hf-symposium.org (HF Symposium) Date: Mon, 24 Apr 2006 23:37:52 -0300 Subject: [HF-FORUM] 136E Autonomic function during CRT. Dr. Moreira Message-ID: In a hypothetical case, what would be your therapeutic recommendation for a patient that after one month under CRT presented BRS decrease (pr? CRT = 6 ms/mmHg; p?s CRT = 3 ms/mmHg) and fall in HRV (SDANN delta change < 0%)? What is the supposed mechanism of this worsening in the autonomic function during CRT? Grateful, Filipe Moreira from Minas Gerais - Brazil - Military Hospital filipe at ipsm.gov.br ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 07:23:37 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 07:23:37 -0300 Subject: [HF-FORUM] 135S RE: Dobutamine. Dr. Montes De Oca Message-ID: I think that if by a clinically instable patient, we mean a patient that presents signs of decompensated HF, with clinical signs of fall of anterograde output, such as signs of obstruction in pulmonary circulation and given the clinical situation, we think that inotropic support should be carried out with dobutamine. In such patients, beta-blockers should be withdrawn until the situation is reversed, and then reinstate them. Dr. Omar Montes De Oca Montevideo-Uruguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 10:53:04 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 10:53:04 -0300 Subject: [HF-FORUM] EXPERTS ASK. What do you think about it? Message-ID: <472C825C-9A13-4C87-A30C-70C7CEF25D8D@hf-symposium.org> Dr. Jose Luis Merino from Spain asks - Is biventricular pacing superior to left ventricular pacing from a hemodynamic point of view in patients with heart failure and left bundlebranch block? What do you think about it? -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 13:21:01 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 13:21:01 -0300 Subject: [HF-FORUM] EXPERTS ASK, EXPERTS ANSWER Message-ID: <21020E4C-AB36-4976-9A00-AE5AB12DD8AA@hf-symposium.org> Dr. Armando Bordalo e S? from Portugal asks - In heart failure patients with atrial fibrillation, what is the "ideal" heart rate to prevent tachycardiomyopathy? What are the therapeutical measures to prevent tachycardiomyopathy? Dr. Jonatham Steimberg from U.S.A. answers The rate at which LV function is harmed, and the duration of time during the day when rates are excessive are not well defined in the clinical milieu. Suffice to say that keeping resting rates below 80 and activity related rates below 110-130 (depending on patient's age) would be logical strategy. Generally speaking, primary rate control medications are beta blockers and digoxin. Amiodarone is sometimes required. Diltiazem may be used, but can be problematic in heart failure. AV nodal ablation is sometimes required. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 13:23:44 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 13:23:44 -0300 Subject: [HF-FORUM] 120S RE: Stem cells. Dr. Rondon Message-ID: <2ACBB1A7-8FC6-44BF-B497-9C9228DEDB48@hf-symposium.org> Dr. Luciano Pereira, About this topic, I also think that there is no clear and well-defined protocol yet, to obtain an evaluation system for the results. For instance, we cannot follow the same protocol for dilated cardiomyopathies of non-ischemic origin, as with those with ischemic origin, autoimmune ones or those with associated degenerative symptoms; so the protocols cannot be the same, nor the results obtained will be the same. Intraarterial application cannot be the same either, as well as implantation by puncture through the coronary sinus directly on the injury area. The preparation condition of these stem cells, as well as the origin of these cells (umbilical cord, bone marrow, etc.) may generate differences and clear answers. Likewise, we cannot have a stabilized parameter for a response or not to stem cells?likewise there should be response effectiveness markers, and a stratification for such response, to be able to choose if the implantation was effective or more doses are needed, because we don't know either if 2 or 4 implantations are better or worse to obtain a proper response. Then, I think that very clear and stratified protocols with clear response parameters are the ones that would provide the information we want to be able to offer this option to our patients, and not to generate false expectations from unclear protocols that are not well documented in their responses before applying them massively. Mauricio Rond?n MD Hospital Universitario de Caracas Unidad de Electrofisiolog?a y Marcapasos -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 13:24:47 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 13:24:47 -0300 Subject: [HF-FORUM] 137E RE: Sino atrial block. Dr. Safer Message-ID: Fatigue and daytime sleepiness are typical signs of sleep apnea. First attempt is to improve respiration by a continuous Positive Airway Pressure device (cPAP). You should convince the patient to accept such a device and wear it during all sleep time. That probably will help significantly. Sleep apnea seems to be an inherited syndrome, which in higher degree of severity dramatically increases the risk for CHF, hypertension, stroke and sudden cardiac death. Currently there is no drug that really helps, unfortunately. With obese patients it will be recommended to convince them for weight loss, which generally improves the condition. There are two EMEA- and FDA-approved drugs to support that: Sibutramine & Orlistat. Sibutramine also seems to help improve SA. Best regards Dr. Anton Safer from Weisenheim (Germany) -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 13:28:37 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 13:28:37 -0300 Subject: [HF-FORUM] 134S RE: Restrictive cardiomyopathy in pediatrics. Dr. Alvarez In-Reply-To: <48134773-1A66-41A7-A679-E38809CCEB32@grupoakros.com.ar> Message-ID: I'm very grateful about this symposium and the chance to participate from my country. I think it is very interesting and the lectures, case presentations and other activities, as well as interviews have a high scientific level. I would like to get information about the subject of Restrictive Cardiomyopathy in Pediatrics by Dr. Virgini. I recently worked in an Asian country and we assessed some cases with this disease. Thank very much for everything. Profesora Alicia Alvarez Rodriguez Profesora de Pediatria de Cuba -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 17:31:52 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 17:31:52 -0300 Subject: [HF-FORUM] 138E RE: Autonomic function during CRT. Dr. Zareba Message-ID: Regarding HRV an improvement is usually observed in HRV after CRT, but it takes longer than a month. Probably one should ask whether the patient shows signs of clinical, echo improvement on CRT or he/she is a nonresponder. Again, improvement in ANS takes time, Best regards Wojtek -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 17:40:03 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 17:40:03 -0300 Subject: [HF-FORUM] 139E RE: Autonomic function during CRT. Dr. La Rovere Message-ID: > In a hypothetical case, what would be your therapeutic > recommendation for > a patient that after one month under CRT presented BRS decrease > (pr? CRT > = 6 ms/mmHg; p?s CRT = 3 ms/mmHg) and fall in HRV (SDANN delta > change < > 0%)? > What is the supposed mechanism of this worsening in the autonomic > function > during CRT? > > Grateful, > > Filipe Moreira from Minas Gerais - Brazil - > Military Hospital > filipe at ipsm.gov.br Dear Dr Moreira what I would check first is is the effectiveness of CRT in this hypothetical case. The patient could be a non-responder to treatment or there could be problems with CRT itsself. I would not be surprised of not seeing any change in autonomic markers after only one month treatment (it may take more time to reset the autonomic function following the hemodymanic improvement) however in this case you suggest a worsening of the autonomic function is taking place. Thus I woud guess that the patient is deteriorating further despite CRT or that other drugs which can positively affect the autonomic markers had been withdrawn or reduced (ie beta-blockers or ace-inhibitors). Another point which has to be taken into account is the condition the patient has been tested (was the patient studied at the same time of the day, following the previous protocol etc....?). Best regards Maria Teresa La Rovere -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 18:57:01 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 18:57:01 -0300 Subject: [HF-FORUM] 142E Nebivolol. Dr. Pojskic Message-ID: <62413430-977F-4B93-BD0A-7182FD4DC9A2@hf-symposium.org> Dear colleagues, Do you have experience with small doses of Nebivolol in case of elderly pts( SENIOR study)?Thank You for Your attention and well organized symposium. Belma Pojskic Bosnia and Herzegovina -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 19:14:01 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 19:14:01 -0300 Subject: [HF-FORUM] 143E RE: CRT in children. Dr. Levine Message-ID: <27EE6108-DC5F-4AAE-9D11-6A864CAC79BE@hf-symposium.org> There was a paper published in late 2005 in JACC focusing on the topic of CRT in a pediatric population. Dubin AM, Janousek J, Rhee E, et al, Resynchronization Therapy in Pediatric and Congenital Heart Disease Patients, An International Multicenter Study, J Amer Coll Cardiology 2005; 46: 2277-2283. This was a retrospective study (not prospective and not randomized) reviewing the experience with CRT at 22 major pediatric centers around the world (US, Canada, Australia, and the Czech Republic). Between these major tertiary care referral centers, there were a total of 103 patients. The study involved in both true pediatric patients with dilated cardiomyopathy as well as any patient with congenital heart disease as complex congenital heart disease is associated with some unique challenges. While the mean age was 12.8 years, the age range was 3 months to 55.4 years. 17 of the patients were over 21 years of age but all had CHF associated with complex congenital heart disease. On top of that the median duration of follow-up was only four months (range 22 days to 1 year). 73 patients had congenital heart disease, 16 had a cardiomyopathy and 14 had congenital complete AV block. The mean QRS duration prior to CRT was 166 ms which decreased by 38 ms after the initiation of CRT. The pre-CRT left ventricular ejection fraction was 26 % ? 11.6%. The LV ejection fraction increased by a mean of 12% with the mean EF after CRT of 40% ? 15% (p < 0.05). Of 18 patients who had undergone CRT while on the cardiac transplant list, 3 were able to removed from the list, 5 underwent a transplant, 2 died and 8 are still on the transplant list. Prior to CRT, all patients were in NY Heart Association functional class III or IV. Following CRT, 15 were reported to be NYHA Functional Class I. The congenital heart problems that were subsequently treated with CRT included left sided obstructive lesions (n = 15), L-transposition with systemic RV failure (n = 12), tetralogy of Fallot (n = 11), AV canal defect (n = 10), d-transposition (n= 12) and a variety of others. 7 of the patients had a single ventricle physiology. Pacemakers had already been implanted in 27 patients for surgically induced AV block and had been paced a mean of 8.6 years (range: 5 months to 35 years). Of the cardiomyopathy patients, 10 had dilated while 4 had hypertrophic cardiomyopathy. As to the implant, a fully transvenous system was able to be implanted in 45 while 48 had epicardial leads placed for CRT. In 10, a combination of transvenous and epicardial leads was utilized. It was the younger patients who received the epicardial systems (4.6 years for epicardial, 16.9 years for transvenous). It was the older population who received a CRT-D system (mean age 17 years, range 9 to 55.4 years) compared to those who received a CRT-P system (mean age 11.5 years, range 4 months to 51.4 years). Patients who were upgraded from a standard pacemaker implanted for AV block obtained a level of benefit similar to those who received a denovo implant for CHF. The relative age, percent improvement of EF and degree of QRS shortening was similar (no significant difference) for the congenital heart disease, cardiomyopathy and AV block groups. Of the patients with single ventricle physiology (n = 7), the QRS shortened in all of them but there was no significant increase in LVEF (mean 7%, p = 0.08) and clinical improvement in only 2 of the 7. Of the 17 patients whose RV was the systemic ventricle, the mean EF increased by 13%, there was a 38 ms decrease in QRS duration and thirteen of these patients showed a clinical improvement. Eleven of the patients were considered non-responders. It was interesting that the non-responders had ?healthier? hearts at the time of CRT implant. The mean LVEF was 32% compared to the mean pre- CRT LVEF of 24% in the group that responded to therapy. The degree of QRS narrowing was similar in both responders and non-responders. Of these 11 patients, three had an improvement in their clinical status after CRT pacing despite any change in EF or other objective measures of ventricular function. As far as complications, there were 23 complications in 20 patients with an overall adverse event rate of 29%. Overall mortality was 5% with coronary sinus issues accounting for 23% of the reported complications. Eighteen percent of transvenous systems had coronary sinus complications. As to indications with respect to the adult population, only 16% had a system implanted for cardiomyopathy while only 54% fulfilled both the QRS duration and ejection fraction criteria used in adults. The majority of patients, and all the adults being followed by the various pediatric centers had complex congenital heart disease. This increases the challenges associated with lead placement for the systemic ventricle. Of 5 of the 6 critically patients on parenteral inotropic support, there were able to be effectively weaned to oral agents after the establishment of CRT. As to Dr. Macarov?s comment about an EF of 50%, the non-responders reported in this paper all had a better EF than the responders. But even then, the EF was below 35% which is one of the standards for the adult population, not 50%. The authors postulate that the lack of response may have been because their ventricles were ?too healthy? and they still had some compensatory mechanisms available to support themselves. In addition, in this report, the indication for CRT was similar to that of the adult population based on a markedly reduced ejection fraction, a very wide QRS (mean 166 ms), symptomatic congestive heart failure (NYHA functional class III or IV) despite appropriate medical therapy. The etiology of the diseases varied significantly from the adult population with only 14 having CHF due to a cardiomyopathy and of this group, only 10 had a dilated cardiomyopathy. Other specific details such as internal LV and RV diameters and the like were not provided in the review article. Perhaps one or more pediatric electrophysiologists and/or heart failure physicians who may be participating in this Symposium will respond to DR. Macarov?s query with their own experience if they have CRT patients at their respective institutions. 103 patients at 22 major tertiary care referral centers with a mean follow-up of only 4 months suggests that these centers have only recently started implanting CRT systems and the number of patients is still very small. The specific number of implants at each center was not reported but there was a mean of 5 patients per center and I suspect that some may have had only 1 or 2 while others had more. Paul Paul A. Levine, MD, FHRS, FACC Vice President, Medical Director St. Jude Medical, CRMD 15900 Valley View Ct. #980, Sylmar, CA 91342 818-493-2900 / Fax: 818-362-2242 ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 19:39:20 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 19:39:20 -0300 Subject: [HF-FORUM] =?iso-8859-1?q?144E_RE=3A_CHF_in_oncological_patients?= =?iso-8859-1?q?=2E_Dr=2E_P=E9rez_Riera?= Message-ID: Dear Dr Jose Acu?a from Uruguay: The spectrum of cardiotoxicity with chemotherapeutic agents includes: 1) Asymptomatic electrocardiographic abnormalities; 2) Hypertension or blood pressure changes; 3) Long QTc interval; 4) Acute cardiomyopathy; 5) Long-term cardiomyopathy; 6) Myocarditis; 7) Arrhythmias; 8) Bradyarrhythmias; 9) Pericarditis; 10) Cardiac tamponade; 11) Acute myocardial infarction; 12) Cardiac failure and 13) Shock. These effects may occur during or immediately after treatment or may not be apparent until months or years after treatment. A major complication of anthracycline therapy is its adverse cardiovascular effects. If these cardiac complications could be reduced or prevented, higher doses of anthracyclines could potentially be used, thereby further increasing cancer cure rates. Moreover, as the incidence of cardiac toxicity resulting in CHF or even heart transplantation dropped, the quality and extent of life for cancer survivors would improve. Preventative strategies that have met with some success have included the use of less cardiotoxic analogs such as epirubicin and liposomal anthracycline preparations. The cardioprotectant agent dexrazoxane reduces cardiomyopathy but there are significant toxicity issues. Therefore, the main strategy for preventing cardiotoxicity remains careful monitoring with radionuclide angiography, ECG and echocardiography. The role of investigational markers of myocardial injury, such as troponin T or BNP, remains of great interest. Management is according to conventional management of CHF. Trastuzumab is an antibody therapy directed against the human epidermal growth factor receptor-2 (HER2), which increases survival in patients with metastatic breast cancer and is under evaluation in the adjuvant setting. It also causes rarely a decrease in LVEF. Incidence is increased if trastuzumab is given in conjunction with paclitaxel or anthracyclines. It differs from anthracycline cardiotoxicity in that it is not cumulative dose- dependent and often improves after withdrawal of treatment. Re-treatment with trastuzumab is often possible. Novel agents under development offer a different spectrum of toxicity to existing anticancer drugs and it appears likely that cardiovascular toxicity will be an important issue for many of these drugs, particularly those that target the tumor vasculature(1). Circulating apoptotic proteins (Tumor necrosis factor (TNF) alpha, sTNF-receptor (sTNF-R) 1 and 2, sFas, sFas ligand, sTNF) are increased in patients with HF. Apoptosis-related proteins and inflammation markers are increased in long-term disease free breast cancer survivors and associated with cardiotoxicity (2). Atrasentan is an anti-cancer drug from a new class of agents called selective endothelin-A receptor antagonists. The orally administered drug is being studied in a subset of patients with advanced prostate cancer. Phase II and III studies evaluating time to clinical and radiographic progression failed to demonstrate a significant benefit with atrasentan versus placebo. The adverse effects, observed more frequently in those treated with atrasentan than in placebo-treated patients, were peripheral edema, rhinitis, headache, infection, dyspnea, and HF. Atrasentan's role in the various stages of advanced prostate cancer, and relative to the chemotherapeutic agent docetaxel, has not been determined (3). Alkylating agents cyclophosphamide, ifosfamide, cisplatin, busulfan, and mitomycin, have also been associated with cardiotoxicity. Other agents with toxic cardiac effects are: vinca alkaloids, fluorouracil, cytarabine, amsacrine, and asparaginase and the newer agents, paclitaxel, etoposide, teniposide and trastuzumab. The last one is an effective treatment in patients with HER2-overexpressing metastatic breast cancer. Risk of trastuzumab-induced cardiotoxicity raises concerns regarding combined use with anthracyclines or other potentially cardiotoxic agents following anthracycline treatment (4). Patients with age >/=50 years or receiving multiple course of high-dose chemotherapy should be considered at risk for cardiac dysfunction (5). The heart is vulnerable to oxidative injuries from O2 radicals generated by chemotherapy. Mild myocardiocyte injury from chemotherapy may be of more concern in children than in adults because of the need for subsequent cardiac growth to match somatic growth and because survival is longer in children. Primary prevention is therefore important. Patients should be educated about the cardiotoxic risks of treatment and the need for long-term cardiac monitoring before chemotherapy is begun. Cardiotoxicity may be prevented by screening for risk factors, monitoring for signs and symptoms during chemotherapy, and continuing follow-up that may include ECG, echocardiography, angiography, and measurements of biochemical markers of myocardial injury. Secondary prevention should aim to minimize progression of LV dysfunction to overt HF. Approaches include: 1) Altering the dose; 2) Using analogs or new formulations with fewer or milder cardiotoxic effects; 3) Using cardioprotectants and agents that reduce oxidative stress during chemotherapy; 4) Correcting for metabolic derangements caused by chemotherapy that can potentate the cardiotoxic effects of the drug; and 5) Cardiac monitoring during and after cancer therapy. Avoiding additional cardiotoxic regimens is also important in managing these patients. Treating the adverse cardiac effects of chemotherapy will usually be dependent on symptoms or will depend on the anticipated cardiovascular effects of each regimen. Treatments include beta-adrenoceptor antagonists, ACE inhibitor or an angiotensin II receptor blocker, aldosterone receptor antagonist and diuretics. Diuretic therapy is useful in treating acute and chronic renal insufficiency, CHF, cirrhosis, overhydration and hypertension (6). References 1) Youssef G, Links M. The prevention and management of cardiovascular complications of chemotherapy in patients with cancer. Am J Cardiovasc Drugs. 2005; 5:233-243. 2) Perik PJ, Van der Graaf WT, De Vries EG, Boomsma F, Messerschmidt J, Van Veldhuisen DJ, Circulating apoptotic proteins are increased in long-term disease-free breast cancer survivors. Acta Oncol. 2006;45:175-183. 3) Murphy G. Atrasentan for metastatic hormone refractory prostate cancer. Issues Emerg Health Technol. 2005; 77:1-4. 4) Konecny GE, Pegram MD. Gemcitabine in combination with trastuzumab and/or platinum salts in breast cancer cells with HER2 overexpression. Oncology (Williston Park). 2004;18: 32-36. 5) Bengala C, Zamagni C, Pedrazzoli P, Matteucci P, Ballestrero A, Da Prada G, et al. Cardiac toxicity of trastuzumab in metastatic breast cancer patients previously treated with high-dose chemotherapy: a retrospective study. Br J Cancer. 2006; 94:1016-20. 6) Simbre VC, Duffy SA, Dadlani GH, Miller TL, Lipshultz SE. Cardiotoxicity of cancer chemotherapy: implications for children. Paediatr Drugs. 2005; 7:187-202. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 22:38:32 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 22:38:32 -0300 Subject: [HF-FORUM] 141R RE: Digoxin and carvedilol. Dr. Pereira Message-ID: I think the opinion by Dr. Mykola Yabluchansky from Ukraine, about the dose of carvedilol is guided by common sense. I agree with her in that we should use clinical criteria to guide us, and not work blindly to achieve maximal doses. Dr. Luciano Pereira Paraguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 22:49:45 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 22:49:45 -0300 Subject: [HF-FORUM] 145E RE Left ventricular pacing and the individualized pacing site. Dr. Levine Message-ID: <72BD0CDA-50A0-4750-8BB8-095DB4F22148@hf-symposium.org> Dr. Li Zhang wrote: Based on the recent study (Jia P, et al. Heart Rhythm 2006;3(3): 296-310), the efficacy of CRT is depended strongly on patient- specific electrophysiologic substrate. For patients with left ventricular ischemic cardiomyopathy, left ventricular (LV) pacing, although it increases QRS duration and dispersion, may do as good as bi-ventricular pacing in improving the mechanical uniformity. Another issue is the LV pacing site. As we know there are multiple factors involved in the cardiac remodeling process in the failing hearts, such as depressed myocardial excitability, changes in the extracellular matrix due to scar tissue or diffused fibrosis and decreased gap junction functions, etc (Akar FG, et al Trends Cardiovasc Med 2005;15(7):259-64). Those factors may have contributed to the outcome as non-responders to CRT. The non- invasive ECG imaging (ECGI) developed by Dr. Rudy's group, as well as the advanced MRI techniques (Helm Pa, et al Cir Res 2006;98(1): 125-32) may not only help predict the non-responders in some degree, but also help identify the optimal pacing site. I wonder if you would be willing to make comments about the ideas of LV pacing and the individualized pacing site. Reply: Dear Dr. Zhang, While I agree that the efficacy of CRT is related to the underlying substrate however this should be both electrical and mechanical. In general, non-ischemic dilated cardiomyopathy patients usually respond better than ischemic cardiomyopathy patients although this is not to say that the ischemic patients do not respond. Many do respond and respond very well. In my personal experience and based on some recent studies presented at the American College of Cardiology this past March, those patients who have a reduced EF and refractory congestive heart failure in association with a large akinetic or even dyskinetic (aneurysm) area from a prior myocardial infarction with the remaining heart muscle functioning well, even being hypercontractile, do not do very well with CRT. It is very difficult to pace scar tissue and induce it to actively contract. Still, many patients with ischemic heart disease do not have a major well defined scar. Rather, they have diffuse fibrosis from ischemia and these patients seem to experience some improvement from CRT. I think that a key to responding is that the muscle still be able to contract and if, with CRT, we can improve the contraction pattern and reduce some of the pathologic wall stress associated with the abnormal contraction pattern, some of the weakened muscle can recover (reverse remodeling). I have a strong bias that pre-implant studies should be done to not only demonstrate the abnormal contraction pattern but to also identify the area of latest contraction. The goal would be to then place the LV lead in that location presuming that capture thresholds are adequate and that it does not induce phrenic nerve stimulation. Indeed, it has been recommended that if the transvenous LV epicardial lead (coronary sinus to cardiac vein) can reach the area of latest contraction, then an epicardial lead should be utilized so that it can be placed in the optimal location. With that being said and even knowing that most patients with poor ventricular function and overt congestive heart failure have periodic routine echocardiograms, these are usually standard studies and the physician is rarely looking for marked dyssynchrony. EF, ventricular and atrial dimensions and the degree of MR and TR are most commonly assessed and followed. Hence, if a patient is being considered for CRT therapy, a detailed echo study should be performed specifically examining the patient for dyssynchrony. There is an occasional patient with complete left bundle branch block who has a dilated and hypokinetic but still synchronous contraction pattern, this patient would not benefit from CRT. We are also beginning to recognize patients with refractory congestive heart failure, a narrow QRS pattern who have marked dyssynchrony and these patients may benefit from a CRT system. The role of CRT in this population of patients is being evaluated in a prospective randomized trial sponsored by St. Jude Medical titled RETHINQ. There is absolutely no data available from this study at the present time. Few centers, however, perform a detailed echo-Doppler, tissue Doppler or some other more sophisticated imaging technique pre-implant study to evaluate whether the patient is a good candidate for CRT and to also serve as a guide for ?optimal? LV lead placement. Even if the patient is not a "good candidate", but by the time CRT is being recommended, intensive pharmacologic therapy has failed whether or not cardiac transplantation is an option, (see Dr. Moss' earlier comments about CRT and Transplant - they are not mutually exclusive), CRT is commonly undertaken as a last therapeutic option with the hope that it will help the patient. In these and many cases, the placement of the LV lead is not based on echo studies but rather on practicality accepting anyplace that the lead can be placed with an adequate capture and sensing thresholds and without phrenic nerve stimulation. This might then be a setting in which the ability to adjust the V-V interval between RV and LV can play an additional role in optimizing therapy. I realize that this is a relatively new capability but it is one that is available in many current generation CRT systems. One could theoretically compensate for delays in conduction to the area of latest contraction to improve the degree of synchronization and hopefully, a further improvement in cardiac function. There have been a few published studies and more abstracts looking at this issue. A number of these are briefly summarized below. Even when the patients have responded to standard CRT pacing, a V-V interval of something other than simultaneous has often resulted in a demonstrated acute hemodynamic benefit (the long term consequences are not available from most of these studies). 1. Chan et al. ?Tissue Doppler Guided Optimization of A-V and V- V Delay of Biventricular Pacemaker Improves Response to Cardiac Resynchronization Therapy in Heart Failure Patients? J of Cardiac Failure 2004; 10, 4 (suppl.): S72 (abstract 199). ? This study evaluated 45 patients who were non-responders and converted 38 (85%) to responders through timing cycle optimization using echo-TDI. The most favorable AV delay was between 130 to 150 ms and the optimal VV delay was between 24-28 ms. This study did not evaluate the individual effects of AV optimization and VV optimization so that it is difficult to say which timing cycle optimization was the major contributor in each patient. 2. Bordachar et al. ?Echocardiographic Parameters of Ventricular Dyssynchrony Validation in Patients with Heart Failure Using Sequential Biventricular Pacing? JACC 2004 Dec 7; 44 (11): 2157-2165. ? This study was performed at implant with acute optimization utilizing a multiplicity of echo-Doppler techniques comparing RV pacing, LV pacing, simultaneous LV-RV and sequential with both RV first and LV first in a random order. More than 85% of patients were optimized at a V-V timing interval other than simultaneous. However, patients whose LV lead was not on the posterior or lateral wall were excluded from study so there is no information available as to whether V-V timing can compensate for a less than optimal lead location. 3. Vanderheyden et al. ?Tailored echocardiographic interventricular delay programming further optimizes left ventricular performance after cardiac resynchronization therapy? Heart Rhythm, Volume 2, No. 10, Oct 2005 1066-1072 4. VanGelder et al. ?Effect of Optimizing the VV Interval on Left Ventricular Contractility in Cardiac Resynchronization Therapy? American Journal of Cardiology 2004; 93, 1500-1503 ? This study compared simultaneous biventricular pacing with AV optimized to sequential biventricular pacing with AV and VV optimization using a Millar catheter placed in the LV to measure dP/ dt. A total of 53 patients were studied (chronic AF with complete heart block, ischemic cardiomyopathy patients and non-ischemic cardiomyopathy patients, the last two groups being in sinus rhythm). 89% were optimized to something other than simultaneous RV and LV stimulation. Optimized sequential CRT provided a 44% relative improvement (8% absolute improvement) over simultaneous CRT with optimized AV delay. While 8% may not seem like a lot and the long term clinical impact cannot be determined from this acute study, these patients are so very compromised that they need every little bit of help that we can provide. 5. Sogaard et al. ?Sequential Versus Simultaneous Biventricular Resynchronization for Severe Heart Failure: Evaluation by Tissue Doppler Imaging? Circulation 106: 2078-2084 (2002) ? This study used tissue tracking and 3D echo to evaluate the impact of sequential CRT vs simultaneous CRT. Delayed longitudinal contraction (DLC) and LV ejection fractions (LVEF) were measured in 20 patients with 11 different V-V delays. DLC was reduced over 50% between no CRT and simultaneous CRT. It was reduced an additional 50% from simultaneous CRT when the V-V delay was optimized. Similar, LVEF improved by an additional 13% with V-V optimization compared to simultaneous even though simultaneous CRT resulted in an improvement over no CRT. 6. Rosanio et al. ?Non-Simultaneous Pacing of the Right and Left Ventricles for Heart Failure: Is It Worth It?? AHA Abstract: 1618 (2003) AHA 76th Scientific Sessions, Orlando, Nov. 9-12, 2003 ? This study evaluated a series of 22 patients who received a CRT system for standard indications. They had AV delay optimization performed at implant and were then followed for 2 months. At the end of 2 months, the V-V delay was optimized using mitral valve Doppler echocardiography and followed for another 2 months. While AV interval optimization resulted in a statistically significant improvement based on the 6 minute walk test, LVEF and NYHA functional class over pre-implant status, V-V interval optimization resulted in a further improvement over simultaneous CRT. The optimal V-V interval ranged between 20 to 80 ms and in most cases, LV preceded RV pacing. 7. O?Cochlain et al. ?The Effect of Variation in the Interval Between Right and Left Ventricular Activation on Paced QRS Duration? PACE 2001; 24: 1780-1782 ? This study evaluated the impact of V-V interval adjustment on the QRS duration as a marker of CRT. LV and RV coupling was evaluated over a range of ? 50 ms. Optimization resulted in a further 13% narrowing of the QRS duration. With the LV lead on the lateral or anterolateral wall of the LV, LV pacing prior to RV pacing gave the best results for this end-point. When the lead was in the posterolateral location, there was not as great a benefit. Using this endpoint (a relatively weak endpoint as QRS duration is not the best endpoint for hemodynamic improvement), 75% of patients were optimized at a V-V delay other than simultaneous. 8. Perego et al. ?Simultaneous vs. Sequential Biventricular Pacing in Dilated Cardiomyopathy: An Acute Hemodynamic Study? The European Journal of Heart Failure 2003; 5: 305-313 ? This study compared sequential to simultaneous biventricular pacing. Invasive measurements of LV and RV pressures and LV dP/dt were measured acutely at VV intervals ranging from LV first by 60 ms to RV first by 40 ms. The average increase in dP/dt was higher with sequential compared to simultaneous stimulation and in most patients (but not all), results were better with LV first. 9. Bracke et al. ?Importance of Interventricular Delay to Optimize Cardiac Resynchronization Therapy? JACC 41: (2003) ACC 52nd Annual Scientific Sessions March 30*-April 2nd, 2003, Chicago ? This study evaluated 13 patients at the time of CRT implant using maximum LV dP/dt as the endpoint. They compared AAI, BiV and LV pacing. With regard to BiV pacing, the V-V delay varied from RV first and then LV first up to a maximum of 80 ms. LV dP/dt was better in 9 of the 13 patients with LV first by an average of 48 ms (? 23 ms). 10. Mortenson et al. ?Sequential Biventricular Pacing: Evaluation of Safety and Efficacy? PACE 2004; 27: 339-345 ? This is a large study involving 189 patients comparing baseline (no CRT), simultaneous BiV and sequential BiV using a multiplicity of echo-Doppler measurements, NYHA functional class and the 6 minute walk test. All patients had their AV delay optimized. Paired data was available for 34 patients in which V-V optimization was performed. VV optimization did not have a significant impact on NYHA functional class or 6 minute walk test, it did increase the aortic velocity time integral and stroke volume measurements by 23% at pre-hospital discharge and by 18% at 3 months follow-up compared to simultaneous biventricular pacing. The optimized VV interval determined prior to discharged also remained stable by the 3 month follow-up visit. 11. Leon et al. ?Effect of Cardiac Resynchronization Therapy with Sequential Biventricular Pacing on Doppler-Derived Left Ventricular Stroke Volume, Functional Status and Exercise Capacity in Patients with Ventricular Dysfunction and Conduction Delay? PACE 25: 141 (2002) NASPE 23rd Annual Scientific Sessions, May 8-11, 2002, San Diego ? This study is similar to the Mortenson study involving the US InSync III trial with sequential biventricular pacing showing a significant improvement in sequential biventricular pacing over simultaneous biventricular pacing. 12. Kurzidim et al, ?Optimization of Cardiac Resynchronization Therapy by Sequential Biventricular Stimulation: Results of an Acute Hemodynamic Study, JACC 2003; 41: 1110-68, ACC 52nd Annual Scientific Session, March 30 ? April 2, 2003, Chicago ? This study involved 34 patients to evaluate the acute effects of individually optimized biventricular pacing on LV systolic function between sequential to simultaneous pacing. The VV interval ranged from LV first by 80 ms to RV first by 80 ms in 20 ms steps. The primary endpoint as maximum left ventricular dP/dt. The highest LV dP/dt was obtained in 50% of the patients with LV first by a mean of 32 ms ?21 ms. Paul A. Levine, MD, FHRS, FACC Vice President, Medical Director St. Jude Medical, CRMD 15900 Valley View Ct. #980, Sylmar, CA 91342 818-493-2900 / Fax: 818-362-2242 -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 22:59:21 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 22:59:21 -0300 Subject: [HF-FORUM] 146E RE: Restrictive cardiomyopathy in pediatrics. Dr. Perez Riera Message-ID: Dear Prof. Alicia Alvarez Rodriguez from the nice Cuba: Restrictive cardiomyopathy (RCM) is most notable for abnormal relaxation of the ventricles and well preserved pumping function. RCM, the least common type of cardiomyopathy in the US, occurs when the myocardium of the ventricles becomes excessively rigid, and the filling of the ventricles with blood between heart beats is impaired.As a result, , the atria, become enlarged while the ventricles, remain normal in size. This is a rare form of cardiomyopathy in children. Differentiation from constrictive pericarditis, a clinically similar entity, is difficult but important because the treatment options and prognosis differ drastically. RCM usually results from another disease, which occurs elsewhere in the body. However, there are idiopathic occurrences as well. Restrictive cardiomyopathy does not appear to be inherited, but some of the diseases that lead to the condition are genetically transmitted. Proposal of classification of RCM I) Idiopathic (cause unknown); II) Familiar/genetic pseudo-idiopathic restrictive cardiomyopathies (result from a genetic or secondary to a heart muscle disease that manifests as restrictive physiology); III) Others non genetic secondary causes. The mains causes of familial/genetic restrictive cardiomyopathies are II.A) Familial/genetic restrictive cardiomyopathies (FRCMs) are: (II.3a) Familial Noninfiltrative restrictive myocardiopaty (II.3b) Familial pseudo-Idiopathic (II.3c) Familial Sclerodermya. II.B) Familiar Infiltrative Restrictive cardiomyopathies (FRCMs): (II.a) Familial amyloidosis restrictive cardiomyopathy (II.b) Mucopolysaccharidosis (a condition in which mucopolysaccharides, or carbohydrates that bond with water to form a thick, jelly-like substance, accumulate in body organs) (II.b.1) Gaucher disease type I (II.b.2) Hurler syndrome. II.C) Storage disease: (III.1) Hereditary hemochromatosis (III.2) Fabry disease or Sphingolipid: It is an X-linked recessive genetic disorder of glycosphingolipid metabolism, due to deficiency of the lysosomal enzyme alpha- galactosidase A. (III.3)Glycogen storage disorder, Pompe disease, acid maltase deficiency, infantile acid maltase II. C) Endomyocardial fibrosis-2. Locus Xq28OMOM NO: 302060, GENE SUMBOL: TAZ, III) Others non genetic secondary causes of RCM 1) Scleroderma is an uncommon autoimmune connective tissue disease or progressive systemic sclerosis Scleroderma (a chronic, degenerative disease that affects the joints, skin, and internal organs); 2) Senile cardiac amyloidosis; 3) Sarcoidosis (a rare inflammation of the lymph nodes and other tissues throughout the body) 4) Radiation therapy for cancer; 5) Metastatic malignancy; 6) Loeffler eosinophilic endomyocardial disease; 7) Anthracycline toxicity; 8) Carcinoid heart disease. Comentaries about Endomyocardial fibrosis (EMF), is an idiopathic disorder of the tropical and subtropical regions of the world that is characterized by the development of restrictive cardiomyopathy that occurs most commonly in children and young adults Africa, primarily in Uganda and Nigeria, India and South America( my dear Brazil) that are within 15? of the equator. EMF may account for up to one fourth of deaths due to cardiac disease in those areas. Tropical EMF and L?ffler endocarditis should be distinguished from endocardial fibroelastosis, which is characterized by cartilaginous thickening of the mural endocardium, chiefly of the LV. This disease is most common in the first 2 years of life and, in some patients, appears to be an inherited disorder that is associated with congenital cardiac malformations. In equatorial African nations, such as Nigeria, EMF is the fourth most common cause of cardiac disease in adults, and EMF accounts for 22% of cases of HF in Nigerian children. EMF is the most common type of restrictive cardiomyopathy in tropical countries. The surgical experience and early results obtained at four surgical centers in the northeast and south of Brazil. From December 1977 to September 1986, 95 operations were performed on 93 patients, ages 11-59. Bilateral lesions occurred in 42 patients, right lesions in 39, and left lesions in 12. Ventricular decortication and removal of thrombi were performed in all. In right-sided lesions, the tricuspid valve was substituted by a bioprosthesis in 34 cases, and substituted by a tilting disk valve in 1 case. In 4 patients, the valve could be preserved. The left-sided lesions led to valve substition by a bioprosthesis in 11 cases, and preservation of the valve in 1. The bilateral lesions needed bioprosthesis in the mitral position in 37 patients, and a disk valve in 2. In these 39 instances, the valvular procedure was insertion of a tricuspid bioprosthesis. Three tricuspid and three mitral plasties were performed. The overall mortality was 20% (26.2% for bilateral lesions, 14.6% for the right-sided lesions, and 20% for the left-sided lesions). The main cause of death was low cardiac output. Aside from a variable degree of right and left ventricular failure, many other non-fatal complications clouded the postoperative course. Complete AV blocks occurred in 10 cases, with the need for permanent pacing in 7 survivors. The mortality and morbidity in the present series is in keeping with the results reported in current literature. Regarding the advanced stage of their patients' disease, the authors agree with the recommendation for earlier surgical intervention (1) 1) da Costa FD, Moraes CR, Rodriques JV, de Mendonca JT, de Andrade JC, Buffolo E,et al. Early surgical results in the treatment of endomyocardial fibrosis. A Brazilian cooperative study. Eur J Cardiothorac Surg. 1989;3:408-413. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Tue Apr 25 23:14:47 2006 From: info at hf-symposium.org (HF Symposium) Date: Tue, 25 Apr 2006 23:14:47 -0300 Subject: [HF-FORUM] 147C Rhythm control in HF patients with AF. Dr. Yunlong Xia Message-ID: <65259A40-9E6A-42B9-AB6D-371B37EEAF24@hf-symposium.org> Dear Dr Jonatham Steimberg In treatment of heart failure patients with atrial fibrillation (AFib), what's the position of rhythm control? In your Webcast of this symposium, rhythm control looks better than rate control in these patients. Especially in Dr Hsu's study, the patients benefit a lot from the rhythm control by catheter ablation. In my mind, AFib ablation should be at least an alternative method for prevention of 'tachycardiomyopathy'. On the other hand, atrial arrhythmias are important predictors for those non-responders under CRT therapy, and rhythm control by ablation might be an ideal strategy for these patients. However, no further comment on this issue could be found either in your Webcast or in the other lectures. What's your opinion of rhythm control, especially by ablation, in heart failure patients with AFib? Best regards Yunlong Xia Department of Cardiology The First Affiliated Hospital of Dalian Medical University -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 26 13:10:41 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 26 Apr 2006 13:10:41 -0300 Subject: [HF-FORUM] 133S RE: Peripartum cardiomyopathy. Dr. Pereira Message-ID: <93F74E82-7716-492A-A84E-94D65F7C161B@hf-symposium.org> Dr. Rondon, Thank you for your reply, but I don't agree with your expression "in our small country." It is not real, if you let me say it. A country with 912,050 Km2 of surface, with more than 25 million inhabitants is in no way small. And a country with Bolivar as its maximal historical figure will never be a small country either. About the topic of peripartum cardiomyopathy, the evolution of patients is also intriguing. Some experiment a regression of dilatation and become absolutely normal, and others progressively worsen. This clinical markers quoted by you, do they correlate to evolution too? Warm regards, Dr. Luciano Pereira Paraguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 26 13:11:45 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 26 Apr 2006 13:11:45 -0300 Subject: [HF-FORUM] 140C RE: Bloqueio sino-atrial. Dr. Lu Message-ID: <11B20FB1-CF56-4CE2-B5B9-EC433178DB25@hf-symposium.org> > Respectable Professors > > Really glad to have chance to ask questions during HF-FORUM. Now > there is a female patient whose age is 59, and she is diagnosed as > SAB (sino atrial block), degree, type 1. Her mother and elder > brother died in sleeping some years ago, not clearly of the > disease history of them. And recently she felt dizzy or suffocating > sometimes. It's quite difficult to persuade her to implant > pacemaker. The question is: is it ok of using drugs to cure her? > what drugs have assured effect? is there any heredity factors of > this disease? > > Thanks in advance for your replies. > > > Dr. Xiuling Tan > > China Thanks for your question. First, you should give a definite diagnosis, for SSS yes or not, for heart disease, yes or not. Holter, UCG, esophageal electrocardiography for sinus node function and the level of serum potassium should be done. If she has not heart disease, only SAB, Wenckebach sinus-atrial block, it is not necessary to implant pacemaker. If she has a heart disease with definited cause, just for etiology treatment. Because the positive family history, some important clues should be looked for, such as the characteristics EKG of Brugada syndrome, it is more to sudden death during sleep; such as Long QT syndrome, hypertrophy cardiomyopathy and so on. If convenience, let her to Wuhan Union Hospital . Yongxin Lu China -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 26 16:33:13 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 26 Apr 2006 16:33:13 -0300 Subject: [HF-FORUM] EXPERTS ASK. What do you think about it? Message-ID: Dr. Ricardo Sarmiento from Argentina asks - In a patient with degree III heart failure, with sinus rhythm, (with history of atrial fibrillation) medicated with cardiovedilol 50 mg/day, espironolactone 25 mg/day, fursemide 40 mg/day, amiodarone 200 mg/day (except two days a week), dicumarinic agents (INR 2.5), enalapril 10 mg/day. With this medication the patient is currently in class II. His urea and creatinine figures have increased progressively in the last year. With the increase of the enalapril dose his symptoms improved more, but his urea increased. What would you do with this patient, currently in class II with urea 1.80 and creatinine 2.7? Would you add digoxin? Would you increase the doses ofdiuretics? What do you think about it? -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 26 16:41:22 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 26 Apr 2006 16:41:22 -0300 Subject: [HF-FORUM] 148S RE: Stem cells. Dr. Pereira Message-ID: <819B4D28-119C-4B6F-8516-078386196B2E@hf-symposium.org> Dr. Rondon, Thank you for your opinion. I think there is a lot yet to be told about this issue and we have to be cautious. I remember last year when -at the very beginning of the Conference of the Argentine Society of Cardiology- we heard Dr. Valentin Fuster say that using stem cells in ischemic heart disease had no relevant value, and the lecturers who had to speak after him about their own experience, did not dare to by fear of losing their audience. With all due respect to Dr. Fuster, who maybe inadvertently caused the affair I just told you about, we could not listen anything more on this topic. In October, already in Asuncion in Paraguay, I heard a professor from the University of Bahia, Brazil, speak in promising terms about the use of stem cells in chagasic cardiomyopathy. So as you say, "protocols cannot be the same, neither the results we obtain will be the same." Kind regards, Dr. Luciano Pereira PARAGUAY -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Wed Apr 26 20:24:46 2006 From: info at hf-symposium.org (HF Symposium) Date: Wed, 26 Apr 2006 20:24:46 -0300 Subject: [HF-FORUM] 149S RE: Rehabilitation. Dr. Bertolasi Message-ID: To answer the clever question by Dr. Wagner Samaniego, we could say in brief: "lack of proper information." This is exaggerated, paradoxically in societies with less budget and level of education. As to the use of the resource, for example it isn't rare to observe the popular impact of the indication of heart transplantation; instead no one thinks of stating the need to make autopsies as a routine. It is true that transplantations save human beings, but it is also true that autopsies indicate the road to treat better our future patients. With the success of the treatment of acute ischemic syndromes, secondary prevention becomes more relevant everyday. Among the proper measures, hygiene and diet guidelines are the ones that show a better risk-benefit ratio (although of scant economic benefit); I think for this reason they receive less support. Anyway, cardiovascular rehabilitation is a slow process, not spectacular, but hugely important for our patient. Interacting with the community to reinforce these concepts is a priority, especially in countries with scant resources and few or no sanitary policies. The difficulty of sending resources to Public Hospitals is explained by our traditional insistence on skimping support to those who need it the most. Carlos Bertolasi -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 27 07:18:33 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 27 Apr 2006 07:18:33 -0300 Subject: [HF-FORUM] 150E RE: Autonomic function during CRT. Dr. Perez Riera Message-ID: Dear Dr. Filipe Moreira from Military Hospital Minas Gerais - Brazil -CTR is able to significantly modify the sympathetic- parasympathetic interaction to the heart, as defined by HR profile and HRV. Lack of HRV improvement four weeks after CRT identifies patients at higher risk for major cardiovascular events(1). Low -frequency component of RR variability power values predict an increased risk of malignant VT/VF; after 1 year of CRT most non- spectral and spectral data, including LF power, improved. Whether these improvements lead to better long-term survival in patients with CHF remains unclear(2). Biventricular pacing in heart failure improves autonomic function by increasing HR variability. This may have important prognostic implications(3). Improvement in ventricular performance from CRT shifts cardiac autonomic balance toward a more favorable profile that is less dependent on sympathetic activation(4). Median atrial-atrial intervals (SDAAM) continuously measured from an implanted CRT is lower in patients at high mortality and hospitalization risk. SDAAM declines as patient status decompensate. Continuous long-term SDAAM may be a useful tool in the clinical management of patients with CHF. SDAAM <50 ms when averaged over 4 weeks was associated with increased mortality risk and SDAAM were persistently lower over the entire follow-up period in patients who required hospitalization or died. SDAAM decreased a median of 16 days before hospitalization and returned to baseline after treatment. Automated detection of decreases in SDAAM was 70% sensitive in detecting cardiovascular hospitalization, with 2.4 false-positives per patient-year of follow-up(5). References 1) Fantoni C, Raffa S, Regoli F, Giraldi F, La Rovere MT, Prentice J,et al. Cardiac resynchronization therapy improves heart rate profile and heart rate variability of patients with moderate to severe heart failure. J Am Coll Cardiol. 2005; 46:1875-1882. 2)Piccirillo G, Magri D, di Carlo S, De Laurentis T, Torrini A, Matera S,et al. Influence of cardiac-resynchronization therapy on heart rate and blood pressure variability: 1-year follow-up. Eur J Heart Fail. 2006 Feb 28; [Epub ahead of print] 3) Livanis EG, Flevari P, Theodorakis GN, Kolokathis F, Leftheriotis D, Kremastinos DT. Effect of biventricular pacing on heart rate variability in patients with chronic heart failure. Eur J Heart Fail. 2003;5:175-178. 4) Adamson PB, Kleckner KJ, VanHout WL, Srinivasan S, Abraham WT.Cardiac resynchronization therapy improves heart rate variability in patients with symptomatic heart failure. Circulation. 2003;108:266-269. 5)Adamson PB, Smith AL, Abraham WT, Kleckner KJ, Stadler RW, Shih A, et al. Continuous autonomic assessment in patients with symptomatic heart failure: prognostic value of heart rate variability measured by an implanted cardiac resynchronization device. Circulation. 2004;110:2389-2394. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 27 07:28:10 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 27 Apr 2006 07:28:10 -0300 Subject: [HF-FORUM] 151E SAB and sudden death in sleep. Dr.Makarov Message-ID: <858F7F0F-68C0-443F-AFCB-CC04ACC1897F@hf-symposium.org> > Respectable Professors > Really glad to have chance to ask questions during HF-FORUM. Now > there is a female patient whose age is 59, and she is diagnosed as > SAB, ???degree, type 1. Her mother and elder brother died in sleeping > some years ago, not clearly of the disease history of them. And > recently she felt dizzy or suffocating sometimes. It's quite > difficult to persuade her to implant pacemaker. The question is: is > it ok of using drugs to cure her? what drugs have assured effect? is > there any heredity factors of this disease? > Thanks in advance for your replies. > > Dr. Xiuling Tan > China > Dear Dr. Xiuling Tan. It is very intresting patient in your letter. For my opinion only SA block during sleep without evidence connection beetwen arrhythmia and symptoms and long pauses is not direct indication to pacemaker. But sudden death of mother and brother need first of all in excluding of hereditary diseases with high risk of sudden death during sleep (syndrome Brugada, LongQT3, diseases Lev- Lenegra, and Sudden Unexplained death syndrome typical for South- Asian countries). I think usefull will be to make: 1) ECG study in family (very important to assess ECG of died relatives; 2) 72 hr Holter monitirng for assessement of the arrhythmias, connection between symptoms and arrhythmia, may be event-recorder; 3) giluritmal test for detection of Brugada pattern; 4) stress test and EPI study for detection of lifetthreathening VT; 5) tilt-test for induce and assess of the typical symptoms. It is possible more actually dicussion about indication for antiarrhythmic or ICD therapy in this case, especially if the patient will be having syncope. Concerning drug therapy of SA block, we sometime use in patient with noncritical bradyarrhythmias and autonomic complaines drugs with adrenomimetic or cholinilitic effects, especially if we nave combination with low level of the blood pressure, but firstly need to exclude diseases with risk of lifethreathening VT. Dr.Leonid Makarov -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 27 07:48:49 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 27 Apr 2006 07:48:49 -0300 Subject: [HF-FORUM] 152C Nonresponders prediction of CRT: what's the next step?. Dr. Yunlong Xia Message-ID: <891A0869-C6C1-4668-BC92-9720BBDC298E@hf-symposium.org> Nonresponders to CRT treatment is a major problem in device management of HF patients. In several lectures of this forum, the methods for prediction of nonresponders of CRT treatment have been recommended, such as noncontact mapping, MRI, echocardiography etc. In Dr Ali Oto's lecture, he listed Algorisms to predict responders to CRT by Tissue Synchronization Imaging (TSI), which are helpful even in HF patients with narrow QRS. Those with the most severe delay not at lateral ventricular wall are likely to be non-responders. Then several questions raised here: 1. When you find the patients are LIKELY to be nonresponders, will you go on CRT treatment under present situation? 2. Echocardiography can help us avoiding 'site of delay - site of pacing' mismatch, and optimizing the lead positioning. In some cases, however, the LV lead can hardly be located wherever you want with adequate sensing and capture threshold. Could you please give us some technique recommendations for lead positioning? 3. Could we try to use some other alternative pacing sites, such as RVOT pacing, when we find the possible nonresponders? Best regards Yunlong Xia Department of Cardiology The First Affiliated Hospital of Dalian Medical University ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 27 07:50:40 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 27 Apr 2006 07:50:40 -0300 Subject: [HF-FORUM] 153S RE: Digoxina and carvedilol. Dr. Melo Message-ID: <90302532-6589-409D-9C68-ABD6534B7BC1@hf-symposium.org> Please, tell me your guide for use of Carvedilol in Ischemic cardiomyopathy My regards, Dr. Melo -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 27 10:25:07 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 27 Apr 2006 10:25:07 -0300 Subject: [HF-FORUM] 154C Anterior myocardial infarction. Dr. Li Ying Message-ID: Here is a patient with extensive anterior wall myocardial infarction. She/He didin?t receive a thrombolysis therapy due to certain limitations. No money for PTCA. Since 3 months after the onset, there was pleura effusion on right side. It was no effect for repeated thoracentesis and anti-tuberculosis for 6 months. The anti-TB treatment had been stopped for 3 month, and pleura effusion was drawn, about 1000ml every month. Do you think this patient suffers from heart failure? Li Ying -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 27 14:57:38 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 27 Apr 2006 14:57:38 -0300 Subject: [HF-FORUM] EXPERTS ASK. What do you think about it? Message-ID: <6B805F8A-9256-402B-B805-028B13C76FFF@hf-symposium.org> Dr. Oswaldo Gutierrrez from Costa Rica asks - What is the current role of invasive hemodynamic monitoring with catheter in the pulmonary artery and the measurement of wedge pressure? What do you think about it? -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 27 16:05:26 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 27 Apr 2006 16:05:26 -0300 Subject: [HF-FORUM] 156E Ultrafiltration. Dr. Blicharz Message-ID: <38BD4968-4591-413C-A35A-2A2E7A828FB4@hf-symposium.org> Dear Colleagues, It is a pleasure to take part in such a great opinion exchange on treatment of HF patients. From my current practice: currently we have in our dept. 40yr old male patient with end stage DCM of primary origin. He have not responded to standart treatment with ACE-I, carvedilol (doses limited by low BP), methyldigoxin and combination of diuretics with diffrent sites of action. We do observe a fluid overload with high cntral venous pressure (28 mm H2O). After 3 weeks of pharmacological treatment we decided to use an ultrafiltration (normal renal function) as a way of preload lowering and we are able to observe constant improvement of patient status. What is our expert opinion on utility of this method of HF patient treatment? Jaroslaw Blicharz, MD St. Luke District Hospital, Tarnow, Poland -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Thu Apr 27 18:49:31 2006 From: info at hf-symposium.org (HF Symposium) Date: Thu, 27 Apr 2006 18:49:31 -0300 Subject: [HF-FORUM] Pediatric Electrophysiology Society. Synchronicity Symposium - Boston May 13, 2006 Message-ID: The Division of Electrophysiology at Children?s Hospital Boston cordially invites you to a pre-HRS symposium ?SYNCHRONICITY ? A multidisciplinary approach to cardiac resynchronization in congenital heart disease? The program will be held at Children?s Hospital Boston on May 16, 2006, preceding the HRS conference. Please see attached invitation and registration form for more information****. There is NO COST but please register in advance as seating is limited. REGISTRATION FORM and PROGRAM INFORMATION ATTACHED There will be a dinner to follow (sponsored by Guidant) at the Hampshire House (the real setting on which the TV series ?Cheers? was based). Please do NOT respond to this email, as it will go to everyone on the list server! SEE REGISTRATION FORM and PROGRAM INFORMATION http://www.hf-symposium.org/files/Synchronicity-Childrenssavethedate.pdf -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 28 13:31:37 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 28 Apr 2006 13:31:37 -0300 Subject: [HF-FORUM] 157E RE: Ultrafiltration. Dr. Perez Riera Message-ID: Dear Dr. Jaroslaw Blicharz from St. Luke District Hospital, Tarnow, Poland: The CHF (IV cl. NYHA) refractory to medical therapy can be treated with ultrafiltrative method such as: 1) Extracorporeal ultrafiltration; 2) Intermittent veno-venosus hemofiltration; 3) Intermittent peritoneal dialysis; 4) Sustained low-efficiency dialysis or; 5) Chronic ambulatory peritoneal dialysis. In patients with decompensate HF and diuretic resistance results in euvolemia and early discharge without hypotension or worsening renal function. In HF patients with volume overload and diuretic resistance, ultrafiltration before intravenous diuretics effectively and safely decreases length of stay and readmissions. Clinical benefits persist at three months (1). In patients with refractory CHF, the ability to provide continuous, daily, large volume removal not only improves volume status but also the clinical symptoms of the acute decompensate patient. A thorough literature review supports the premise that starting hemofiltration is an appropriate alternative for difficult and unstable cardiac patients. An optimal strategy utilizing continuous renal replacement therapy can dramatically improve the patient's clinical condition, mitigate the neurohumoral stimulation, increase urinary output and promote absorption of excessive extravascular fluid(2). Fluid overload may occur in patients with CHF. Under normal conditions, this is treated with inotropic support and diuretics. However, when diuretics fail, fluid removal becomes uncontrolled and other therapeutic options must be undertaken. Extracorporeal ultrafiltration is a possible solution to restore a status of fluid balance close to normal. Several new technologies have made ultrafiltration available today in all centers and easy to be instituted. Acute isolated schedules of ultrafiltration may, however, be too aggressive and result in severe hemodynamic instability. For this reason, continuous extracorporeal techniques have been applied in such patients and the therapy is generally carried out with success. Excellent hemodynamic stability, a good cardiovascular response and often diuresis restoration are the most common effects encountered using continuous forms of extracorporeal fluid removal. The potential for a home-based application of these techniques represents a further stimulating concept to be investigated (3). When Systolic refractory HF to conventional medical treatment is associated with chronic renal failure it is necessary to treat the body liquid composition alterations, and the alterations in the hemodynamic state without creating low flow conditions, trying to achieve an electrolytic and an acid-base balance to reduce the plasmatic volume and permit refilling between the interstitium and plasm. Sustained low-efficiency dialysis is a dialysis technique allowing the maintenance of hemodynamic stability through a reduced ultrafiltration rate, it allows an adequate clearance of small solutes, and with sustained treatment it maximizes the dialysis dose and determines a clinical improvement through the removal of the hydric overload. Sustained low-efficiency dialysis is a substitutive treatment for acute dialysis in patients with systolic HF refractory to conventional medical treatment (4). Ultrafiltration method together with pharmacological therapy allows a resetting of neuro-endocrine and electrolytic system in refractory CHF patients and a recovery of a pharmacological response. Without such a response a cardio-circulatory balance can be maintained through a chronic ambulatory peritoneal dialysis method (5). References 1) Costanzo MR, Saltzberg M, O'Sullivan J, Sobotka P. Early ultrafiltration in patients with decompensated heart failure and diuretic resistance. J Am Coll Cardiol. 2005; 46:2047-2051. 2) Sharma A, Hermann DD, Mehta RL.Clinical benefit and approach of ultrafiltration in acute heart failure. Cardiology. 2001; 96:144-154. 3) Ronco C, Ricci Z, Bellomo R, Bedogni F. Extracorporeal ultrafiltration for the treatment of overhydration and congestive heart failure. Cardiology. 2001; 96:155-168. 4) Iorio L, Violi F, Simonelli R, Nacca RG, Rossi G, Caliendo A, et al. Sustained low-efficiency dialysis (SLED) in patients with prevalent systolic heart failure G Ital Nefrol. 2006; 34:71-73. 5) Ragazzoni E, Sacco A, Cusinato S, Agliata S, Schweiger K, Cavagnino A, et al. Heart failure resistant to drug therapy. Nephrologic approach Minerva Urol Nefrol. 1998;50:133-138. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. ----- Edgardo Schapachnik Director General y Cient?fico Grupo AKROS edgardoschapachnik at mac.com -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 28 13:45:50 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 28 Apr 2006 13:45:50 -0300 Subject: [HF-FORUM] 160E RE: Nonresponders prediction of CRT: what's the next step?. Dr. Saksena Message-ID: This is an interesting discussion. This year we will be presenting data on the use of intracardiac echocardiography for patient selection and optimizing programming of CRT devices. This has reduced the number of non-responders very substantially. The pilot clinical data will be presented at a symposium at the upcoming Heart Rhythm Society meetings. Sanjeev Saksena Sanjeev Saksena MD FACC FESC FHRS FAHA Professor of Medicine, UMDNJ-Robert Wood Johnson Medical School Medical Director, Electrophysiology Research Foundation Editor in Chief, Journal of Interventional Cardiac Electrophysiology Past President, Heart Rhythm Society -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 28 15:14:50 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 28 Apr 2006 15:14:50 -0300 Subject: [HF-FORUM] 158E RE: Digoxina y carvedilol. Dr. de Souza Message-ID: <0F51008A-84BA-4C49-A07F-E57CEDED7771@hf-symposium.org> Dear coleagues, I appreciate the opportunity of changing experiences with so many experts. The european guidelines and the american guidelines for heart failure (ischemic or not) recomend a target dose of 50 mg of carvedilol. The american guidelines allows even a maximum dose of 100 mg/day (50 mg twice daily) in patients over 85 kg. Both the Capricorn study (in patients after AMI) and Copernicus (in patients with heart failure ischemic and non-ischemic) showed benefit using a target dose of 50 mg (25 mg of carvedilol twice daily). There is a very interesting discussion about this issue in: Gheorghiade and Goldstein. Beta-Blockers After MI. Circulation. 2002;106:394-398. Other references of importance are: 1- The CAPRICORN Investigators. Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial. Lancet. 2001;357:1385-1390. 2- COPERNICUS Study. Circulation. 2002;106:2194-2199. 3- European Society of Cardiology Guidelines 2005 www.escardio.org 4- Hunt et al. 2005 ACC/AHA Practice Guidelines www.acc.org or www.americanheart.org Thank you, Marcos R. de Sousa - Brazil ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 28 18:53:23 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 28 Apr 2006 18:53:23 -0300 Subject: [HF-FORUM] 155S RE: CHF in oncological patients. Dr. More Message-ID: <6AC86019-9CB9-4DEB-8F18-5BD1206FFE6A@hf-symposium.org> Dear Dr. Perez Riera, Thank you for your contribution. From the echocardiographic point of view, we still think that ejection fraction is still a delayed pattern to consider when we should stop administering cardiotoxic drugs. Everyday we see a request for ejection fraction or systolic shortening fraction to determine myocardial function, and we suffer deeply when we observe by tissue Doppler, the segmentary alterations observed much earlier than the ejection fraction being globally altered, i.e. we see S wave and E and A wave alterations, altered QS times before the ejection fraction is altered. Wouldn't it be timely for our colleagues, echocardiographists who hold significant positions, to warn about the possibility of detecting myocardial disease by drugs early and decide to conduct a new protocol to anticipate iatrogenics suffered by these poor patients? There are other echocardiographic indexes to be able to detect cardiotoxicity early: The Tei Index Identifies a Differential Effect on Left and Right Ventricular Function with Low-dose Anthracycline ChemotherapyMark Belham, MD, MRCP, MB, ChB?, Anton Kruger, MB (FRCP, FRCPath)?, Colin Pritchard, BA, BPhil, MA, MSc, PhD?. I just meant to make a small contribution about something we experience everyday. DR ALBERTO MORE RIO TERCERO CORDOBA ARGENTINA -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 28 20:45:05 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 28 Apr 2006 20:45:05 -0300 Subject: [HF-FORUM] 159S RE: Digitalis. Dr. Nunez Message-ID: <43F68A0D-8D5C-4C1B-9F8B-EBCB444D10EC@hf-symposium.org> Dear Dr. Perez Riera, As usual your expositions are very clear. I would like to know more or have access to material about the use of digoxin in septic shock. This is not a medication used regularly during sepsis, and I don't recall having seen it in the last guidelines of the Surviving Severe Sepsis Campaign: Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock R. Phillip Dellinger, MD; Jean M. Carlet, MD; Henry Masur, MD; Herwig Gerlach, MD, PhD; Thierry Calandra, MD; Jonathan Cohen, MD; Juan Gea- Banacloche, MD, PhD; Didier Keh, MD; John C. Marshall, MD; Margaret M. Parker, MD; Graham Ramsay, MD; Janice L. Zimmerman, MD; Jean-Louis Vincent, MD, PhD; Mitchell M. Levy, MD; for the Surviving Sepsis Campaign Management Guidelines Committee Thank you, Dr. Edgardo N??ez -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 28 22:08:28 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 28 Apr 2006 22:08:28 -0300 Subject: [HF-FORUM] 161S Anterior myocardial infarction. Dr. Gorini Message-ID: <7B83D1DF-CB2D-4A29-AC47-37C6BA34850B@hf-symposium.org> >> Here is a patient with extensive anterior wall myocardial infarction. >> > She/He didin?t receive a thrombolysis therapy due to certain > limitations. No > money for PTCA. Since 3 months after the onset, there was pleura > effusion on > right side. It was no effect for repeated thoracentesis and > anti-tuberculosis for 6 months. The anti-TB treatment had been > stopped for 3 > month, and pleura effusion was drawn, about 1000ml every month. > Do you > think this patient suffers from heart failure? > Li Ying Dear colleague, I think you should provide data about the features of the liquid obtained after pleural punctions (physical ?pH, color, etc-, chemical ? including LDH and ADA if possible-, bacteriological and cytological). These elements first, would allow us to establish whether it is exudate or transudate. In case of being exudate, a hemodynamic etiology for the pleural liquid would be ruled out (pure or exclusive, at least). Regards, N?stor Gorini -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 28 23:06:35 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 28 Apr 2006 23:06:35 -0300 Subject: [HF-FORUM] 163S RE: Chagasic cardiomyopathy. Dr. Schapachnik Message-ID: Dear friends, Almost finishing the Symposium, I finally have a few minutes with no messages to process in 5 languages, so I can submit a reflection that I think underlies the exchange of opinions between Dr. Pellizon and Dr. Dubner, concerning the results of the LABOR registry. Let's remember that in the message 94S by Dr. Pellizon, he pointed out that "according to the characteristics of these patients (Dubner) concludes that the results obtained in the ICD-Labor DO NOT support the automatic transference from indications used for ICD implantation in patients with ischemic heart disease, into those patients with Chagas disease," and he continued "According to his criteria, which patients today with chronic chagasic cardiomyopathy should have an ICD implanted?" In turn, Sergio in the message 122S said "The results of the ICD- Labor registry show that chagasic patients with an ICD implanted as secondary prevention, are different from patients with ischemic heart disease (greater incidence of women and less ejection fraction between the groups) and this cannot be extrapolated to which patients should receive an ICD." I think I interpret that chagasic patients, with identical severity regarding ventricular arrhythmias as ischemic patients -to the extent that all of them received an indication for ICD implantation- had less diffuse involvement than the latter, and therefore better EF. That is to say, I think that when indicating the implantation of the device, the treating cardiologists were sensible and took into account the severity of the arrhythmia (for instance, patients who recovered from a VF episode), not paying much attention to its underlying mechanism. This reminds me that chagasic cardiomyopathy is a "micronodular cardiomyopathy" as Mauricio Rosenbaum taught in his pioneer work of the Progress in 1964. Therefore, hypothetically the presence of a single inflammatory micronodule with lymphocytes, macrophages and eosinophils, release of cardioaggresive cytokines, etc., which do not alter the echocardiogram or generate EF fall, would be enough to generate mechanisms for reentries and triggering fatal arrhythmias. Instead, the anatomy of dilated cardiomyopathy (DCM) with ischemic origin, involves the heart in a more diffuse way. For this reason, the ischemic patients of the Labor registry had worse EF than chagasic ones. Their arrhythmias were due to diffuse involvement of the ventricular mass. Consequently, in this exchange of ideas, maybe the extrapolation of ICD implantation indications may INDEED be possible to patients whether chagasic or carriers of other etiologies, since the determining factor is the severity of the arrhythmia, potentially fatal. If this reasoning was true, we may think in an INFLAMMATORY origin of ventricular arrhythmias in chagasic patients, which may be treated with other specific pharmacological steps. What I think is that maybe, following Sergio's reflection, this could explain the differences found between the groups of patients in the LABOR registry; but such finding should not modify the indication for device implantation, at least until more consistent results are achieved. Warm regards for everyone and go on enjoying the last few days of the Symposium. Edgardo -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Fri Apr 28 23:19:15 2006 From: info at hf-symposium.org (HF Symposium) Date: Fri, 28 Apr 2006 23:19:15 -0300 Subject: [HF-FORUM] =?iso-8859-1?q?164E_RE=3A_CHF_in_oncological_patients?= =?iso-8859-1?q?=2E_Dr=2E_P=E9rez_Riera?= Message-ID: <8A1E247F-3246-4F62-B157-F15582847950@hf-symposium.org> Dear friend Dr. Alberto More from Rio Tercero C?rdoba Argentine: I agree absolutely with your cleavers commentaries. The Tei index is a new Doppler index, combining systolic and diastolic time intervals as an expression of global myocardial performance ("index of myocardial performance"). Tissue Doppler Tei index is pointed to be more effective in the evaluation of global cardiac function than systolic and diastolic measurements alone in various heart diseases. Natriuretic peptides and Tei index are useful indices for risk stratification in advanced LV dysfunction. TD myocardial performance index can rapidly quantify alterations in LV contractile state but is affected by acute alterations in preload and afterload(1). TDE-Tei index increased with worsening of LV diastolic function and can identify the pseudonormal/restrictive mitral inflow pattern. It also correlated with the echocardiographic parameters of LV systolic and diastolic function and filling pressure. It suggests that TDE-Tei index is a simple and feasible marker in assessing global LV function (2). Utility in congenital heart disease: The Tei index has utility also in congenital cardiopathy. In asymptomatic or minimally symptomatic patients with tetralogy of Fallot, biventricular dysfunction is detected by the Tei index(3). Utility in Hypertension: Tissue Doppler Tei index is gaining importance in evaluating LV function after drug intervention in hypertensive patients (4). Utility in coronary heart disease: Tei index, is an independent predictor for LV dysfunction in acute myocardial infarction. Patients with preinfarction angina had better preserved systolic LV function and Tei index values (5). An increased Tei index suggests the absence of adequate coronary reperfusion in patients with first anterior AMI without other lesion (6). References 1) Cannesson M, Jacques D, Pinsky MR, Gorcsan J 3rd. Effects of modulation of left ventricular contractile state and loading conditions on tissue Doppler myocardial performance index. Am J Physiol Heart Circ Physiol. 2006; 290:1952-1959. 2) Su HM, Lin TH, Voon WC, Lee KT, Chu CS, Lai WT, et al. Differentiation of left ventricular diastolic dysfunction, identification of pseudonormal/restrictive mitral inflow pattern and determination of left ventricular filling pressure by tei index obtained from tissue Doppler echocardiography. Echocardiography. 2006; 23: 287-294. 3) Norozi K, Buchhorn R, Bartmus D, Alpers V, Arnhold JO, Schoof S, et al. Elevated brain natriuretic Peptide and reduced exercise capacity in adult patients operated on for tetralogy of fallot is due to biventricular dysfunction as determined by the myocardial performance index. Am J Cardiol. 2006;97:1377-1382. 4) Tan HW, Li L, Zhang W, Ma ZY, Zhong XZ, Zhang Y.Effect of cilnidipine on left ventricular function in hypertensive patients as assessed by tissue Doppler Tei index. J Hum Hypertens. 2006 Apr 20; [Epub ahead of print]. 5) Orem C, Kucukosmanoglu M, Kaplan S, Kasap H, Durmus I, Eminagaoglu S, et al. Evaluation of left ventricular function using Tei index in patients with preinfarction angina. Anadolu Kardiyol Derg. 2006;6:3-8. 6) Kuwahara E, Otsuji Y, Takasaki K, Yuasa T, Kumanohoso T, Nakashima H,et.al. .Increased Tei index suggests absence of adequate coronary reperfusion in patients with first anteroseptal acute myocardial infarction. Circ J. 2006;70:248-253. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 29 08:44:08 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 29 Apr 2006 08:44:08 -0300 Subject: [HF-FORUM] 162S RE: Stem cells. Dr. Flores In-Reply-To: Message-ID: In Mexico there is a program for stem cells implantation that according to the author is promising, and it displays "favorable" results; I think that as in the world experience, we should wait until we get more results and reports with reproducible results to start truly thinking that this is a promising future. Dr. Ramon Flores -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 29 16:43:20 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 29 Apr 2006 16:43:20 -0300 Subject: [HF-FORUM] 165S RE: Digital and sepsis. Dr. Perez Riera Message-ID: Dear Dr. Edgardo N??ez: Thanks very much for your complimentary words. About 400,000 cases of sepsis, 200,000 cases of septic shock, and 100,000 deaths from both occur each year in the US (1). Sepsis is defined as the systemic response to infection. In the absence of infection, it is called systemic inflammatory response syndrome and is characterized by at least two of the following: 1) Temperature greater than 38?C or less than 36?C; 2) HR greater than 90 bpm; 3) Respiratory rate more than 20/minute or PaCO2 less than 32 mm Hg and 4) Alteration in white blood cell count (>12,000/mm3 or <4,000/ mm3). Septic shock is a subset of severe sepsis defined as sepsis-induced hypotension that persists despite fluid resuscitation and is associated with tissue hypoperfusion. Patients receiving vasoactive agents are also considered to have septic shock if they have tissue hypoperfusion despite correction of the hypotension (2). Digoxin should be considered in all patients with systolic HF where, in addition to angiotensin conversion enzyme inhibitors and diuretics, it reduces the incidence of pulmonary edema, and in the management of patients with supraventricular tachycardia, where it reduces the ventricular rate, in association with other treatment, as a single dose of 750 -1000 mug/ 70 kg in patients not treated previously with digoxin who have septic shock. It should be avoided in patients with critical coronary artery disease and ischaemic or hypertrophic diastolic failure (3). Experimental studies have documented that myocardial dysfunction is precipitated between 3 and 6 hr after beginning of sepsis shock. A "Hinshaw-modified" isolated working LV preparation has been used to document and assess the degree of HF. It was found that the HF is often severe and reversible only temporarily by adrenergic agents but reversible by digoxin or insulin. Dopamine administration may be associated with increased mortality rates in shock (4). Dopamine sensitivity septic shock patients is associated with decreased mortality rate. Early recognition of dopamine resistant septic shock (mean arterial pressure <70 mm Hg despite the use of 20 mug/kg/min dopamine.) could allow for better screening of patients with an ominous prognosis(5). Levosimendan improves systemic hemodynamics and regional perfusion in patients with septic cardiac dysfunction under conditions where administration of 5 microg/kg dobutamine per minute is no longer efficacious. Levosimendan can be an alternative to the strategy of increasing the dose of dobutamine under such conditions. The cause of the HF has not been identified, but evidence is presented against a myocardial depressant factor being the causative factor. Hearts subjected to a 2-4 hr period of hypotension on the threshold of HF show no signs of failure when subjected to blood circulating from an animal in splanchnic arterial occlusion shock. Hearts from pancreatectomized animals subjected to endotoxin shock with their source of myocardial depressant factor removed demonstrate the typical failure in 4-6 hr. Other factors are suggested that contribute to myocardial dysfunction are: 1) Hypotension; 2) Nonuniform perfusion of subendocardial regions of the heart; 3) Depressed responsiveness to inotropic and chronotropic stimuli; 4) Intracardiac ionic and fluid disturbances, and; 5) Cardiomegalia and muscle stiffness. Since steroid/antibiotic therapy increases the probability that an animal will survive lethal sepsis, investigating the effect of this therapy on myocardial function may aid in determining whether or not this degree of HF contributes in the animal to irreversible shock and death. In patients treated with cardiac glycosides nonocclusive mesenteric ischemia a rare but serious disorder with a high mortality rate could be causal factor include in addition to severe hypotension, decompensate HF, and septic shock(6). Septic shock is a common problem in hospitalized patients. Optimal management depends on rapid recognition, aggressive restoration of circulating volume with fluid boluses, initiation of appropriate antibiotic therapy, implementation of adequate monitoring, and meticulous attention to the details of care. Mean arterial pressure should be increased to between 65 and 75 mm Hg as soon as possible to reduce the likelihood of multiorgan dysfunction. Despite these therapeutic maneuvers, however, mortality rates are likely to remain high until the development of therapies that better target the underlying mechanisms of sepsis. References 1) Parrillo JE, Parker MM, Natanson C, et al. Septic shock in humans: advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. Ann Intern Med 1990; 113:227-242. 2) Fitch SJ, GossageJR Optimal management of septic shockRapid recognition and institution of therapy are crucial Postgrad Med. 2002;111:53-6, 59-60, 63-64. 3) Worthley LI, Holt AW. Digoxin in the critically ill patient. Crit Care Resusc. 1999;1:252-264. 4) Sakr Y, Reinhart K, Vincent JL, Sprung CL, Moreno R, Ranieri VM, et al. Does dopamine administration in shock influence outcome? Results of the Sepsis Occurrence in Acutely Ill Patients (SOAP) Study. Crit Care Med. 2006;34:589-597. 5) Cardiovascular response to dopamine and early prediction of outcome in septic shock: a prospective multiple-center study. Crit Care Med. 2005;33:2172-2177. 6) Weil J, Sen Gupta R, Herfarth H. Nonocclusive mesenteric ischemia induced by digitalis. Int J Colorectal Dis. 2004; 19:277-280. All the best Andr?s Ricardo P?rez Riera, MD Chief of the Sector of Electro-Vectocardiography of the Discipline of Cardiology, School of Medicine, ABC Foundation Santo Andr? - S?o Paulo - Brazil. ---- Dr. Edgardo Schapachnik edgardoschapachnik at grupoakros.com.ar Director General y Cient?fico Grupo AKROS -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sat Apr 29 16:51:47 2006 From: info at hf-symposium.org (HF Symposium) Date: Sat, 29 Apr 2006 16:51:47 -0300 Subject: [HF-FORUM] 166E RE: Chagasic cardiomyopathy. Dr Furlani Message-ID: <7FF49969-0EDB-4948-85F6-0DC28015316A@hf-symposium.org> Dear colleagues: First of all, I would like to thank Drs Pellizon, Dubner and Schapachnik for their clever comments about the ICD LABOR registry and the difference between chagasic and coronary artery disease (CAD) patients receiving and ICD for secondary prevention of sudden cardiac death (SCD). I have enjoyed this discussion as well as other points of view about distinct topics posted in this wonderful symposium. Congratulations to the organizers! Many large, randomized trials have studied the value of ICDs in secondary prevention of SCD in both CAD and idiopathic dilated cardiomyopathy (IDC) patients, such as: AVID, CIDS and CASH. Regarding to primary prevention of SCD, results from MADIT and MADIT II in patients with CAD and DEFINITE in those with IDC are available. Likewise, SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial) included both CAD and IDC patients with severe LV dysfunction and no history of sustained ventricular arrhythmias nor SCD. All these studies and some metanalysis including them have helped members of the ACC/AHA/HRS and European Society of Cardiology to develop guidelines with indications for ICD implantation in different population of patients at risk for SCD. Unfortunately, none of these studies included patients with chagas disease. Few studies have been conducted in patients with Chronic Chagasic Cardiomyopathy (CCC) and hard data about this subject are lacking. We know that a history of sustained ventricular arrhythmias or SCD, frequent and complex ventricular arrhythmias (mainly NSVT), history of syncope, an abnormal ECG and inducible sustained VT during programmed ventricular stimulation and even a history of congestive heart disease are predictors of higher mortality and SCD in Chagasic patients (1-3) but, so far, prospective, adequately-powered and randomized studies have not been conducted in this population to determine the value and the impact of ICD therapy on mortality and SCD. Chagas disease is seen in developing countries and this illness grows with poverty in regions economically unprotected. This population is not ?attractive? for pacemaker/ICD companies and this fact may explaine at least in part the lack of appropriate trials. On the other hand, we would need about 1000 patients to demonstrate a statistically significant decrease in total mortality with ICD versus Amiodarone in patients with chagasic cardiomyopathy and severe LV dysfunction (below 35%) without a history of sustained ventricular arrhythmias or SCD, what means that this ?MADIT II like trial in chagasic patients? would have to be a multicenter, international trial. Maybe the time has come for the Latin-American Cardiac Societies to get together and design and conduct this ?MADIT II like trial in chagasic patients? and other studies to determined new risk factors of SCD in this population (for instance, the value of microvolt T wave alternans or heart rate turbulence in predicting SCD in chagasic patients). In the meantime, sometimes we will have to extrapolate results from trials including ?idiopathic dilated cardiomyopathy patients? to manage chagasic patients although extrapolating is not ?evidence based medicine?. My best regards, Aldo Alberto Furlani MD, Buenos Aires, Argentina. Sosa E, et al: Risk stratification to sustained ventricular tachycardia in chagasic heart disease. Circulation 1994; 90:I-179. Carrasco HA, et al: Ventricular arrhythmias and left ventricular myocardial function in chronic chagasic patients. Int J Cardiol 1990;28:35-41. Predictive Value of Clinical and Electrophysiological Variables in Patients with Chronic Chagasic Cardiomyopathy and Nonsustained Ventricular Tachycardia. Arq Bras Cardiol 2000; 75:41-47. -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 30 08:24:21 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 30 Apr 2006 08:24:21 -0300 Subject: [HF-FORUM] 167S About Dr. Sarmiento's question. Dr. Pereira In-Reply-To: <17821B62-E5EC-4894-9C2B-ED6BD8B711A5@grupoakros.com.ar> Message-ID: Dr. Ricardo Sarmiento, About enalapril and renal performance, it is good to remember that it is contraindicated with creatinine clearance below 30 ml/min. I suggest determining this, besides electrolytes (serum potassium may increase with the association of enalapril and spironolactone, even more if the patient has renal failure). Current guidelines do not mention digoxin in patients with heart failure and sinus rhythm. On the other hand, amiodarone interacts with digoxin increasing the plasma levels of the latter, which may lead to digitalis intoxication. Kind regards, Dr. LUCIANO PEREIRA Paraguay -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 30 17:07:26 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 30 Apr 2006 17:07:26 -0300 Subject: [HF-FORUM] 168P NS-VT and S-VT. Dr Almeida Message-ID: <6F89A164-4616-4157-9A0E-8A4B52FA2050@hf-symposium.org> Dear colleagues, I thank you for the chance to participate of the Virtual Conference by ISHNE, with an excellent and high scientific content. I seize this opportunity to send to the Forum this case, which I submit in the attached file. Dr. Adail Paix?o Almeida - Brasil Dear colleagues, Although I did not participate with opinions but very rarely, I have been reading with interest and evidently, I learn a lot with this forum. I took the liberty to present this case to ask opinions about if I should follow the suggestion by the arrhythmologist: antiarrhythmic therapeutics with amiodarone 400 mg/day and other classical drugs for CHF (furosemide, spironolactone and captopril), or if I should indicate implantable cardiodefibrillator in this patient. Clinical history: Male, 50-year-old patient, with good clinical aspect. Eight months ago he was referred by a clinician for a consultation about chronic dilated cardiomyopathy of which he is carrier (ECHO = mild left ventricular (LV) dilatation, mild hypertrophy, moderate global LV dysfunction, discrete aortic failure. Ejection fraction = 42%) and mild hypertension. No smoking or alcoholism. Diagnosis = CHF II/III NYHA. Normolipemic. History of hypertension and coronary artery disease in the family. Prescription = furosemide, captopril and carvedilol adjusted up to 12.5/2 per day. He was evolving well until 33 days ago, when he presented non-sustained ventricular tachycardia (NS-VT) (Figure 1). 48 hours later, sustained ventricular tachycardia (S-VT) (Figure 2). Hemodynamically stable and hospitalized in Intensive Care Unit with amiodarone being administered, infusion pump 900 mg/EV/24 hours with a successful reversion (Figure 3). The electrophysiological study (EPS) (Figures 4,5,6,7) did not detect focus or induce NS-VT or S-VT. Amiodarone has been maintained in 400 mg. Current ECG with no arrhythmia, CHF II/III. Carvedilol has been suspended. My question is: 1. Should ICD be implanted? 2. Should carvedilol be started again? Figures 1 ? 2 ? 3 http://www.hf-symposium.org/files/Almeida.pdf Figures 4 ? 5 ? 6 ? 7 They were not sent by the author -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 30 17:10:26 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 30 Apr 2006 17:10:26 -0300 Subject: [HF-FORUM] 169S Amiodarone in ventricular arrhythmias of chagasic cardiomyopathy In-Reply-To: Message-ID: <04682E89-CE49-4656-B8B1-56B02D33EB2A@hf-symposium.org> I would like to ask the specialists in treating ventricular arrhythmias in chronic chagasic cardiomyopathy, if amiodarone is still the drug of choice and if there are papers associated to aspirin, and the doses of both drugs. Thank you, Dr. Rosendo Rivero Melgar Santa Cruz-Bolivia -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 30 17:14:24 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 30 Apr 2006 17:14:24 -0300 Subject: [HF-FORUM] 170S Heart failure + renal failure. Dr. Bartolomeo In-Reply-To: Message-ID: My question is the following: in patients with HF who also present renal failure, what drug therapy do you use and about ACEI, don't you use them or do you prefer some in particular? Dr. Mario Bartolomeo -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 30 17:49:42 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 30 Apr 2006 17:49:42 -0300 Subject: [HF-FORUM] Translators In-Reply-To: <3AA74B40-CEFE-47ED-9B22-4B0B362B6371@grupoakros.com.ar> Message-ID: The ISHNE Worldwide Symposium on Heart Failure through the Internet is coming to an end, and we couldn't let it finish without expressing the fact that if we could indeed call this event WORLDWIDE, it is because of the titanic work by the international team of translators that made it possible for the opinions of the colleagues from different areas of the world, to be known by their peers. Thus we would like to express with these words, our most sincere gratefulness and congratulations to: Maria Isabel Ayala (Argentina) Georgina Warlet (Argentina) Federico Epstein (Argentina) Andrly Voroniak (Argentina) F?tima Dumas Cintra (Brazil) Tha?s Nascimento.(Brazil) Cuilan Li (China) Danshi Li (China) Donghui Yang (China) Huabin Sun (China) Jingmin Zhou (China) Jinqiu Liu (China) Lingjie Wang (China) Xingpeng Liu (China) Xuesi Wu (China) Yiqiong Xu (China) Yongxing Lu (China) Yunlong Xia (China) Zhihong Han (China) Miaomiao (China) Pei Pei (China) Once again, THANK YOU! Sergio and Edgardo -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee From info at hf-symposium.org Sun Apr 30 18:01:12 2006 From: info at hf-symposium.org (HF Symposium) Date: Sun, 30 Apr 2006 18:01:12 -0300 Subject: [HF-FORUM] Symposium's Closing words Message-ID: <460D5DC0-0B34-404C-8FA4-E28F9E402696@hf-symposium.org> Dear Colleagues: The April 2006 Symposium on Heart Failure is coming to an end. After 30 intense days with a lot of questions and replies still to be answered, we plan to end this scientific event according to our original schedule. We are proud of what we have achieved, for we all have obtained better insight into this prevalent and complex disease that is associated with high morbidity and mortality. We had 11,893 registrants from 107 different countries, and this response far exceeded our expectations. The Symposium has been translated into 4 simultaneous languages, we have added Chinese and Russian to our usual Spanish and Portuguese translations, we have obtained CME credits provided by ACCME from USA, and we have added numerous registrants from "non-traditional" countries in our Symposium. Approximately 10 daily questions were added to the 4 discussion forums in their respective languages. In addition, 35 lectures (with 116 translations in HTML and 232 in PDF formats), 3 clinical cases, 2 webcasts, 1 multimedia presentation, and 6 international interviews (Argentina, USA, Russia, India, China and Brazil) were provided. Access was made available to 134 heart failure trials, and international diagnostic and therapeutic guidelines were highlighted. The International Society of Holter and Noninvasive Electrocardiography (ISHNE) is proud of having presented this event that is now part of the series started with the First Virtual Symposium on the Brugada Syndrome held in 2001. Since then, we have held the Long QT Syndrome (LQTS), the Arrhythmogenic Right Ventricular Dysplasia (ARVD), and the Atrial Fibrillation (AF) Symposia, and we will continue with one on Sudden Cardiac Death next October. Renowned colleagues from different countries have presented very topical lectures, either written, through PowerPoint presentations, or through radio interviews. The forum involved ongoing questions and replies. This approach made this symposium an international event, and we feel very satisfied for having been its organizers. We thank our faculty who with their lectures provided a high level of academic excellence to the symposium, our cardiology experts for their presentations, all the physicians who interactively participated in this Symposium, the authorities of ISHNE for their ongoing support for this innovative approach to Continuing Medical Education, and St. Jude Medical with its generous support of this program. We would like to especially mention and thank Dr. Li Zhang who coordinated all the activity of the Symposium in China and the corresponding translation, Dr. Leonid Makarov who enabled us to transmit and discuss this knowledge in Russian, Dr. Wojciech Zareba for his coordination of the CME credits, and Dr.Ricardo Perez Riera for his unwavering collaboration. We also thank Bruce Meredith and his SJM team for the suggestions and help provided. Finally, we want to thank all our team of professional translators and interpreters, computer technicians, specialists in networks, graphic designers, sound technicians, radio presenters, and secretaries who anonymously provided behind the scenes support that enabled our symposium to operate efficiently and effectively. As you may imagine, the size of this list is such that it would be impossible to include them by name in this letter, but each one of them is listed in our minds and hearts because they have been the real makers of this Symposium. Thank you very much for all you involvement. We invite you to join us in October for our next educational program on Sudden Cardiac Death. Arthur, Sergio, and Edgardo Arthur J. Moss, MD (Rochester, NY, USA) Sergio Dubner, MD (Buenos Aires, Argentina) Edgardo S. Schapachnik, MD (Buenos Aires, Argentina) -- Dr. Sergio Dubner President of Scientific Committee Dr. Edgardo Schapachnik President of Steering Committee