From info at myocardial.ischemia-symposium.org Thu Jan 10 22:40:48 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 10 Jan 2008 23:40:48 -0200 Subject: [ISCHEMIA-FORUM] Dr. Bayes de Luna and Dr. Dubner's letter Message-ID: <4786C920.3030204@myocardial.ischemia-symposium.org> Dear colleagues, It is a great pleasure and pride to announce that next January 15th the ISHNE-ISCP Internet Symposium on "Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia" will begin. This is the first time that our two societies conduct a joint scientific activity through the Internet, joining our efforts to approach this topic of great cardiological topicality. The Symposium will be similar to all the ones performed previously by ISHNE, with text presentations, webcasts, or videos, most of which will be translated into the five official languages; this depending on the date in which they were received by the scientific committee. There will be a double access to the lectures, which can be found in the "virtual halls" or by topic according to the contents (Acute, Chronic, and Prevention). A library with automatic updating will also be available, enabling access to all published guidelines, and also ongoing studies published by Medline. On the same day, the Discussion Forum will be enabled and will remain open for all the questions, opinions, doubts, consultations on specific clinical cases related to our topic, and so on, where the guest lecturers will answer when required. We would like to express our deep gratefulness to the Directors of the Symposium, Drs. P. Stone, R. Verrier, A. Bayes de Luna, and JC Kaski, due to the high scientific quality of the program and the presentations of guest colleagues, to all the lecturers for their efforts, the scientific/technical team responsible of the design and management of the site, to the translators, and your presence that accompany us permanently, and without which all efforts would be useless. We would also like to express our special thanks to all the companies that made this event possible. We are certain that all of us will enjoy a symposium with a high scientific level, and we will be waiting for you on January 15th. Best regards, Dr. Antoni Bayes de Luna Dr. Sergio Dubner President of ISCP President of ISHNE -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 10 22:40:48 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 10 Jan 2008 23:40:48 -0200 Subject: [ISCHEMIA-FORUM] Dr. Bayes de Luna and Dr. Dubner's letter Message-ID: <4786C920.3030204@myocardial.ischemia-symposium.org> Dear colleagues, It is a great pleasure and pride to announce that next January 15th the ISHNE-ISCP Internet Symposium on "Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia" will begin. This is the first time that our two societies conduct a joint scientific activity through the Internet, joining our efforts to approach this topic of great cardiological topicality. The Symposium will be similar to all the ones performed previously by ISHNE, with text presentations, webcasts, or videos, most of which will be translated into the five official languages; this depending on the date in which they were received by the scientific committee. There will be a double access to the lectures, which can be found in the "virtual halls" or by topic according to the contents (Acute, Chronic, and Prevention). A library with automatic updating will also be available, enabling access to all published guidelines, and also ongoing studies published by Medline. On the same day, the Discussion Forum will be enabled and will remain open for all the questions, opinions, doubts, consultations on specific clinical cases related to our topic, and so on, where the guest lecturers will answer when required. We would like to express our deep gratefulness to the Directors of the Symposium, Drs. P. Stone, R. Verrier, A. Bayes de Luna, and JC Kaski, due to the high scientific quality of the program and the presentations of guest colleagues, to all the lecturers for their efforts, the scientific/technical team responsible of the design and management of the site, to the translators, and your presence that accompany us permanently, and without which all efforts would be useless. We would also like to express our special thanks to all the companies that made this event possible. We are certain that all of us will enjoy a symposium with a high scientific level, and we will be waiting for you on January 15th. Best regards, Dr. Antoni Bayes de Luna Dr. Sergio Dubner President of ISCP President of ISHNE -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 14 23:02:02 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 15 Jan 2008 00:02:02 -0200 Subject: [ISCHEMIA-FORUM] BEGINNING OF ACTIVITIES Message-ID: <478C141A.9080004@myocardial.ischemia-symposium.org> Dear colleagues, As of today and up to the end of the Symposium, the Lecture Hall will be enabled. There you may obtain access the full Scientific Program, made up by texts, presentations, webcasts, and videos grouped according to the thematic index proposed by the Program. http://www.myocardial.ischemia-symposium.org/lectures.php Likewise, all the scientific material has been grouped into three great chapters that include the corresponding trends of ischemic heart disease: Acute Coronary Disease, http://www.myocardial.ischemia-symposium.org/lectures_acute.php Chronic Coronary Disease http://www.myocardial.ischemia-symposium.org/lectures_chronic.php and Prevention http://www.myocardial.ischemia-symposium.org/lectures_prevention.php We hope you will enjoy it. Likewise, the Discussion Forum will be enabled in 5 languages. You may send your questions, doubts, opinions, and so on, by sending messages to this e-mail address: mi-forum at myocardial.ischemia-symposium.org Kind regards Sergio and Edgardo -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 14 23:01:40 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 15 Jan 2008 00:01:40 -0200 Subject: [ISCHEMIA-FORUM] Opening speech Message-ID: <478C1404.1070606@myocardial.ischemia-symposium.org> http://www.myocardial.ischemia-symposium.org/opening-speech.php -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 14 23:02:45 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 15 Jan 2008 00:02:45 -0200 Subject: [ISCHEMIA-FORUM] Passwords Message-ID: <478C1445.60402@myocardial.ischemia-symposium.org> Dear Colleagues: If you don't remember your personal passwords, you can use the following ones: USER ID: qrst PASSWORD: QRST Best regards Edgardo and Sergio -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 15 12:08:52 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 15 Jan 2008 13:08:52 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASKS, EXPERTS ANSWER Message-ID: <478CCC84.2060306@myocardial.ischemia-symposium.org> Dr. Ricardo Pizarro from Panama asks - Dear Dr. Perez Riera, About your lecture on Identification of ACS in patients carriers of CLBBB, I would like to consult with you about the following case: Female patient, 67 years old, diabetic, with symptoms that made us suspect of ACS, and with background of syncope or pre-syncope, mild to moderate sweating, regular general aspect, good conscience state, anxious. Since six hours ago, she denies chest pain, and in onset ECG she shows CLBBB, the existence of which was previously ignored, and "unspecific ST/T segment disorders", capillary glycemia 150 mg/%. She doesn't show prior history of similar symptoms. Since the ECG and the clinical history are not reliable to establish an accurate diagnosis: a) Would it be advisable to wait for the result of cardiac enzymes (CPK/CPKMB, Troponin T or I or other accepted ones) to make a "decision" to apply thrombolysis to such patient?; b) Or considering an invasive treatment such as PCI would be less risky and/or more appropriate in this case?; c) If cardiac enzymes are not conclusive or borderline, should we consider tomographic coronary angiography (if she has no chronic renal failure), which increasingly seems to be used more in ER scenarios, according to current medical literature? Since this patient is diabetic, I would also like to know the opinion of Dr. Tziakas about whether this condition should turn management more aggressive. What is the management to follow then? What is the opinion of other Faculties and Participants? Thank you very much for your consideration to answer. Dr. Ricardo Pizarro Panama ------------------------------------- Dr. Andres Perez Riera from Brazil answers - Dear Dr. Pizarro, I understand this woman is elderly (>65 years old), diabetic, supposedly with suggestive or doubtful pain accompanied by pre-syncope or syncope and concomitant sweating, and over the last 6 hs she is painless and the admittance ECG shows CLBBB without prior tracing and this dromotropic disorder was previously ignored. The most important symptom, typical of AMI, is pain or intense retrosternal (behind the sternum) discomfort, which often is described as pressure, oppression, weight, or burning feeling, that could irradiate into the neck, jaw, upper limbs and back. These symptoms are frequently accompanied by the so-called "concomitant" symptoms: nausea, vomits, sweating, paleness, and feeling of imminent death. The duration is characteristically >20 minutes. Pain with typical characteristics, but with a duration <20 minutes suggests angina where there is no cardiac muscle death. Elderly diabetics of the female gender (your case) have a greater chance of presenting atypical pain or discomfort, i.e. with characteristics and intensity different from the classical ones. The association of CLBBB completely overshadows the symptoms. In such cases, it is possible to be before an AMI without pain, atypical or silent, and in the great majority of cases, the patient is just as this lady, anxious and with discomfort due to the hypersympathotonia. If necrotic involvement at random exceeds an involvement of > 40% of LV mass, it may evolve into HF, acute pulmonary edema and shock. In spite of the WHO stating that for the diagnosis of AMI the presence of clinical, electrocardiographic, and biochemical criteria should be present, the management in this case in particular, if you have such resource available, is immediate hemodynamic study to clarify the real situation. The earlier, the greater the chance of recovery is. The test is essential when blood flow is attempted to be restored into the infarction area, whether by angioplasty or by revascularization surgery. It should not be performed only when the risk is greater than the possible benefit, and this doesn't seem to be the case. Each minute that goes by without therapeutic management, the rate of failure increases and a life-saving chance is missed. Since the end of the 60's, it is known that most deaths occur during the first hours of the disease manifesting, being 40% to 65% in the first hour from the onset of symptoms and approximately 80% over the first 24 hours. Thus, most deaths by AMI occur outside the hospital, often without medical care, and sometimes even from the family. The most frequent modality of cardiorespiratory arrest during the first hours of AMI is ventricular fibrillation, which can only be reversed by electric defibrillation; if performed in the first minute after the collapse, electric defibrillation reverses more than 90% of cases. They are related to delay in searching for help, ignoring the pain of AMI, advanced age, low socio-economic level, female gender, and self-medicating. The reduction of pre-admission delay not only decreases the number of cases of pre-admission sudden cardiac death, but also in-hospital mortality. The time elapsed between the onset of pain and coronary, chemical or mechanical rechanneling, is the essential factor to obtain benefits from the treatment, both immediate and in the long run, regarding mortality and morbidity, in patients treated in up to 12 hours since the onset of pain. I hope I have clarified your doubt. Andr?s Ricardo P?rez Riera. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 15 12:19:29 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 15 Jan 2008 13:19:29 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASKS, EXPERTS ANSWER (Dr. Tziakas answers) Message-ID: <478CCF01.9060200@myocardial.ischemia-symposium.org> Dr. Ricardo Pizarro from Panama asks - Dear Dr. Tziakas, Since this patient is diabetic, I would also like to know the opinion of Dr. Tziakas about whether this condition should turn management more aggressive. What is the management to follow then? What is the opinion of other Faculties and Participants? Thank you very much for your consideration to answer. Dr. Ricardo Pizarro Panama ------------------------------------- Dr. Dimitrios Tziakas from Greece answers - I would like to thank Dr Pizzaro for his query regarding the aforementioned diabetic female patient. In my opinion, the aforentioned case is an atypical presentation of a possible ACS in a diabetic plus a complete LBBB background. I think that a more thorough analysis of her past medical background (presence of hypertension, family CAD history, dyslipidemia, current smoking status, presence of valvular disease) as well as the history of present complaint (swaeting, nausea) would be of help. Furthermore, findings from her clinical examination (cardiac ausciltation - murmurs / pulmonary ausciltation - lung rales) as well as a chest x-ray (cardiothoracic ratio, findings of pulmonary congestion) would also be of value in order to diagnose or reject the presence of an ACS or other cardiac condition (i.e congestive heart failure, aortic stenosis, ruptured aortic aneurysm). As a general concept, diabetic patients should receive a maximized medical treatment and also if the diagnosis of an ACS is certain could benefit more from an invasive managment. As far as thrombolysis is concerned, since we our not certain of the ACS diagnosis in the absence of a positive cardiac necrosis marker (i.e early marker: myoglobulin in the 1st hour) I would not recommend thrombolysis. If a positive marker for myocardial necrosis is positive (like Troponin which becomes positive in the first 6 hours since the acute event)then a balanced decision should be made regarding the benefits and the adverse effects of a relatively late lysis treatment in a background of an atypical presentation. In this setting, if symptoms persist I would recommend a diagnostic coronary catheterization following a possible revascularization procedure. If such an approach is not feasible, I would recommend maximazation of medical treatment with anti-platelets, statin, beta-blocker (query of bifascicular or trifascicular block on the ECG in view of her past medical history of syncope), angiotensin-receptor blocker, and intense glucemic control. Dr Dimitrios Tziakas, MD,PhD,FESC,FAHA Asst Professor in Cardiology Democritus University of Thrace Alexandroupolis, Greece -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 15 19:30:30 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 15 Jan 2008 20:30:30 -0200 Subject: [ISCHEMIA-FORUM] 2S Dr. Pizarro's clinical case. Dr. Valdes Message-ID: <478D3406.2010409@myocardial.ischemia-symposium.org> Dear Dr. Pizarro, The clinical case you present is particularly significant, because it is difficult to differentiate from the classical one in triad, characteristic of AMI. It is important to remember these points: 1) diabetic patient; 2) age; 3) female; 4) neurovegetative symptoms; 5) CLBBB. The patient should be admitted into an intermediary (if there was no clinical involvement)/intensive care unit. ECG follow up: if ischemic, there may be changes with the management (ASA, nitroglycerin) that could help to get closer to the goal, measurement of CK MB/Tr T, and if positive, I would act according to the resources available in the place; if I was in a high-complexity center I would choose (undoubtedly) primary angioplasty because; a) the type of injury (complicated calcified plaques) that these patients usually present; b) this is a patient in high risk; c) in expert hands, the results are better than pharmacological treatment. Sincerely, Dr Valdes - Formosa -Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 15 19:57:55 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 15 Jan 2008 20:57:55 -0200 Subject: [ISCHEMIA-FORUM] 3E Cardiac X Syndrome. Dr. Cremer Message-ID: <478D3A73.9010203@myocardial.ischemia-symposium.org> First of all, thank you very much for this nice opportunity for improving our knwoledge based on the net. Second, a question to G. Lanza, respect to treatment of patients with cardiac syndrome X: Which is your opinion about antiplatelet therapy in this clinical scenario and if necessary, which should be our first option? Thank you very much in advance, David Cr?mer, MD. Clinical Cardiologist. Palma de Mallorca, Spain. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 16 06:46:55 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 16 Jan 2008 07:46:55 -0200 Subject: [ISCHEMIA-FORUM] 4E LBBB. Dr. Ortiz Message-ID: <478DD28F.3090409@myocardial.ischemia-symposium.org> Dear Doctors, In left bundle branch block (LBBB) with antero-septal infarction, is it possible to see r wave appear in V1 and V2? Dr. Justiniano Ortiz Paraguay -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 16 07:53:10 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 16 Jan 2008 08:53:10 -0200 Subject: [ISCHEMIA-FORUM] 1R Message of acknowledgement by Dr.Yabluchanski Message-ID: <478DE216.6030605@myocardial.ischemia-symposium.org> Dear Organizers of the Symposium, Thank you very much for your scientific and educational work. This time we will be able to enjoy a great event devoted to ischemia and myocardial infarction. I was eagerly waiting for this Symposium. Sincerely, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 16 12:57:47 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 16 Jan 2008 13:57:47 -0200 Subject: [ISCHEMIA-FORUM] 5S RE: Dr. Pizarro's clinical case. Dr. Bonzon Message-ID: <478E297B.9040501@myocardial.ischemia-symposium.org> Dear colleagues, Ricardo, Andres, and Dimitrios, What added value for decision making in this case, do you consider a simple transthoracic echocardiogram (made with a simple portable device) may contribute, conducted in the Emergency Room, or immediately after entering this patient into the Intensive Coronary Care Unit? Cordially, Dr. Gustavo R. Bonz?n Resistencia, Chaco, Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 16 18:37:37 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 16 Jan 2008 19:37:37 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASKS, EXPERTS ANSWER Message-ID: <478E7921.9070101@myocardial.ischemia-symposium.org> Dr. Andriy Vorotniak from Russia and Argentina asks - For Drs. Atar, Shaul/Birnbaum, Yochai, When a young man (35-45 years old) presents in the Department of Emergencies with precordial pain and signs of "early repolarization" in his ECG, a lot of uncertainty and concern arises. We know that a significant percentage of patients with ACS do not meet the classical morphological criteria for ST segment elevation. Is there a standard protocol to assess the patients with signs of "early repolarization" (for instance, tachycardizing maneuvers, hyperventilation, etc.)? ------------------------------------- Dr. Yochai Birnbaum and Dr. Shaul Atar from USA answers - It is a great question. However, there is no answer. The ACC/AHA guidelines simply ignore this problem. It is the combination of the clinical impression with the ECG. Even experienced cardiologists make a lot of mistakes in interpreting these ECGs. We need to do more research and develop criteria and protocols as you had suggested. Thank you Yours truly, Yochai Birnbaum and Shaul Atar Yochai Birnbaum, MD Edward D. and Sally M. Futch Professor of Medicine, Biochemistry and Molecular Biology, Medical Director, Cardiac Intensive Care Unit Medical Director, The Heart Station The Division of Cardiology The University of Texas Medical Branch 5,106 John Sealy Annex 301 University Blvd. Galveston, Texas 77555-0553 Tel: 409-772-2794 Fax: 409-772-4982 -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 16 18:35:56 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 16 Jan 2008 19:35:56 -0200 Subject: [ISCHEMIA-FORUM] 6P LBBB. Dr. Perez Riera Message-ID: <478E78BC.4070800@myocardial.ischemia-symposium.org> Yes, it is possible. The phenomenon occurs in the cases in which the necrosis selectively attacked the left septal surface, leaving the low right surface of the septum unharmed. In such cases, the initial r wave of the V1-V2 complex, increases voltage or appears if it did not exist previously. Additionally, initial q wave appears in left leads. In brief, a strict infarction of the region of the left septal surface that doesn't reach the low right septal mass, may cause the following in surface ECG: 1) Increase of voltage of initial r in right precordial leads V1-V2; 2) Appearance of initial r wave, where there was QS complex before in the right precordial leads, thus transforming QS complex into rS; 3) Appearance of initial q wave in left precordial leads V5-V6. Best regards for everyone and thanks, Andr?s Ricardo P?rez Riera. > Dear Doctors, > In left bundle branch block (LBBB) with antero-septal infarction, is it > possible to see r wave appear in V1 and V2? > > Dr. Justiniano Ortiz > Paraguay -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 16 19:58:32 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 16 Jan 2008 20:58:32 -0200 Subject: [ISCHEMIA-FORUM] 7S Positive T wave. Dr. Alais Message-ID: <478E8C18.7030109@myocardial.ischemia-symposium.org> First, thank very, very much for the chance of such important scientific group giving us an opportunity to have a scientific update. My doubt is about when in a complete left bundle branch block, we find positive T wave, particularly in leads V4-V6. Would this indicate that there could be an overlapped pathology? Thank you very much for your attention, Dr. Alais -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 16 20:21:05 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 16 Jan 2008 21:21:05 -0200 Subject: [ISCHEMIA-FORUM] 8S RE: Dr. Pizarro's clinical case. Dr. Solano Message-ID: <478E9161.9030307@myocardial.ischemia-symposium.org> Question for Dr. Pizarro from Panama, I think it is wise to perform an echocardiogram and assess sectorial motility, besides serial ECG to try to establish the presence of ischemic heart disease. Cardiac enzymes would be part of a pre-established protocol. A coronary cineangiography would be a wise and revealing measure. Dr. Yamil Solano Costa Rica -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 17 14:06:45 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 17 Jan 2008 15:06:45 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASKS, EXPERTS ANSWER Message-ID: <478F8B25.4010400@myocardial.ischemia-symposium.org> Dr. Gustavo Bonzon from Argentina asks - Question for Dr. Magda Heras, Your presentation, "ACS without ST elevation. Optimizing Antithrombotic Therapy" is excellent. Besides the correction of IIb-IIIa inhibitors dose based on renal function, what additional adjustment do you suggest in such drugs according to the weight of the patient? Cordially, Dr. Gustavo R. Bonz?n Resistencia, Chaco, Argentina ------------------------------------- Dr. Magda Heras from Spain answers - "The inhibitors of the glycoprotein IIb/IIIa are given always considering the weight of the patient and also taking into account renal function, just as correctly pointed out. In slide number 7 of the presentation, we indicate the doses by Kg, both for bolus and endovenous infusion of the three available drugs: abciximab, eptifibatide, and tirofiban. Of note, currently there are some studies that are evaluating the efficacy and safety of higher doses of tirofiban." Thank you for your interest in this presentation. Happy 2008! Kind regards, Magda Dra. Magda Heras Cap de Secci? de Cardiologia Cl?nica ICT Hospital Cl?nic Villarroel, 170. 08036 Barcelona Tel 34 93 227 9305 Fax 34 93 451 4148 e-mail: mheras at clinic.ub.es -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 17 14:07:59 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 17 Jan 2008 15:07:59 -0200 Subject: [ISCHEMIA-FORUM] 12E High heart rate and ST elevation. Dr. Doval Message-ID: <478F8B6F.9070208@myocardial.ischemia-symposium.org> How a high heart rate may influence on ST elevation and mimic a STEMI? Best regards Dr. Henry Doval. France -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 17 14:19:02 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 17 Jan 2008 15:19:02 -0200 Subject: [ISCHEMIA-FORUM] 13E Culprit Coronary Artery. Dr. Madias Message-ID: <478F8E06.7090505@myocardial.ischemia-symposium.org> Dear Colleagues: Greetings!!!!!!! I am grateful to the organizing Committee for giving me the opportunity to participate in this forum on myocardial ischemia/infarction I read with great interest the lecture by Drs. Bayes de Luna, Fiol, and Carrillo, enttled "the Culprit Coronary Artery and the Location of Coronary Occlusions in patients with STEMI - A New Algorithm" in which the authors elaborate on employing the vecorial characteristics of the ischemic injury to predict the occluded coronary vessel, and in the case of LAD to differentiate the level of occlusion (proximal, distal, above/below the diagonal or septal branches. They refer to a cut-point of >2.5 mm for the sum of ST-depression from leads III and aVF in anterior wall MI with ST-elevations in the precordial leads. Wouldn't it may more sense to use ratios of the sums of ST-elevations from the precordial ledas to sums of ST-depressions from leads III and aVF, instead of using the absolute value of 2.5 mm? The absolute values of ST-segment elevations (and consequently the reciprocal ST-depressions) must be time of inception of occlusion to ECG recording-dependent, and therefore changing, mostly decreasing after clinical presentation, and thus the rations rather than the absolute values might be more appropriate to employ. Thank you for the opportunity to comment. Wishing to all a fruitful and joyful interaction with our colleagues, Sincerely, John E. Madias, MD Mount Sinai School of Medicine -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 17 14:21:06 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 17 Jan 2008 15:21:06 -0200 Subject: [ISCHEMIA-FORUM] 9R Ventricular fibrillation. Dr. Kosolapov Message-ID: <478F8E82.6030304@myocardial.ischemia-symposium.org> Dear colleagues, My question is for all the participants in the Forum. What management would you follow in a patient, who during the treatment with thrombolytic agents had an episode of ventricular fibrillation? Electric cardioversion was conducted on this patient, successfully reversing to sinus rhythm. Would you indicate endovenous amiodarone (loading and maintenance) and for how long? Would you indicate long-term treatment combined with beta-blockers and amiodarone, or would you manage it in a conventional way (as a post-infarction patient without ventricular arrhythmia)? Dr.Yuriy Kosolapov Hospital de urgencias n?mero 2, Ciudad de Novosibirsk, Russia. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 17 14:23:42 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 17 Jan 2008 15:23:42 -0200 Subject: [ISCHEMIA-FORUM] 10S RE: Dr. Pizarro's clinical case. Dr. Pizarro Message-ID: <478F8F1E.5010007@myocardial.ischemia-symposium.org> Greetings for everyone, Congratulations and my respect goes to the Organizers, Faculties, and Participants of this great event, which we started off with the right foot along with this New Year. Thank you very much for the active participation to this moment; I have really learnt a lot, and we are just beginning. About this case, that is an "average case" that we see and will increasingly see more in our Emergency Services (there will be more diabetics, so much so, that experts on the topic have been saying over the last two years that DM is becoming the Epidemics of the 21st C.), and which I attempted not to "personalize" as our dear and respected Dr. Dimitrius Tziakas would have preferred (which is completely understandable and proper to manage this patient), but precisely I presented him as a "general" case to foster lucubrations, commentaries, personal experience, or experience-based medicine, and of course, what we have available on evidence-based medicine about the topic (which keeps evolving and changing all the time, to the extent that the Organizers have to start thinking and planning another great Symposium for next year, what do you think?), and I'm sure that we are reaching this goal. About this issue, there is a lot to be said, and this is the time to do it; thank you very much for your consideration and I appreciate the chance to participate and help each other to understand more and the best possible way this topic. Sincerely, Dr. R. Pizarro -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 17 14:29:01 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 17 Jan 2008 15:29:01 -0200 Subject: [ISCHEMIA-FORUM] 11S RE: Dr. Pizarro's clinical case. Dr. Pizarro II Message-ID: <478F905D.2010805@myocardial.ischemia-symposium.org> Greetings for everyone, Dear Dr. Gustavo R. Bonzon, I am no expert in echocardiograms, but since you mention it, I remember that a couple of years ago, I read an article on the new devices of bedside or portable echocardiographs, and its authors had made a comparison between "static" and "portable" models, and the latter had the honor of being quite reliable to measure left ventricular ejection fraction, which seems to be a rough measurement, but quite accurate for the contractile strength of the heart (in general), but for the rest of measurements (if I remember well) not much credibility was given to it, but who knows? Probably those authors are participating in this current event and may contribute further data about this; if they are not (and they are missing it), I'm sure there will be other colleagues that may answer, contribute, and share their knowledge and experience. Sincerely, Dr. R. Pizarro. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 17 14:34:42 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 17 Jan 2008 15:34:42 -0200 Subject: [ISCHEMIA-FORUM] 14E Positive T wave. Dr. Perez Riera Message-ID: <478F91B2.4010305@myocardial.ischemia-symposium.org> Dear Dr. Alais, Classically, in non-complicated Complete LBBB depression upwardly convex of ST segment followed by negative asymmetrical T wave in left leads (DI, aVL, V5 and V6) is normally observed. Ventricular repolarization in not complicated Complete LBBB has secondary alteration of ventricular repolarization with QRS/ST-T angle near the 180?. Positive T waves from V4 to V6 in presence of Complete LBBB frequently indicate precordial T transition pattern in V5 and V6 and not isquemia. This hypothesis is stronger if concomitantly is observed the presence of the Rs pattern in the left precordial leads. This association may indicate: 1) Transitional recording for LVE the left leads may show Rs pattern followed of positive T wave pattern in absence of another associated problem: Non-complicated LBBB. 2) Association with LAFB. 3) Association of LBBB with Right Ventricular Enlargement (RVE). 4) Association of LBBB with electrically inactive area in the LV free wall. All the best Andr?s Ricardo Perez Riera, MD Chief of Electro-Vectorcardiography Sector ABC?s Medical School, ABC Foundation, Santo Andr?, S?o Paulo, Brazil > First, thank very, very much for the chance of such important scientific > group giving us an opportunity to have a scientific update. My doubt is > about when in a complete left bundle branch block, we find positive T > wave, > particularly in leads V4-V6. Would this indicate that there could be an > overlapped pathology? Thank you very much for your attention, > > Dr. Alais -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 17 15:40:37 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 17 Jan 2008 16:40:37 -0200 Subject: [ISCHEMIA-FORUM] 18E Chest pain and early repolarization. Dr. Perez Riera Message-ID: <478FA125.50108@myocardial.ischemia-symposium.org> Dr. Andriy Vorotniak from Russia, Please, theses criterias are important for the diagnosis decision: Criteria for early repolarization are the following: 1) Sinus bradycardia is often present. Sinus bradycardia is the rule in athletes with VER. 2) PR interval: shorter and depressed P-R interval is referred. 3) QRS morphology: notching or slurring of the terminal QRS complex; (Brady WJ, Chan TC. Electrocardiographic manifestations: benign early repolarization. J Emerg Med. 1999; 17: 473-478) on end of descending ramp of R wave (J point). Relatively deep but narrow q waves may appear in the left precordial leads 4) S?QRS or QRS axis: Vertical electrical axis is the rule. 5) The frontal plane QRS axis and ST segment axis and T wave axis are all in the same direction. 6) Abrupt transition with counterclockwise rotation on precordial leads is observed. About two-thirds of clockwise rotation and counterclockwise rotation could be attributed to the septal angle by anatomical rotation of the heart in one plane around the long axis, but other factors appear to be responsible for such electrocardiographic findings in the remaining one-third of cases. Relatively higher positions of the precordial ECG leads, as observed in the vertical heart, appeared to be responsible for clockwise rotation in the some patients, and left septal fascicular block is suspected to be responsible for counterclockwise rotation in others patients 7) Widespread STE precordial greater than limb leads. It is considered present when at least two adjacent or anatomically contiguous leads on electrocardiogram show elevation of the ST segment, with values ?2 mm in the precordial leads and/or ?1mm in the limb leads. 8) minimally elevated J point . Notching or irregular contour of J point 9) Concavity of initial up-sloping portion of ST segment: ST segment: Diffuse or widespread persistent ST segment elevation, upward concavity of the initial portion of the ST segment most commonly seen in the mid-to-left precordial leads, and they are also sometimes seen in both the limb leads (I, II, II, aVF and aVL) and chest leads (V2to V6). Unfortunately, concave ST morphology cannot be used to exclude ST elevation MI with left anterior descending coronary occlusion because it is common in this circumstances. 10) Prominent, concordant T waves: T Typical pseudo-asymetrical or slightly asymmetrical, concordant T waves often of larges amplitude upright tall peaked T waves most conspicuously from V2 to V4 or V5 sometimes seen in leads DII, DIII and aVF is the rule. The T waves may appear "peaked" or pointed. 11) Stable ECG pattern: There are no evolutionary short-term changes in the ST segment and T waves( persistent ECG features) 12) U wave: because frequently bradycardia U waves are frequent in ERV best observed in V3 lead. 13) The QT maximum: The maximum Q-onset-T-end interval. This parameter is higher in ERV subjects than in normal controls (Dilaveris P, Pantazis A, Gialafos E. Assessment of ventricular repolarization alterations in subjects with early repolarization. Int J Cardiol. 2004; 96:273-279) 14) Negative cardiac injury markers: Exercise and isoproterenol tend to normalize the ST segment elevation. A progressive decrease in ST segment elevation and normalization of the ECG with mild exercise was a predictable response in patients who have early repolarization with otherwise normal 15) The QTp maximum: maximum Q-onset-T-peak interval. This parameter is higher in ERV subjects than in age-matched healthy controls. 16) The rate-corrected QTc maximum: This parameter is lower in ERV subjects than in age-matched healthy controls. 17) The QTpc maximum: This parameter is lower in ERV subjects than in age-matched healthy controls. 18) The QRS duration: This parameter is higher in ERV subjects than in age-matched healthy controls. 19) VCG markers spatial T amplitude: This parameter is higher in ERV subjects than in age-matched healthy controls. Spatial QRS amplitude: This parameter is higher in ERV subjects than in age-matched healthy controls. 20) Normal cardiac stress test or angiography. All the best Andr?s Ricardo Perez Riera, MD Chief of Electro-Vectorcardiography Sector ABC?s Medical School, ABC Foundation, Santo Andr?, S?o Paulo, Brazil -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 17 17:04:30 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 17 Jan 2008 18:04:30 -0200 Subject: [ISCHEMIA-FORUM] =?iso-8859-1?q?16S_Variant_angina=2E_Dr=2E_Bonz?= =?iso-8859-1?q?=F3n?= Message-ID: <478FB4CE.20705@myocardial.ischemia-symposium.org> Questions for Drs. Kaski, Juan Carlos, and Arroyo-Espliguero, Ram?n. Dear colleagues, In your outstanding lecture titled "Variant Angina", you state this: "The implantation of stents could also be effective in patients with refractory symptoms and mild to moderate obstructive CAD, in whom a vasospastic arterial segment is identified, taking into account that most of the patients with positive provocative test and recurring symptoms usually present vasospasm located on the same arterial segment. However, the spasm may recur in different segments, including multiple spasm." My questions are: 1- Would you advice the use of drug-eluting stents (DES) or bare-metal stents (BMS)? 2- In case of using drug-eluting stents, what length of stent do you advice using regarding the length of the documented vasospastic segment? 3- In the cases of vasospasm of the main trunk of the left coronary artery in women, would you advice indicating an implant of stent or CABG? Thanking you in advance for your reply, Cordially, Dr. Gustavo R. Bonz?n Resistencia, Chaco, Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 17 17:01:17 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 17 Jan 2008 18:01:17 -0200 Subject: [ISCHEMIA-FORUM] =?iso-8859-1?q?15S_Precordial_pain_and_early_rep?= =?iso-8859-1?q?olarization=2E_Dr=2E_Garc=EDa?= Message-ID: <478FB40D.1030107@myocardial.ischemia-symposium.org> Dear colleagues, Considering that the symptoms in such a young patient could result in myocardial infarction, I think that this patient at least should be admitted in a precordial pain unit, with serial ECG and evaluation of serum markers (troponins, CPK, etc.). This would demand approximately 10 hs, and the margin for error would decrease significantly. Sincerely, Dr. Edgar Garc?a. Corrientes. Argentina. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 17 17:28:45 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 17 Jan 2008 18:28:45 -0200 Subject: [ISCHEMIA-FORUM] 20E Cardiac X Syndrome. Dr. Lanza Message-ID: <478FBA7D.6090003@myocardial.ischemia-symposium.org> With regard to Dr. Cr?mer question about use of antiplatelet therapy in patients with cardiac syndrome X., there is no evidence at present that these drugs (including aspirin) can be in some way helpful in this group of patients. Antiplatelet agents reduce cardiovascular events significantly in several groups of patients with obstructive coronary artery disease who present an appreciable increase of events compared to general healthy people. In contrast, syndrome X patients have excellent long term prognosis, with an incidence of events that seems to be similar to that of the general population. Accordingly, it seems unlikely that antiplatelet drugs may significantly improve prognosis in these patients, and therefore, in my opinion, they do not have indication at present in the the general population of cardiac syndrome X. Gaetano A. Lanza -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 18 11:58:57 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 18 Jan 2008 12:58:57 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASKS, EXPERTS ANSWER Message-ID: <4790BEB1.8070903@myocardial.ischemia-symposium.org> Dr. Ricardo Pizarro from Panama asks - Dear Drs. Kaski and Lanza, In the so-called cardiac X syndrome, and regarding the pain perceived by patients, what role has the CNS, maybe specifically the sympathetic system? I will be grateful if you could let me know if someone has attempted to research this or treat it as if it was a neuropathic pain (intermittent drip of xylocaine at 2% and other medications), for instance, or something similar. Let us remember that emotions-stress-pain are closely linked, and we should consider the organism as a whole: Hans Bruno Hugo Selye, when mentioning the "General Syndrome of Adaptation" mentions emotions a lot. The only way to understand all this subject better, is to never forget that the organism is a "WHOLE". It is impossible to separate a stimulus from the normal reaction of the organism, whether on "eustress" or "distress" and to think on the emotions it originates and the pain, as not connected. Therefore, would it be possible that the initial event in a person with X Syndrome was triggered by a very stressful or frightening event, and the "memory" of it remained, unsolved, and it is still affecting the patient in the form of the pain that troubles them? Have Psychiatrists been consulted for these patients? Sincerely, Dr. R. Pizarro Panama ------------------------------------- Dr. Gaetano Lanza from Italy answers - Dear Dr. Pizarro, Many thanks for your intriguing questions about cardiac syndrome X (CSX). The possible role of nervous system alterations in CSX has been suggested by several observations: 1. A group of studies demonstrated that, in at least a group of these patients, chest pain can be evoked by mechanical (e.g. intracardiac injection of saline, intracardiac catheter manipulation), electrical (pacing stimulation) or chemical (adenosine) stimuli at intensity usually not causing pain in patients with other cardiac problems. These data suggest that a reduced pain threshold for cardiac stimuli can present and contribute to the characteristics of chest pain in CSX patients. 2. Whether the abnormal pain sensitivity is a ?systemic? or a ?cardiac? disorder is a matter of discussion. Indeed, some studies suggested reduced pain threshold to peripheral skin stimuli. However, using a controlled protocol Cannon et al. failed to show increased pain sensitivity during thermal stimuli and we recently showed no differences between CSX patients and patients with coronary artery disease or healthy controls in chest and right hand pain threshold in response to laser stimuli. Thus, on the whole the data suggest that the nociceptive abnormality exclusively or mainly concerns the heart. 3. Some abnormality in the central elaboration of pain stimuli, however, has recently been reported by our group in a study in which we found the lack of the physiological habituation to skin laser painful stimuli during repeated sequences of impulses in CSX patients. How this apparent central abnormality influences chest pain characteristics of patients, however, remains to be established. 4. Finally, some abnormality in the specific function of nervous adrenergic activity in CSX patients was suggested by indirect data, as an increased heart response to exercise or reduced heart rate variability. We, on the other hand, documented an impairment of cardiac uptake of meta-iodo-benzyl-guanidine (MIBG), an analogue of norepinephrine, by adrenergic nerve fibres, thus suggesting functional or structural abnormalities in the efferent cardiac sympathetic nerve fibres. Interestingly, MIBG uptake was not impaired in other organs (lungs, liver, salivary glands), thus again suggesting a nervous abnormality exclusively or mainly localized in the heart. At present it is difficult to give a complete explanation of the relationship among these different observations. However, the following considerations, in my opinion, can be done: 1. As we suggested in a previous Editorial article, there can be a link between the abnormal cardiac MIBG uptake (which indicates an abnormal efferent cardiac adrenergic function) and the increased cardiac pain sensitivity (which suggests an impaired afferent cardiac nerve function). Thus these data combined may suggest an abnormality of the cardiac nerve system; 2. Although a primary alteration of the cardiac nervous system cannot be excluded, the abnormal cardiac nerve abnormalities might be secondary to chronic coronary microvascular dysfunction, which may affect not only the myocardium but also the cardiac nerve fibres (the involvement of the efferent cardiac adrenergic nerve fibres can influence, in turn, coronary microvascular function); 3. The involvement of cardiac nerve structures may determine some neuropathic characteristics of chest pain of these patients, although this statement is merely speculative; 4. A possible clue to the assumption of neuropathic aspects of chest pain in CSX patients can be suggested by the efficacy of neromodulatory techniques (mainly spinal cord stimulation) on anginal pain episodes. 5. It remains to be clarified how the lack of habituation to peripheral pain stimuli shown in CSX patients is generated and contributes to the characteristics of angina episodes in these patients (our still unpublished data indicate that SCS seem to restore habituation to pain induced by skin laser stimuli). As far as your hypothesis that a very stressful or frightening event can be responsible for the anginal chest pain symptoms in CSX patients, it is certainly fascinating. However, my personal clinical experience points out that it is unlikely. Although clinical cardiologists may not be very good at identifying minor or latent psychiatric disorders, patients with clear or doubtful such problems are usually identified and excluded from the diagnosis of CSX. On the other hand, it is difficult to establish whether minor behavioural disorders are a cause or a consequence of a clinical status of angina symptoms. Finally, how acute emotional events or status can influence cardiac and vascular function is not completely clear yet, but there might be some stricter relations than previously believed. For example, it is now clear that dramatic negative emotional events may cause an acute form of cardiomyopathy (so-called takotsubo disease or apical ballooning syndrome), likely mediated by an abnormally activation of the adrenergic system, with severe, although transient, impairment of ventricular function. Interestingly, an acute severe coronary microvascular constriction is among the possible mechanisms involved in this particular form of cardiomyopathy. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 18 12:04:09 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 18 Jan 2008 13:04:09 -0200 Subject: [ISCHEMIA-FORUM] 22E Coronary spasm and VF. Dr. Bayes de Luna Message-ID: <4790BFE9.1070501@myocardial.ischemia-symposium.org> About the question, this is my opinion: 1- Coronary spasm very rarely induces ventricular fibrillation. In our experience (J of Electrocardiology 1985;18:267-276) we haven't seen any case. On occasions, it did induce runs of ventricular tachycardia (see the article on coronary spasm in this symposium). In the attached case it is clear that the spasm produced ventricular fibrillation, but also it is clear that calcium antagonists prevented this from recurring. Moreover, does the patient smoke? Smoking could be a trigger and all possible triggers, drugs, etc., have to be discontinued. Conclusion: discontinue triggers, DO NOT discontinue calcium antagonists, and very likely the crisis will not occur again. Dr. Antoni Bayes de Luna -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 18 11:59:51 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 18 Jan 2008 12:59:51 -0200 Subject: [ISCHEMIA-FORUM] 21E Coronary spasm and VF. Dr. Wasserman Message-ID: <4790BEE7.1080207@myocardial.ischemia-symposium.org> Dear Drs. Bayes de Luna and Kaski, Congratulations on your presentations! I would like to present a personal case: 51-year-old patient, female, who was admitted in the ER of our service with ventricular fibrillation, and electrical cardioversion was applied successfully. Her coronary angiography showed total spasm of the anterior descending artery, produced by ergonovine without coronary lesions; she was treated with calcium antagonists. On treatment, a new coronary angiography did not show spasm, and the electrophysiologic study did NOT induce ventricular tachycardia. Would you agree with ICD implantation? Her medical insurance denies granting the device because they tell us that according to guidelines, it would be excluded in this case as she has reversible or transitory causes. Dr. Faiwel Wasserman Poland -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 18 12:11:42 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 18 Jan 2008 13:11:42 -0200 Subject: [ISCHEMIA-FORUM] 19S Ventricular fibrillation. Dr. Orlando Message-ID: <4790C1AE.2060901@myocardial.ischemia-symposium.org> Dear colleagues from the forum, In patients who are suffering AMI, and the decision is made to perform reperfusion with thrombolytic agents, if a VF event occurs, one of the possibilities is that the latter could be evidence of the reperfusion; if in evolution during monitoring the patient does not present a new event, he/she should be treated as a conventional patient, with post-reperfusion beta-blocking therapy. Querencio Orlando Jefe del servicio de Emergencias Instituto de Cardiologia Corrientes - Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 18 12:49:34 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 18 Jan 2008 13:49:34 -0200 Subject: [ISCHEMIA-FORUM] 25E Coronary spasm and VF. Dr. Vanerio Message-ID: <4790CA8E.8040805@myocardial.ischemia-symposium.org> Dear Dr. Faiwel Wasserman I would like to know if your patient was a smoker Thank you Gabriel Vanerio, MD Montevideo Uruguay -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 18 13:06:13 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 18 Jan 2008 14:06:13 -0200 Subject: [ISCHEMIA-FORUM] 27E Early Repolarization and Elderly Ages. Dr. Zamarripa Message-ID: <4790CE75.3050003@myocardial.ischemia-symposium.org> Dear colleagues, Do anyone knows what's the prognostic and long term survival of the early repolarization. We use to consider the early repolarization as a "positive" factor, however what's the real impact of this EKG marker in the older age population ? Thanks for your comments. Daniel Zamarripa MD Somerset, New Jersey -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 18 14:29:06 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 18 Jan 2008 15:29:06 -0200 Subject: [ISCHEMIA-FORUM] 30E High heart rate and ST elevation. Dr. Birnbaum Message-ID: <4790E1E2.2000604@myocardial.ischemia-symposium.org> Dear Dr. Doval. Indeed, heart rate may affect ST elevation. It is well known that ST elevation related to early repolarization is rate dependent and disappear with faster heart rates. On the other hand, ST elevation in leads V1-V3 (a "normal variant", secondary to LVH or LBBB) may increase with tachycardia. Moreover, in patients with old or recent Q wave infarction and baseline mild ST elevation, tachycardia may cause ST elevation in these leads. this phenomenon is often see during post infarction exercise stress tests. On the other hand, tachycardia may cause ST depression in leads V4-V6 with reciprocal ST elevation in leads V1 and aVR. Although this pattern is generally ascribed to circumferential subendocardial ischemia due to significant left main stenosis or diffuse coronary artery disease, this is true especially when seen as dynamic changes with relatively slow heart rate. When seen during tachycardia, the significance of such changes is similar to positive electrocardiographic stress test; it may indicate ischemia, or non-specific changes in patients with hypertension, LVH or cardiomyopathy. It has to be remebered that according to the AHA/ACC guidelines, ST should be measured at the J point, and not 0.06-0.08 seconds after the J point, as recommended for ST depression during stress tests. If measured at 0.06 seconds after the J point, ST elevation could be falsely detected during tachycardia (measuring the T wave instead of the ST segment). Thank you Yochai Birnbaum, MD Professor of Medicine, Biochemistry and Molecular Biology The Division of Cardiology The University of Texas Medical Branch 5.106 John Sealy Annex 301 University Blvd. Galveston Texas 77555-0553 -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 18 15:39:18 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 18 Jan 2008 16:39:18 -0200 Subject: [ISCHEMIA-FORUM] 24S Several replies. Dr. Pizarro Message-ID: <4790F256.6070800@myocardial.ischemia-symposium.org> Greetings for everyone: 1) Dear Dr. Gustavo R. Bonzon, as a physician working in an Emergency Room, I see and read that tests are being increasingly performed in patients, since the initial care in the ER to "shorten distances" with management, and to make decisions as soon as possible about whether the patient should go to a Ward (stable and with low risk), a Coronary Unit, Semi-Intensive Care Unit, Hemodynamic Lab, Operating Room, or Chest Pain Unit, which are increasingly more frequent, and after a short stay there, even to home. So I think it would be a great idea (it is just a suggestion for experts and Faculties), that when an enough sophistication degree for the portable echocardiogram devices is reached, and once the corresponding studies are started with such devices, Guidelines should be prepared to use them. We see it in the great advancement of genetics, to the extent that everyday new findings are published, including the clinical application (even free of charge), so don't be surprised if within 2 decades, most Diagnosis are made in the ER. Well, all this is just lucubration and good wishes, but I see we are on the right road. Sincerely, Dr. R. Pizarro. 2) Dear. Dr. Yamil Solano (Costa Rica), I think your approach to the patient is very appropriate, and I agree with you. Sincerely, Dr. R. Pizarro. 3) Dear Dr. John E. Madias, from the prestigious Mount Sinai University (I am subscribed to the excellent Journal of the Mount Sinai Hospital, and it is among the best), about you comments (which are also very instructive), let me tell you that I completely agree with you, since this is a case to apply the algorithm by Dr. Elena Sgarbossa, and other prestigious colleagues that participated in the study, which was so fascinating, to the extent that I have still recorded in my PC, and I checked it every time I need it, and although I have read some criticisms to its sensitivity, I think (not being an expert on the topic) that it is good, and for this reason I still use it (N Engl J Med 1996;334:481-7); (if any of the participants wants it, please write to my personal e-mail, and I will gladly send it, as well as a summary of abstracts by Dr. E. Sgarbossa). On the other hand, I did not mention the amplitude of ST segment (elevated or depressed), since I presented a hypothetical case, but that we see increasingly more frequently, and I left the "details" for all of you, to be able to "enjoy and seize to the most" this very interesting topic, that will be and will continue being one of the most frequent and important; I have also written about this in another message that I have sent yesterday night, to this formidable Symposium. Thank you very much for your didactic and timely input, and please, go on participating. Sincerely, Dr. R. Pizarro. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 18 17:06:20 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 18 Jan 2008 18:06:20 -0200 Subject: [ISCHEMIA-FORUM] 31E Coronary spasm and VF. Dr. Wasserman In-Reply-To: <4790CA8E.8040805@myocardial.ischemia-symposium.org> References: <4790CA8E.8040805@myocardial.ischemia-symposium.org> Message-ID: <479106BC.4060508@myocardial.ischemia-symposium.org> Dear Dr. Vanerio, My patient is not a smoker neither pasive smoker Best regards F. Wasserman > Dear Dr. Faiwel Wasserman > > I would like to know if your patient was a smoker > Thank you > > > Gabriel Vanerio, MD > Montevideo Uruguay > -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 18 17:58:30 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 18 Jan 2008 18:58:30 -0200 Subject: [ISCHEMIA-FORUM] 26E Discussion Dr. Kaski VAP. Dr. Bousik Message-ID: <479112F6.2070501@myocardial.ischemia-symposium.org> Dear colleagues, I am thankful to have the opportunity to participate in this interesting Internet symposium on variant angina pectoris presented by Dr.Kaski. In my opinion another method - Body Surface Potential Mapping is useful for the diagnostics of VAP. This almost forgotten but useful screening diagnostic tool in the Prague modification can help in the diagnostic of different cardiopathies incl. VAP as it can be seen on the following example description. BSPM examinations and the provocative tests (hyperventilation combined with handgrip) were carried out in our laboratory with following results: substantial potential increase in the repolarization. In Figure 1*** the lower map represents a rest potential map in 70% repolarization before the test The red color represent the electropositivity, the blue color represents the electronegativity, the left half of the map belongs to the anterior chest wall, the right half to the posterior chest wall. The distance of isopotential lines is given in microvolts m V). The maximal value of the potential in the electropositivity on this map before the test was 311 m V, in the electronegativity it was -150 m V. The upper map was obtained 5 minutes after the provocative test (hyperventilation combined with handgrip). After the test substantial increase of potential values appeared (949 m V res. 340 m V). In Figure 2*** the lower map was obtained 5 minutes after the test (it is the same map as in the upper part of the Figure 1). The upper map in the Figure 2 was obtained 2 minutes after the inhalation of isosorbide dinitrate (/ISDN) in form of a spray. The potential values on the BSPM after ISDN decreased practically to the starting values (308 m V, res. -159 m V). The explanation: with high probability after the test the occlusion of the left anterior descending coronary artery appeared and the normalization was followed after the ISDN. BSPM nowadays does not enjoy wide spread applicability. Prague modified version of BSPM increased substantially as the sensitivity as the specificity when compared with situation at the end of eighties. Our 20 years lasting experience with the clinical application of BSPM as a screening method we found it to be reliable, easily reproducible and very cheap. The examination can be carried out by an experienced nurse in 20 minutes. References: Boud?k F, Stojan M, Anger Z et al: Evaluation of body surface potential mapping changes after successful percutaneous transluminal coronary angioplasty Can J Cardiol 1996; 12:745-749. Boudik F, Anger Z, Aschermann M et al: Dipyridamole body surface potential mapping: noninvasive differentiation of syndrome X from coronary artery disease. J Electrocardiol; 2002; 35:181-91. Boudik F, Reissigova J et al: Primary prevention of coronary artery disease among middle aged men in Prague: Twenty-years follow-up results. Atherosclerosis 2006; 184:86-93. Prof.Dr.F.Boudik, Charles University Hospital2nd Medical Dept., U nemocnice 2 rague 2 Czech Republic Note: Figures are in the attached Word document.**** **** Click here http://lists.ischemia-symposium.org/files/KASKI_BSPME.doc -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 19 07:33:05 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 19 Jan 2008 08:33:05 -0200 Subject: [ISCHEMIA-FORUM] 32E E Early Repolarization and Elderly Ages. Dr. Perez Riera Message-ID: <4791D1E1.90105@myocardial.ischemia-symposium.org> Dear Dr Daniel Zamarripa: Thank you very much for your intelligent question. Early repolarization variant (ERV) or early repolarization pattern (ERP) is common in people under the age of 30 years old. There is a decreasing incidence with advancing age. It is absolutely exceptional in older age. Dr Lee wrote 4 years ago a manuscript entitled: Ask the doctor. I am a fit and healthy 42-year-old man. So I was disturbed when my latest electrocardiogram said I had "ST elevation consistent with early repolarization." I know from reading the Heart Letter that ST elevation can mean a heart attack, although I don't think I have had one of these. Should I be worried about this?. (1) This paper answers your cleaver question. The ER pattern is predominant in athletically active people and more infrequent in sedentary. Recently, there has been renewed interest in ERV because of similarities to the arrhythmogenic Brugada syndrome (BrS). Not much is known about the epidemiology of ERV and several studies have reported that this condition is associated with a good prognosis. Both syndromes exhibit some similarities including the ionic underlying mechanism, the analogous responses to changes in heart rate and autonomic tone, sympathicomimetics (isoproterenol test) as well as in sodium channel and beta-blockers. These observations raise the hypothesis that the ERV may be not as benign as traditionally believed. The ERV shares remarkable cellular, ionic, and electrocardiographic similarities with the BrS and idiopathic ventricular fibrillation (a variant of the BrS with ST-segment elevation in inferior leads (2). ST-segment elevation in an apparently structurally normal heart is associated with an ECG J wave, which can be observed in the ERV, idiopathic ventricular fibrillation (VF), and BrS(3) In ERV, there is a voltage gradient but no dispersion of AP duration. POSSIBLE SIMILARITIES BETWEEN ERV AND BrS 1) Both more frequent in males; 2) Both occur more frequently in young adults; 3) Both occur in individuals without apparent structural heart disease; 4) Both can influence just the V1-V2 leads: Rarely (9%), can ST elevation be observed in ERV only in the right precordial leads: V1-V2, or in the inferior ones. When ST elevation is normal, it can reach up to 3 mm in V2-V3, especially in young people. In those individuals over 40 years, it seldom exceeds 2 mm. Both can show incomplete RBBB patent or right bundle branch conduction disorder: in BrS, it can present atypical features, RBBB-like and of the saddle type by exclusive elevation of the J point. S wave with delay in the left leads: DI, aVL, V5 and V6, could be absent as it is to be expected in a classic RBBB. The elements considered as typical in BrS are: 1) elevation of the terminal part of QRS (prominent J wave): 2) elevated and descending ST, not related to lesion of ischemic (idiopathic) injury; 3) negative T wave in the right precordial leads; 4) normal QTc; 5) absence of final delay in left leads as it would be expected in a classic RBBB(4). In ERV, when associated to athlete heart, QRS can present a moderate extension (100 ms to 110 ms) in 15% of the cases, which in nonathlete, normal population, in a 2.4% is called outflow tract hypertrophy. In this case r' does not exceed the 5 mm and is lower than S in the same lead: rSr'; 5) Both can improve repolarization during the stress test; 6) Both can improve with use of isoproterenol; 7) Both respond to a shortening of AP phase 2 in a part of ventricular thickness, and intensification of fast repolarization notch (phase 1) mediated by transmural dispersion of ventricular repolarization by a larger notch in the Ito channel(5). 8) The alteration of the Ito and ICa2+-L channels in BrS and in ERV are the electrophysiologic substrate that explains the J point and ST segment elevation, because they cause the intensified notch in phase 1 and suppression in phase 2 duration in the epicardium and in the endocardium of ventricular wall thickness. Elements for differential diagnosis: 1) Family background ERV: negative BrS: frequently positive 2) Race: ERV: predominantly in African?s descendents(6). BrS: predominantly in Asian (58%) and Caucasian people(7). 3) Response to IC group antiarrhythmic agents: BrS: flecainide, used in a 10mg/Kg dosage in 10 minutes, increases ST elevation and QRS duration in a more significant way in patients with BrS than in individuals without the entity, and only in those it triggers ventricular extrasystoles(8). ERV: it can induce a pattern similar to BrS; however, the degree of ST elevation caused by the drug is much higher in patients with BrS than in patients without the disease. Table 2 makes a comparison among ERV acute pericarditis, AMI and BrS. Additionally, there are documents showing that ST-segment height in the man is greatly influenced by central sympathetic nervous activity, both at baseline and during physiologic and pharmacological stress. There is a higher prevalence of ERV in individuals with spinal cord injury at levels of injury that can disrupt central sympathetic command of the heart (at the C5 to C6 levels) with high vagal tone and loss of sympathetic tone(1). In these cases the prognosis is not good(9).. Central sympathetic dysfunction regularly results in multilead ST-segment elevation or J wave that decreases or below isoelectric baseline during low dose isoproterenol infusion. Critical discussion of semantics: denominations used in literature The denomination Early Repolarization Syndrome (ERS) is not correct if we define syndrome as a group of symptoms that collectively indicate or characterize a disease, psychological disorder, or other abnormal condition, or a complex of symptoms indicating the existence of an undesirable condition or quality. However, there is a third meaning of the term that could make the denomination of syndrome appropriate: a distinctive or characteristic pattern of behavior. A syndrome is a characteristic ECG pattern, and its behavior always or nearly always has a benign course. We do not think the denomination Benign Early Repolarization (BER) today is appropriate, because it indicates a type of given clinical evolution, and recent papers have cast a doubt about whether this electrocardiographic pattern is really benign. The ERV may not always be benign and it can become a substrate for ventricular arrhythmias, sudden cardiac death (SCD), and hypercontractility cardiomyopathy in certain subjects, including certain high-performance athletes. Athletes with symptoms of syncope, especially if exertion, warrant a complete evaluation. The treatment of athletes and other individuals with life-threatening ventricular arrhythmias has been revolutionized by the implantable cardioverter defibrillator (ICD), a device that offers excellent protection from SCD. Defining those athletes who would benefit from an ICD is not always clear. Furthermore, participation in competitive athletics for athletes with life-threatening arrhythmias or structural heart disease known to put the athlete at risk for life-threatening arrhythmias is usually prohibited2. Additionally ERV probably represents part of a spectrum of cardiovascular anomalies related to nonischemic ST elevation, including Brugada syndrome (BrS), and that it may also have a molecular genetic origin of variable penetrance (10) The denomination Early Repolarization Pattern is correct, since it indicates that it is characterized by a given electrocardiographic pattern. Therefore, we believe that the most appropriate denominations are Early Repolarization Variant or Early Repolarization Pattern, because both refer to the existence of a given electrocardiographic variant or pattern. References 1) Lee TH Harv Heart Lett. 2003;14(4):8. ) 2) Letsas KP, Efremidis M, Pappas LK, Gavrielatos G, Markou V, Sideris A, Kardaras F. Early repolarization syndrome: is it always benign? Int J Cardiol. 2007; 114: 390-392. 3) Shu J, Zhu T, Yang L, Cui C, Yan GX. ST-segment elevation in the early repolarization syndrome, idiopathic ventricular fibrillation, and the Brugada syndrome: cellular and clinical linkage. J Electrocardiol. 2005; 38(4 Suppl): 26-32.) 4) Hiss RG, Lamb LE. Electrocardiographic findings in 122.043 individuals. Circulation 1962; 25:947-961. 5) Antzelevitch Ch, Xin Yan G, Shimuzi W, et al. Electrical heterogeneity, the ECG, and Cardiac Arrhythmias. In Zipes DP, Jalife J Cardiac Electrophysiology From Cell to Bedside, Third Edition. W.B. Saunders Company.2000. Chapter 26 p: 222-238. 6) Grusin H. Peculiarities of the African?s electrocardiogram and the changes observed in serial studies. Circulation 1954; 9: 860-867. 7) Nademanee K, Veerakul G, Nimmannit S, Chaowakul V, Bhuripanyo K, Likittanasombat K, Tunsanga K, Kuasirikul S, Malasit P, Tansupasawadikul S, Tatsanavivat P. Arrhytmogenic marker for the sudden unexplained death syndrome in Thail men. Circulation. 1997; 96:2595-2600. 8) Shimizu W, Antzelevitch C, Suyama K, Kurita T, Taguchi A, Aihara N, Takaki H, Sunagawa K, Kamakura S. Effect of sodium channel blockers on ST segment, QRS duration, and corrected QT interval in patients with Brugada syndrome. J Cardiovasc Electrophysiol 2000; 11:1320-1329. 9) Marcus RR, Kalisetti D, Raxwal V, Kiratli BJ, Myers J, Perkash I, Froelicher VF. Early repolarization in patients with spinal cord injury: prevalence and clinical significance. J Spinal Cord Med. 2002; 25:33-38. 10) Boineau JP. The early repolarization variant--normal or a marker of heart disease in certain subjects. J Electrocardiol. 2007; 40: 3.e11-16. All the best for all Andr?s Ricardo P?rez Riera MD and Master in cardiology area. Chief of Electro-Vectorcardiography Sector ABC?s Medical School, ABC Foundation, Santo Andr?, S?o Paulo, Brazil -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 19 07:40:05 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 19 Jan 2008 08:40:05 -0200 Subject: [ISCHEMIA-FORUM] 33E Coronary spasm and VF. Dr. Jack Chen Message-ID: <4791D385.6030605@myocardial.ischemia-symposium.org> Distinguished Colleagues: I have seen one patient with documented spasm-induced ventricular fibrillation. This gentleman, about age 50, presented to me with 2 episodes of effort-induced syncope associated with chest pain. On the treadmill, he developed precordial ST-elevation, chest pain, and immediate VF. He was easily resuscitated without incident. At catheterization, initial left coronary images were unrevealing. However, during right coronary angiography (which was normal), the patient began to complain of chest pain, with concomitant ST-elevations. Immediate re-imaging of the left system revealed significant spasm of the mid LAD. Intracoronary nitroglycerine relieved the spasm and symptoms. Given the dramatic presentation of this patient's coronary spasm, we proceded with stent implantation. The procedure was successful, and the patient has remained asymptomatic. Therefore, in the rare case of serious arrhythmias induced by coronary spasm, I would advocate stenting. Respectfully, Dr. Jack Chen -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 19 08:18:24 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 19 Jan 2008 09:18:24 -0200 Subject: [ISCHEMIA-FORUM] 37E Coronary spasm and VF. Dr. Kaski Message-ID: <4791DC80.7030001@myocardial.ischemia-symposium.org> Thank you for this important question. In addition to Dr Bayes de Luna's comments, with which I agree completely, the following points need consideration: 1. The prevalence of VF in spasm appears to be relatively low (< 5%) but it is not known due to the fact that many patients who die with coronary spasm before reaching the hospital are not diagnosed as such. 2, Coronary artery spasm can cause life-threatening arrhythmias (~15%) & sudden cardiac death (< 5%). These are common in patients with refractory Variant angina 3. ICD is required in survivors of Sudden death who continue to experience recurrent refractory spasm and/or sustained ventricular life-threatening arrhythmias. I agree with Antonio that if the spasm can be prevented then ICD may not be indicated. In our study on this topic, 10 variant angina patients with NCA, survivors of SCD followed for 6.7 years. In the 3 patients with ICD, interrogation of the device did not reveal sustained ventricular arrhythmias during 83 months of follow-up with effective, aggressive medical therapy. (Parchure et al. Cardiovasc Res 2001). In my view, ICD may not be required for long term management in every VA patient who survived SCD, but may be life-saving during the acute period of the disease. Its need has to be assessed carefully. 4. In relation to the specific case mentioned, if triggers are effectively avoided (and these should be explored carefully; remember smoking, hyperventilation, antimigraine treatment, cocaine, some antibiotics, etc) and vasodilators are effective in preventing the spasm, the ICD is not indicated. Patient has to be monitored carefully and frequently over time though. Hope this helps Best wishes JC Kaski Juan Carlos Kaski MD, DSc, FRCP, FESC, FACC Professor of Cardiovascular Science Director, Cardiovascular Biology Research Centre Division of Cardiac and Vascular Sciences St George's Hospital, University of London Cranmer Terrace, London SW17 0RE, UK Tel. No. + 44 208 725 5901/3963 Fax No. + 44 208 725 3328 -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 19 08:22:37 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 19 Jan 2008 09:22:37 -0200 Subject: [ISCHEMIA-FORUM] 38E Discussion Dr. Kaski VAP. Dr. Kaski (answer to Dr. Bousik) Message-ID: <4791DD7D.8060308@myocardial.ischemia-symposium.org> Thank you. I am aware of this important device and its potential use. We have not mentioned it in our presentations, however, as its use is not widespread and the device is not available in most centres. If further studies could be carried out in larger populations, furtehr documenting its value, it would be certainly excellent to consider it as part of the current diagnostic armamentarium. Regards JC Kaski -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 19 08:28:19 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 19 Jan 2008 09:28:19 -0200 Subject: [ISCHEMIA-FORUM] 39E T wave. Dr. Albornoz Message-ID: <4791DED3.7080102@myocardial.ischemia-symposium.org> Dear Dr Andr?s Ricardo P?rez Riera: Thank you very much for your nice lecture. Could you explain to us the T wave characteristic in coronary heart disease (acute coronary syndrome) and others entities with similar alterations on this wave in reference to polarity, duration, and shape.. Summarizanding, I want to know about the T wave and its differential diagnosis. Thank you in advance Cienfuegos Albornoz MD Habana Cuba. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 19 09:42:53 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 19 Jan 2008 10:42:53 -0200 Subject: [ISCHEMIA-FORUM] 28S Dr. Pizarro's clinical case. Dr. Pero Message-ID: <4791F04D.2070902@myocardial.ischemia-symposium.org> About what has been written, I would like to ask, 1 The graduation of sweating: is it real or subjective? If there are guidelines about it, could you tell me where to read about it? (To show it to the residents, since I haven't read about it before). 2 If there is no pain, a bedside echo may provide us some information, what do you think? If there is syncope or pre-syncope and CLBBB, it is almost certain the patient has structural heart disease, maybe related to VT. 3 If six hours had elapsed, negative troponin would relieve my concern. It may be positive in many cases of patent coronary arteries, but it is rarer in AMI after six hours. 4 The rest of the physical test, how is it? The patient may have digestive bleeding, or any digestive symptom in which thrombolytic agents are not very beneficial. 5 If after this there are still doubts, cineangiography would be essential. 6 Undoubtedly, the one beside the patient and who makes the decision is right, then come others that can only express their opinions. Regards, Dr. Sim?n Pero -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 19 11:45:31 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 19 Jan 2008 12:45:31 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASK, EXPERTS ANSWER Message-ID: <47920D0B.3080206@myocardial.ischemia-symposium.org> Dr. Andriy Vorotniak from Russia and Argentina asks - For Dr. Angiolillo, Dominick, My question is about the most appropriate moment to give clopidogrel (loading dose) in patients with Acute Coronary Syndrome with ST elevation, who are candidates for primary angioplasty. In the center where I work, the average delay between the patient's admittance into the Emergency Room and admittance into the Hemodynamics Service is 1 to 2 hours. Is it advisable to administer the loading dose of clopidogrel 1 hour before the procedure, considering the possible diagnostic mistakes (for instance, an aortic dissection "masked" with ST segment elevation in the inferior side) or the need of a potential urgent myocardial revascularization surgery? ------------------------------------- Dr. Dominick Angiolillo from USA answers - There are no studies evaluating the optimal timing of clopidogrel pretreatment in patients with STEMI undergoing primary PCI. In my opinion, if a patient is committed to primary PCI, the sooner treatment is given, the better. However, this should not delay cath lab times (top priority). Although not evidenced based, in our practice we give a 600mg loading dose of clopidogrel in patients undergoing primary PCI and we try to give this dose as soon as possible (e.g. in the emergency room) as this patient is committed to PCI and not surgery. Indeed, we cannot exclude the need for surgery in patients and some diagnostic errors may occur (e.g. aortic dissection). In these patients were there may be a diagnostic doubt, you should not pre-treat until diagnostic angiography is performed. If you times to the cath lab are also so short in UA/NSTEMI patients you probably should not load in the ER either, as at least 12-15 hrs of pretreatment are needed to see a clinical benefit (post-hoc analysis from the CREDO). -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 19 09:51:19 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 19 Jan 2008 10:51:19 -0200 Subject: [ISCHEMIA-FORUM] 29S Ventricular fibrillation. Dr. Pellizzon Message-ID: <4791F247.70108@myocardial.ischemia-symposium.org> Dear friends, Some years ago, in a project of experimental work in dogs, we performed a ligation of anterior descending artery and the VF always appeared with acute ischemia. When we released the ligation, the most frequent arrhythmia was accelerated idioventricular rhythm (AIVR) or frequent and polymorphic ventricular extrasystoles. At the beginning of clinical studies with thrombolysis, it was thought that AIVR was an arrhythmia exclusive of reperfusion. Later it was proved that this rhythm could appear in occluded artery or unobstructed by thrombolysis. Primary VF does not imply a worse prognosis, although there is a publication that shows that VF in anterior AMI has a worse prognosis than inferior AMI. Subsequent management is the same as noncomplicated AMI. Excellent symposium and interesting questions. Oscar Pellizon. Rosario - Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 20 07:49:24 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 20 Jan 2008 08:49:24 -0200 Subject: [ISCHEMIA-FORUM] 42C Cardiac X Syndrome. Dr. Message-ID: <47932734.7050600@myocardial.ischemia-symposium.org> There is indication to use Asprin, and it is better to use it. 403859118 at qq.com > With regard to Dr. Cr?mer question about use of antiplatelet therapy in > patients with cardiac syndrome X., there is no evidence at present that > these drugs (including aspirin) can be in some way helpful in this group > of patients. > Antiplatelet agents reduce cardiovascular events significantly in > several groups of patients with obstructive coronary artery disease who > present an appreciable increase of events compared to general healthy > people. In contrast, syndrome X patients have excellent long term > prognosis, with an incidence of events that seems to be similar to that > of the general population. > Accordingly, it seems unlikely that antiplatelet drugs may significantly > improve prognosis in these patients, > and therefore, in my opinion, they do not have indication at present in > the the general population of cardiac syndrome X. > > Gaetano A. > Lanza -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 20 08:02:21 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 20 Jan 2008 09:02:21 -0200 Subject: [ISCHEMIA-FORUM] 43C High heart rate and ST elevation. Dr. Message-ID: <47932A3D.7060602@myocardial.ischemia-symposium.org> We should monitor the dynamic changes of ECG, and also the myocardium enzyme marker. 403859118 at qq.com ______________________________________________________________________ > How a high heart rate may influence on ST elevation and mimic a STEMI? > Best regards > > Dr. Henry Doval. > France -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 20 08:23:31 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 20 Jan 2008 09:23:31 -0200 Subject: [ISCHEMIA-FORUM] 44C Variant angina. Dr. Message-ID: <47932F33.4060004@myocardial.ischemia-symposium.org> My comments: 1. Drug eluting stent. 2. longer than the spasm area, 3. CABG lyw660620 at sina.com > > Questions for Drs. Kaski, Juan Carlos, and Arroyo-Espliguero, Ram?n. > > Dear colleagues, > > In your outstanding lecture titled "Variant Angina", you state this: "The > implantation of stents could also be effective in patients with refractory > symptoms and mild to moderate obstructive CAD, in whom a vasospastic > arterial segment is identified, taking into account that most of the > patients with positive provocative test and recurring symptoms usually > present vasospasm located on the same arterial segment. However, the spasm > may recur in different segments, including multiple spasm." > > My questions are: > > 1- Would you advice the use of drug-eluting stents (DES) or bare-metal > stents (BMS)? > 2- In case of using drug-eluting stents, what length of stent do you > advice using regarding the length of the documented vasospastic segment? > 3- In the cases of vasospasm of the main trunk of the left coronary > artery in women, would you advice indicating an implant of stent or CABG? > > Thanking you in advance for your reply, > > Cordially, > > Dr. Gustavo R. Bonz?n > Resistencia, Chaco, Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 20 09:39:20 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 20 Jan 2008 10:39:20 -0200 Subject: [ISCHEMIA-FORUM] 48R Evoking coronary spasm. Dr. Vorotniak Message-ID: <479340F8.6040309@myocardial.ischemia-symposium.org> Dear Dr. Kaski, I would like to ask you a question about evoking coronary spasm: In Ukraine and Russia, to evoke coronary spasms in patients suspected of carrying variant angina, the "cold test" (??????????????) is often used: a bucket with frozen water is prepared, and the patient sinks his/her arms in it up to the elbows; simultaneously the ECG is recorded. When I proposed this method to my colleagues in Argentina (where I currently live), they thought it was too cruel. In your presentations you did not mention this test either. What do you think about it? Dr. Andriy Vorotniak -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 20 09:43:27 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 20 Jan 2008 10:43:27 -0200 Subject: [ISCHEMIA-FORUM] 49E Evoking coronary spasm. Dr. Kaski Message-ID: <479341EF.1040902@myocardial.ischemia-symposium.org> Dear Dr. Vorotniak, Thank you very much for your question. We used the cold test in the 80's, sometimes alone and other times more "sensitive" with hyperventilation. The problem of using is not in that the test is "cruel" but that it has a very low sensitivity. Ergonovine and hyperventilation are superior in this sense. I hope this commentary clarifies my position about the "cruel" cold test! Kind regards, JC Kaski Juan Carlos Kaski MD, DSc, FRCP, FESC, FACC Professor of Cardiovascular Science Director, Cardiovascular Biology Research Centre Division of Cardiac and Vascular Sciences St George's Hospital, University of London Cranmer Terrace, London SW17 0RE, UK Tel. No. + 44 208 725 5901/3963 Fax No. + 44 208 725 3328 -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 20 09:50:39 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 20 Jan 2008 10:50:39 -0200 Subject: [ISCHEMIA-FORUM] 50E Coronary spasm and VF. Dr. Skeberis Message-ID: <4793439F.4030903@myocardial.ischemia-symposium.org> Dear colleagues, Giving my opinion on the prophylactic implantation of an ICD in the patient of Dr Wasserman, I would say that his patient does not belong in any of the classes of the indications for ICDs. Additionally, if the patient has a EF >40% the ICD does not offer benefit. I can imagine that the EPS performed in a full protocol manner. Best regards to Dr Wasserman and the coordinators Vassilis Skeberis MD,FESC Thessaloniki Greece -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 20 10:52:46 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 20 Jan 2008 11:52:46 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASK, EXPERTS ANSWER Message-ID: <4793522E.50104@myocardial.ischemia-symposium.org> Dr. Ricardo Pizarro from Panama asks - Do know if in Latin America there are studies related to the Safety/Efficacy of antithrombotic/anticoagulant therapy, and if there are, are the results similar to those found in other parts of the world (USA and Europe)? Dr. Ricardo Pizarro Panam? ------------------------------------- Dr. Magda Heras from Spain answers - The answer to Dr. Pizarro's question is the following one: I ignore the existence of registries on the safety and efficacy of anti-thrombotic management in ACS, exclusive from South America. However, Argentina and Brazil participate with 7 and 6 hospitals, respectively, in the GRACE registry (http://www.outcomes-umassmed.org/GRACE/bibliography.cfm). The only publication that analyzes data from South America within the context of ACS, although taking into account a very special situation of the country, is: Gurfinkel EP, Bozovich GE, Dabbous O, Mautner B, Anderson F. Socio economic crisis and mortality. Epidemiological testimony of the financial collapse of Argentina. Thromb J. 2005;3:22. In a more general scenario, I would be surprised if there was any difference in efficacy and safety. In Spain we have good ACS registries (PRIAMHO and DESCARTES) that have shown us the same efficacy and safety than the ones obtained in other countries. You may consult such bibliography at: http://www.scisquemica.com/index.aspx?id=6 Kind regards, Dra. Magda Heras Cap de Secci? de Cardiologia Cl?nica ICT Hospital Cl?nic Villarroel, 170. 08036 Barcelona Tel 34 93 227 9305 Fax 34 93 451 4148 e-mail: mheras at clinic.ub.es -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 20 16:14:35 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 20 Jan 2008 17:14:35 -0200 Subject: [ISCHEMIA-FORUM] RE 23R Ventricular fibrillation. Dr. Yabluchansky Message-ID: <47939D9B.1080005@myocardial.ischemia-symposium.org> Dear Yuriy, Your question is interesting and, about another aspect: how to prevent lethal arrhythmias during thrombolysis? This type of arrhythmias develops as a result of a successful thrombolysis and the factors that influence on this process are the following ones: 1 The time from culprit artery occlusion to the onset of thrombolysis; 2 The size of the ischemic focus; 3 The time up to the reperfusion of the culprit artery. All this influences on the gradient of proarrhythmogenic substances, which migrate from the area of the infarction to the peri-infarction area. Indeed, this topic is developed in my presentation in this Symposium. Kind regards, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com > Dear colleagues, > My question is for all the participants in the Forum. > What management would you follow in a patient, who during the > treatment with > thrombolytic agents had an episode of ventricular fibrillation? > Electric cardioversion was conducted on this patient, successfully > reversing > to sinus rhythm. > Would you indicate endovenous amiodarone (loading and maintenance) and for > how long? > Would you indicate long-term treatment combined with beta-blockers and > amiodarone, or would you manage it in a conventional way (as a > post-infarction patient without ventricular arrhythmia)? > > Dr.Yuriy Kosolapov > Hospital de urgencias n?mero 2, > Ciudad de Novosibirsk, Russia. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 20 16:16:10 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 20 Jan 2008 17:16:10 -0200 Subject: [ISCHEMIA-FORUM] 31E Coronary spasm and VF. Dr. Wasserman Message-ID: <47939DFA.4000302@myocardial.ischemia-symposium.org> Dear Dr. Vanerio, My patient is not a smoker, neither active nor passive. Cordially, Dr. Faiwell Wasserman -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 20 17:16:56 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 20 Jan 2008 18:16:56 -0200 Subject: [ISCHEMIA-FORUM] 34S Commentary on a case. Dr. Pero Message-ID: <4793AC38.2030902@myocardial.ischemia-symposium.org> Recently we admitted a 47-year-old woman, dyslipidemic, with no family background, or other risk factors, still in a fertile age, that presented in a setting of emotional stress, nonirradiated retrosternal oppression with ST elevation in DI and aVL of 0.5 mm in both with troponin I of 3.7 for a normal value of 0.04 (CPK and MB were normal) in cineangiography. Left coronary trunk 45% of obstruction with lateral hypokinesis in the ventriculogram. 72 hours later NMR with provocation was normal, with no ischemia, with no infarction or other lesions. Dr. Simon Pero Tucuman - Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 20 17:23:03 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 20 Jan 2008 18:23:03 -0200 Subject: [ISCHEMIA-FORUM] 35P Extrasystole in Acute Infarction. Dr. Campodonico (f) Message-ID: <4793ADA7.9060200@myocardial.ischemia-symposium.org> A clinical study made by Dr. Ramirez in Brazil showed that the incidence and the clinical significance of ventricular extrasystoles (VE) in the hospital phase of acute myocardial infarction (AMI), studied in 43 patients admitted in the hospital, seven hours in average, after the onset of precordial pain symptoms; 21 had anterior wall infarction and 22 inferior wall infarction. The patients underwent electrocardiographic monitoring by 24 hs Holter at hospital admission (H1) and in the third (H2), sixth (H3), 12th (H4) and 18th (H5) days of in-hospital evolution; in H1 there was some VE in 95.3% of patients (90.5% of anterior wall and 100% of inferior wall infarction) and in H5, in 73% of them (58.8% of anterior wall and 85% of inferior wall infarction). On the other hand, from H2 through H5, most patients did not differ from the general population, as to the frequency of VE in 24 hours. There was a significant predominance between the results in H1 and H2. VE did not relate to the electrocardiographic location of infarction; the ejection fraction and the number of injured coronary arteries, both in the acute phase (H1) and in the hospital phase (H5). I would like to have the opinions of the colleagues, and mainly about the use of the High Resolution Electrocardiogram searching for late potentials. Dr. Sidney Campodonico Filho Prof. Cardiologia PUCRS Brasil -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 13:57:16 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 14:57:16 -0200 Subject: [ISCHEMIA-FORUM] RE 36S Ventricular fibrillation. Dr. Rivera Varas Message-ID: <4794CEEC.5030502@myocardial.ischemia-symposium.org> Dear colleague, I would only indicate amiodarone for this patient, if he does not respond to initial electric defibrillation; however, considering that he responded to defibrillation and remained in sinus rhythm, I would check if it is possible to administer beta-blockers cautiously (ruling out that there are no contraindications and according to Killip-Kimball's plan). Dr. Sergio David Rivera Varas -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 15:24:50 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 16:24:50 -0200 Subject: [ISCHEMIA-FORUM] 41S Long stents. Dr. Bonzon Message-ID: <4794E372.6070106@myocardial.ischemia-symposium.org> Dear Dr. Kaski, I dare to ask you about a specific issue, not approached in this Symposium, but which I'm sure that you are researching. Interventional cardiologists the implant drug eluting stents or DES, frequently face a problem: In the patients that have been successfully treated with a DES in the Proximal Anterior Descending Artery, we usually see that noninvasive tests in follow-up (especially the SPECT) yield positive results for apical ischemia (or in a greater territory) in the peak of maximal stress, but with no angina or ST deviation, that after the intervention no longer had it, and the findings of which are almost the same and repeat up to two years of follow up or more. These results lead us to perform many angiographies, the result of which is negative by intrastent restenosis. My questions for you are very concrete: 1- Don't you think that "long" stent implantation (28 or 32 mm) have a restrictive effect on the necessary vasodilation of the greater epicardial vessels in stress to achieve an appropriate perfusion of the myocardial territory in risk? 2- Do you think that the current recommendations about the appropriate length of DES could be objected? 3- What management do you consider appropriate for an asymptomatic patient that had no prior evidence of ischemia distal to the treated vessel and after the implantation of a "long" DES does show symptoms in a single functional test (SPECT), with angina or ST? These questions are addressed to a theory I have: the implantation of a stent limits the maximal vasodilating capacity of the major epicardial coronary vessel before the need of a greater regional perfusion due to stress. Do you agree? Cordially, Dr. Gustavo R. Bonz?n Resistencia, Chaco, Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 15:52:28 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 16:52:28 -0200 Subject: [ISCHEMIA-FORUM] RE 52S Ventricular fibrillation. Dr. Lanzas Rodriguez Message-ID: <4794E9EC.7040209@myocardial.ischemia-symposium.org> Dear colleagues, I agree with the opinion by Dr. Sergio David Rivera about not using amiodarone due to the fact of the patient having presented ventricular fibrillation during thrombolysis. If the acute event occured only then, later the conventional management should be followed: antiaggregation, beta-blockers, ACEI, statins. If clinically, the in-hospital evolution is satisfactory, and the echocardiographic study shows me a good ventricular function, I would not consider this patient as a candidate for management with Amiodarone. It would be different if post-thrombolysis, the evolution is different, with ventricular arrhythmias, clinical or echocardiographic data of ventricular dysfunction. I would use Amiodarone, and evaluate the need of coronary angiography before hospital discharge. Dr Roger A Lanzas Rodr?guez Cardi?logo Cl?nico Costa Rica. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 15:36:27 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 16:36:27 -0200 Subject: [ISCHEMIA-FORUM] 45R Cardiac X syndrome. Dr . Yabluchansky Message-ID: <4794E62B.3000902@myocardial.ischemia-symposium.org> About the commentary by Dr. Gaetano A.Lanza. We treat the patient, not the disease. Since many cardiac X syndrome patients have subclinical atherosclerotic disease, it would be wise to indicate aspirin in these patients. Yabluchansky Mykola (Nickolay ) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 15:41:08 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 16:41:08 -0200 Subject: [ISCHEMIA-FORUM] 46R Ventricular fibrillation. Dr. Yabluchansky Message-ID: <4794E744.2010802@myocardial.ischemia-symposium.org> I agree with Dr. Querencio Orlando. The probability of ventricular fibrillation during thrombolysis is increased; therefore, beta-blockers should be used to prevent it. The incidence of ventricular arrhythmias increases in late thrombolysis cases, of extensive infarction and successful reperfusion. All this is explained in my presentation in the Symposium. Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 16:00:50 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 17:00:50 -0200 Subject: [ISCHEMIA-FORUM] 53P Several answers. Dr. Brindeiro (f) Message-ID: <4794EBE2.2040008@myocardial.ischemia-symposium.org> Greeting for all the colleagues! The commentary by Dr. Pizarro about the usefulness of ECHO in emergency situations is very timely. The use of the test is quite useful to detect areas with contractile deficit to corroborate the diagnosis of AMI, but also to accompany and for the prognostic evaluation of the disease. Besides this, often it is also helpful to establish the differential diagnosis (for instance, aortic dissection, hypertrophic cardiomyopathy, etc.) being essential to establish an appropriate therapeutic management. In Brazil, in all States, there are Hospitals with Units of Chest Pain, and the Brazilian Society of Cardiology has Guidelines about this: 1) Units of Chest Pain. A modern form of management of patients with thoracic pain the Emergency Room. Arq Bras Cardiol, volume 79 (n? 2), 196-202, 2002; 2) I guideline for chest pain in the Emergency Room. Arq Bras Cardiol volume 79, (suplemento II), 2002; 3) Guidelines of the Brazilian Cardiology of Society about unstable angina and acute myocardial infarction without ST segment elevation. Arq Bras Cardiol 2007; 89(4) : e89-e131. Around three years ago, we conducted tests with portable devices ("the mountain goes to Mohammed") at the Alfa Hospital, here in Recife. Recently, in a patient in shock after PTCA and implantation of pharmacological stent, the Echo showed cardiac tamponade by pericardial bleeding. Note: there was no jugular protruding. As it was to be expected, after puncture, the patient went out of shock immediately. I would like to know, what is the frequency with which this condition occurs and is diagnosed? Sincerely, Djair Brindeiro Filho Recife - Brasil. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 16:37:06 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 17:37:06 -0200 Subject: [ISCHEMIA-FORUM] 58E Culprit Coronary Artery. Dr. Bayes de Luna, Fiol and Carrillo Message-ID: <4794F462.3090506@myocardial.ischemia-symposium.org> Answer to Dr. Madias Dear Collegue, We believe that in most of cases the ratio Sum of ST-segment elevation in precordial leads/ Sum of ST-segment depression in inferior leads is not useful in clinical practice because the most important differences between patients with proximal vs. distal LAD were observed in inferior leads. The value of ST analysis in inferior leads in anterior MI to diagnose proximal (ST depression in inferior leads) versus distal LAD occlusion (ST elevation) have been previously reported . However, in all these studies only one separate criteria were considered, and in this paper (Fiol et al Clin Cardiol, 2008) our aim is to establish sequential algorhythm that predict the place of occlusion in LAD and that may be easy to perform in clinical practice. We agree with Dr. Madias that ST-segment elevations (and consequently the reciprocal ST-depressions) mostly decreasing after clinical presentation. We recommended to value the first ECG recorded at admission. Sincerely Drs. A Bayes de Luna, M Fiol and A Carrillo -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 16:43:26 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 17:43:26 -0200 Subject: [ISCHEMIA-FORUM] 59E Ventricular fibrillation. Drs Bayes de Luna, Fiol and Carrillo Message-ID: <4794F5DE.1020002@myocardial.ischemia-symposium.org> Answer to Dr. Kosolapov and Dr Orlando Dear Collegues, The incidence of primary ventricular fibrillation in patients admitted to Coronary Care Unit with ACS has decreased significantly (2-3%) due to the new therapies employed, though it is still higher in more compromised patients (Killip 1:<1%, Killip 3-3:> 4%). The ventricular fibrillation in the setting of acute myocardial infarction in the first 6-hours from onset of symptoms, successfully reversed to sinus rhythm have a good prognosis and we manage it in a conventional way. Only the ventricular fibrillation that occurs in the course of anterior infarction has subsequent negative prognostic implications (Schwartz et al, AJC 1985). When the ventricular fibrillation is recurrent (arrhythmia storm) we indicate endovenous amiodarone (loading dose of 300 mgr followed by maintenance dose of 1200 mgr a day during 3-4 days). There is not evidence that ventricular fibrillation is a reperfusion arrhythmia but probably is a non-reperfusion arrhythmia and is indicated quickly reperfusion treatment (thrombolysis or angioplasty). Dates from TIMI phase II trial (Berger PB et al JACC 1993;22:1773-1779) indicated that the ventricular fibrillation is associated with occlusion of the culprit coronary artery. We have observed (Fiol at al AJC 1993) that once the patient is in the hospital, ventricular fibrillation occurs particularly in presence of: - ST-segment elevation higher than 10 mm - Fast basic heart rate (Adgey et al BHJ 1982) (in absence of any evident contraindication, should be corrected with beta-blocker agents) - Hypotension - Persistence of pain - R-on-T phenomenon before reperfusion We agree with the comments from Dr. Pellizon and Dr. Yabluchansky Sincerely Drs. A. Bayes de Luna, M Fiol and A Carrillo -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 16:54:43 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 17:54:43 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASK, EXPERTS ANSWER Message-ID: <4794F883.4040501@myocardial.ischemia-symposium.org> Dr. Alfredo Piombo from Argentina asks - In order to analyze coronary reperfusion by ECG, is it better to take the lead with the greatest depression or the sum of ST in all leads? ------------------------------------- Dr. Ben Scirica from USA answers - That is a good question. Taking the sum of ST in all leads is the most complete way to assess resolution, but clinically, it is reasonable and easiest to choose the lead with greatest ST elevation and calculate the resolution from that lead. You can see the paper by Cooper HA (Am Heart J. 2002 Nov;144(5):790-5) Best regards Ben Scirica -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 17:03:06 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 18:03:06 -0200 Subject: [ISCHEMIA-FORUM] 54S 75-year-old woman with prolonged precordial pain. Dr. Pizarro Message-ID: <4794FA7A.4000100@myocardial.ischemia-symposium.org> Greetings for everyone! Dear Dr. Magda Heras, Thank you very much for the addresses you sent; they are very good; congratulations for the Studies made in Spain. About the conclusions of the DESCARTES study, it seems that they are repeated in other parts of the world, with the corresponding warning to improve (more aggressively?) management (of NSTEMI). This is the reason why I presented the case of a 75-year-old woman that I saw a few days ago at the ER where I work, and who presented with history of 3 hours and 20 minutes of chest oppression (she referred the feeling of chest oppression (of mild intensity), which on occasions she described as "chest tiredness" but that was constant). 1st episode: she takes pediatric ASA, 1 pill per day, isosorbide dinitrate 10 mg orally twice a day, and other medication about which she couldn't remember the name, and her cardiologist had told her the year before that she suffered of coronary ischemia; as background: her husband had died 15 days ago, and she lived alone. I applied O2, sublingual nitroglycerin and ASA 325 mg orally, as the ACLS states, and I didn't apply morphine because I didn't interpret her "chest oppression" as a severe pain; I placed cardiac monitoring, of blood pressure (160/80, and she said that her BP usually was 130/80) and pulse oximeter (99%). I obtained samples for hematic biometry, blood chemistry (glycose, creatinine, urea level, Na+, K+, Ca++, CPK, CPKMB and Troponin T), and all resulted within normal limits; the patient improved the symptoms more or less in 30 minutes, and of course I performed an ECG at admittance, and another one approximately 2 hours later, with very similar results (almost the same). I attach the first ECG****, in which I seem to observe ST depression in 8 leads (DI, DII, aVL, V2 through V6) and ST elevation in aVR and V1. So, could you consider a circumferential involvement that would correspond to 3-vessel disease or left coronary trunk (LCT) subocclusion. Further, if the T wave is negative in V4-V6, it is usually LCT. I know this from the book (Basic Electrocardiography, 2007) by the excellent Master Dr. Antoni Bayes de Luna, with whom I would be very grateful if he could clarify this tracing, as he is participating as Faculty in this great symposium; moreover, I would be grateful if you could comment on the subsequent management, once you obtain the information I have just sent. Thank you very much, Dr. R. Pizarro. PS: I have no more data about the patient. DOWNLOAD THE ECG in PDF format (2.5 Mb) http://lists.ischemia-symposium.org/files/Pizarro1.pdf -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 17:05:40 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 18:05:40 -0200 Subject: [ISCHEMIA-FORUM] 57R Ventricular fibrillation. Dr.Yabluchansky Message-ID: <4794FB14.6070304@myocardial.ischemia-symposium.org> Dear Dr. Oscar Pellizon, I would like to draw your attention to dogs, in which there is significant anastomosis between the anterior and posterior descending arteries. Therefore, to evoke a true ischemia, it is necessary to ligate the anterior descending artery in 2 sites. In my presentation in this symposium, the factors that influence reperfusion are mentioned, as well as our work on this. Best regards, Dr. Nikolay Yabluchansky -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 21 19:36:04 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 21 Jan 2008 20:36:04 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASK, EXPERTS ANSWER Message-ID: <47951E54.8080200@myocardial.ischemia-symposium.org> Dr. Andriy Vorotniak from Russia and Argentina asks - For Dr. Perez Riera or Dr. Bayes de Luna, About ECG changes, related to the climacteric. In the climacteric period or in hormone disorders, ECG changes are often observed, that are similar to ischemic heart disease (T wave flattened or negative in V1-V4). In these cases the test with propranolol (very economic) is useful. Currently, the test with propranolol is virtually not used. And women with climacteric symptoms and ST-T changes in V1-V4 are managed as the rest of the patients with suspicion of coronary artery disease, which adds costs and makes patients undergo studies that sometimes are unnecessary (myocardial perfusion, cineangiography, etc.) Shouldn't the management of women with characteristic climacteric symptoms and ST-T changes in V1-V4 be less complex? ------------------------------------- Dr. Andres Perez Riera from Brazil answers - Dear Dr. Andriy Vorotniak from Russia: Even though gender-specific differences in ventricular repolarization have gained wide recognition, the underlying mechanisms remain unknown. Information is limited about the independent prognostic value of repolarization abnormalities in women. Ventricular repolarization abnormalities in postmenopausal women are important predictors of Coronary Heart Disease (CHD) events and CHD mortality as ECG myocardial infarction (ECG-MI) and other QRS abnormalities(1). The following features are considered important predictors: 1) Wide QRS/T angle and ECG-demonstrated ECG-MI are the strongest predictors of CHD events 2) Wide QRS/T angle, ECG-MI, and QT prolongation appeared as dominant predictors when evaluated simultaneously with other ECG variables in a multiadjusted risk model 3) QRS/T angle, ECG-MI, and high QRS nondipolar voltage are the strongest predictors of CHD mortality 4) Five ECG abnormalities are identified as dominant mortality risk predictors: a) WIDE QRS/T ANGLE b) ECG-MI c) HIGH QRS NONDIPOLAR VOLTAGE d) REDUCED HEART RATE VARIABILITY (HRV) e) QT PROLONGATION. Estrogen hormones may represent a causative factor for the changes in ventricular repolarization in women. Estrogen Replacement Therapy (ERT) causes alterations in ventricular repolarization dynamics without significantly affecting the autonomic nervous tone. The QT/RR regression slope increased by 93% in the ERT. The variability of RR and QT intervals do not change. CAD is frequent in postmenopausal women. Myocardial ischemia has been induced with stress testing, and a relationship between endothelial dysfunction and perfusion defects has been reported. Female gender and hormonal status affect ECG response to exercise. Both are often cited as factors contributing to the decreased diagnostic accuracy of exercise stress tests in women (2). Peix et al (3) studied 59 postmenopausal patients were each underwent technetium-99m methoxy-isobutyl-isonitrile myocardial scintigraphy (protocol: exercise stress-rest), brachial artery endothelial function measured by ultrasonography, lipidogram, and 24-h Holter. Group I: 21 patients showed perfusion defects in myocardial scintigraphy and Group II: 38 patients did not. Group I patients exhibited endothelial dysfunction more frequently (57 vs. 29%) than those of group II. Among group I patients, 12 showed a reversible perfusion defect that, in 75% of the cases, was associated with poststress LVEF reduction greater than 5% and a regional hypokinesis. 9 patients had fixed defects, which in 56% of the cases were associated with poststress LVEF reduction greater than 5%. LVEF poststress minus LVEF at rest was -5.2% in group I patients versus -1.8% in group II. 3 patients in group I showed evidence of ischemia by Holter compared with four in group II. Stress-induced ischemia is associated with poststress LVEF reduction in postmenopausal women with typical angina, normal coronary angiography, and a trend toward abnormal endothelial-mediated vasodilation. Weissman et al (4) analyzed the ECG response to exercise in female patients who underwent symptom-limited exercise stress testing over a 12-month period with no evidence of ischemia on SPECT myocardial perfusion imaging (N = 404). Hormonal status was defined as: 1) Premenopausal (n = 78); 2) Postmenopausal (n = 277); 3) Postmenopausal on ERT (n = 49). Positive ECG response for ischemia was defined as 1 mm or greater horizontal and/or downsloping ST depression during and/or after exercise. The frequency of a positive ECG response to exercise without evidence of ischemia on gated SPECT imaging was analyzed according to hormonal status. Seventeen of 78 premenopausal women (22%), 48 of 277 postmenopausal women (17%), and 19 of 49 women taking ERT (39%) had a positive ECG response. ECG positivity was significantly higher in ERT users when compared with premenopausal and postmenopausal women. ERT therapy affects ST-segment response to exercise, likely through a nonischemic mechanism. Unless ERT therapy can be discontinued for a prolonged period of time (up to 6 weeks) prior to a stress test, myocardial imaging should be used to improve diagnostic accuracy. Heart rate variability showed no statistically significant changes in the time, frequency or complexity measurements either before or following cessation of ERT in healthy postmenopausal women (5). Sleep affects the RR interval in ECG recordings and ventricular repolarization differentially in men and women. Compared to men, pre-menopausal women have a more pronounced shortening of RR interval and prolongation of QT and QTc ECG waves during rapid eye movement sleep. Sleep-related RR and QT changes in women are not altered by menopausal status or by post-menopausal ERT and progesterone (6). Most frequent risk factors in a group of 40 premenopausal women with history of MI were smoking (70%) and hypertension (62.5%). Reaction to bicycle exercise tests was negative in 42% and ischemic (mainly pain combined with ST-segment changes) in 50% of these women. Ischemic ECG changes were found during both exercise test and 24-hour Holter in 30% and were not found at all in 40% of women. Angiography revealed coronary artery stenosis in 58% of women (7). References 1) Rautaharju PM, Kooperberg C, Larson JC, LaCroix A.Electrocardiographic abnormalities that predict coronary heart disease events and mortality in postmenopausal women: the Women's Health Initiative. Circulation. 2006; 113: 473-480. 2) Vrtovec B, Starc V, Meden-Vrtovec H. The effect of estrogen replacement therapy on ventricular repolarization dynamics in healthy postmenopausal women. J Electrocardiol. 2001; 34: 277-283. 3) Peix A, Garc?a EJ, Valiente J, et la. Ischemia in women with angina and normal coronary angiograms. Coron Artery Dis. 2007; 18: 361-366. 4) Henzlova MJ, Croft LB, Diamond JA. Effect of hormone replacement therapy on the electrocardiographic response to exercise J Nucl Cardiol. 2002; 9: 385-387. 5) Weissman A, Lowenstein L, Porat M, Geva A, Rosenstein Y.The effect of hormone replacement therapy cessation on heart rate variability in postmenopausal women. Clin Auton Res. 2005; 15: 411-413. 6) Lanfranchi PA, Gosselin N, Kara T, et al. Menopause, hormone replacement and RR and QT modulation during sleep. Sleep Med. 2005; 6: 561-566. 7) Svistov AS, Galiullina RKh, Obrezan AG. Risk factors of ischemic heart disease, data of exercise tests, 24-hour ECG monitoring and coronary angiography in young women with history of myocardial infarction Kardiologiia. 2003; 43: 54-58. All the best Andr?s Ricardo P?rez Riera MD -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 22 11:19:04 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 22 Jan 2008 12:19:04 -0200 Subject: [ISCHEMIA-FORUM] 51S Several replies Dr. Bonzon Message-ID: <4795FB58.40709@myocardial.ischemia-symposium.org> Dear Dr. Pizarro, Regrettably, I have to disagree with you in most aspects. The echocardiogram (and I speak of transthoracic and transesophageal color Doppler echocardiogram, I reject any other) in the ER of a Hospital with Cardiology Service, should available the 24 hs of the 365 days of the year. The usefulness that supports this statement is overwhelming. If we have such an easy and rapid study, that is noninvasive, in the ER proper or in Intensive Care, we not only can detect early disorders of segmentary relaxation or contraction that contribute information that serial ECG or lab tests will not provide as soon, but we can also dismiss many other things, such as: ischemic dysfunction of the papillary muscle, aortic dissection, etc. In this discussion Forum we have been reading many of the authors of the AHA/ACC and ESC guidelines on ACS. It would be appropriate, according to my modest point of view, for us to stop this discussion between both of us, and let's yield the floor to them about why they did not include obligatorily such useful and economic tool in the guidelines that nowadays rule the management of cardiologists all over the world. Having an ECHO available in experienced hands 24 hs in the center where I work, has enabled us to reduce the door-to-balloon time from more than 60 to 90 minutes, to 40 to 20 minutes, according to the case (clinical state, echographic window, etc.) with the subsequent better evolution for all our patients with "doubtful AMI". And if this occurs in a small city of the interior of Argentina, it should happen with much better results than ours in the best centers of the world. I think the issue is of such significance, as for Dr. Bassand to pose a IIa indication, Level C of Evidence, at least, in the future Guidelines 2008 of the ESC. About the indication of thrombolytic agents or of primary angioplasty or direct of infarction, I cannot express my opinion, considering that since 1993 we no longer use thrombolytic agents in our center. All of our patients with infarction receive angioplasty. I cannot express my opinion on drugs that I haven't been using or indicating for 15 years, since angioplasty has proven an overwhelming superiority on thrombolytic agents. Best regards, Dr. Gustavo R. Bonz?n Resistencia, Chaco, Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 22 11:24:24 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 22 Jan 2008 12:24:24 -0200 Subject: [ISCHEMIA-FORUM] 55P Extrasystole in Acute Infarction. Dr. Perez Riera Message-ID: <4795FC98.1000602@myocardial.ischemia-symposium.org> Dear colleague, Dr. Sidney Campodonico Filho, High resolution ECG may have a concrete indication in post-AMI patients to stratify the risk this way: a) In patients that suffered AMI, the method should be used between the sixth and thirtieth day after the event, because this is the range with greater probability to detect late potentials (LP). LPs are present in 80% of the cases of patients with S-VT and/or induced, and only in 10% of patients without VT. b) In inferior wall or infero-latero-dorsal infarctions, high resolution ECG is more efficient to predict S-VT occurrence than in anterior or antero-septal infarctions. The phenomenon is explained, because infero-lateral and infero-basal segments activate late, and thus, late potentials are sensed more easily, while when the areas of slow activation are located in regions of early activation (anterior wall) they may be concealed in the QRS (Buxton, A. E. et. al. J. Electrocardiol. 540-5,1988). c) Infarcted patients managed with thrombolytic agents, showed a lower incidence of positive high resolution ECG than those treated conventionally: 5% versus 23%, which is due to less infarcted mass (Gang, E. S. et. al. N. Eng. J. Med.321:712-6, 1989). This verification was confirmed later by other authors (Tranchesi, B. et . al. Am . J. Cardiol. 66:1196-8, 1990). Risk stratification in patients with complex ventricular arrhythmias: High resolution ECG in arrhythmogenic RV dysplasia is positive in 80% of the cases. In this entity, NS-VT or S-VT has LBBB morphology: right VT. It is altered nearly always (positive); however, it could be normal in the forms located in patients with VT. The sensitivity of the method would be around 85% (Leclercq, J. F. e col.; Ann. Cardiol.Angeiol.39:281-5, 1990). Kinoshita et al (Circulation, 91:715-21,1995) observed an improvement of sensitivity maintaining the specificity, combining it to analysis by time and frequency domain. The typical elements of the method are characterized by late potentials, which mean slow and heterogeneous conduction area. It is useful for the differential diagnosis between patients with RV dysplasia and those without structural heart disease with RVOT VT, with LBBB morphology or catecholamine-sensitive. High resolution ECG is indicated in special cases (potentially malignant ventricular arrhythmias, or malignant with hemodynamic involvement), and with the suspicion of S-VT not recorded, and it may reveal late potentials of low amplitude and high frequency filtered at the end of QRS (Grimm, W. e col.; ANE2:20-26, 1997) that is usually more emphasized in the dilated forms with coronary origin. It has a great negative predictive value (95% to 99%); i.e. in the absence of late potentials of low amplitude and very high frequency, in the final portions of the QRS complex, related to fragmented and delayed electric activity of the ventricles, potentially malignant arrhythmias will hardly appear, and a low positive predictive value (15% to 25%), i.e. in the presence of late potentials, the probability of appearance of fatal ventricular arrhythmias is not so high. Research of patients with syncope with unknown origin. The method could be useful as a guide to indicate invasive electrophysiologic study in those patients where S-VT is suspected, that is not documented yet (concealed VT); however, with III or IV clinics (pre-syncope, syncope and/or cardiac arrest). In patients with syncope and carriers of heart disease, the probability of being secondary to S-VT is around 33%. In such cases, mortality is 30% in 18 months. In absence of structural heart disease, mortality is 6% in this period (Vatterot, P. J. et. al. Mayo Clin Proc. 63:931-42, 1988). The absence of positive high resolution ECG in patients with syncope and heart disease does not rule out invasive study. In brief: Indications of high resolution ECG 1) Risk stratification in patients with NS-VT and/or complex premature ventricular contractions. In such cases, a positive high resolution ECG indicates positive predictive value for sudden cardiac death. High resolution ECG has the capacity to predict inducibility in invasive electrophysiologic study (EPS). Thus, inducibility in this study is more frequent in patients that has positive high resolution ECG and require treatment. 65% of patients with positive high resolution ECG, i.e. with late potentials (LP) and NS-VT showed inducibility in EPS; while only 10% of the patients with NS-VT in Holter and negative high resolution ECG showed inducibility in EPS (Turito, G et. al. Am. J. Cardiol.61:1272-8, 1989). 2) Risk stratification in patients with complex ventricular arrhythmias, frequently in: a) Nonischemic dilated cardiomyopathy; b) Arrhythmogenic RV dysplasia: in this entity, high resolution ECG is positive in more than 80% of the cases; c) Brugada syndrome (Ikeda T, Sakurada H, Sakabe K, Sakata T, Takami M, Tezuka N, Nakae T, Noro M, Enjoji Y, Tejima T, Sugi K, Yamaguchi T.: Assessment of noninvasive markers in identifying patients at risk in the Brugada syndrome: insight into risk stratification. J Am Coll Cardiol 2001 May;37(6):1628-34). d) Hypertrophic cardiomyopathy. e) Chagas disease. High resolution ECG is very useful for: 1) Evaluation of efficacy obtained in surgery of refractory TV. E.g.: foreseeing surgical results of aneurysmectomy in patients with S-VT. 30% of the patients that underwent surgery of refractory VT, normalized high resolution ECG and it was no longer possible to induce arrhythmia in the electrophysiologic study (Hat?m, D. M. et. al. Arq. Bras. Cardiol. 60:5; 357-360, 1993); 2) Investigation of patients with syncope with unknown origin; 3) Identification of patients tending to crises of acute atrial fibrillation: filtered P waves with total duration superior to 135 ms, indicate a tendency to develop this arrhythmia. Best regards for everyone, Andr?s Ricardo P?rez Riera Chefe do setor de eletro-vetorcardiografia da Faculdade de Medicina do ABC Santo Andr? S?o Paulo Brasil -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 22 11:42:50 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 22 Jan 2008 12:42:50 -0200 Subject: [ISCHEMIA-FORUM] 60E High heart rate and ST elevation. Dr. Peter Stone Message-ID: <479600EA.3010803@myocardial.ischemia-symposium.org> Dear Dr. Doval, Your question is a very important one. The answer is in large part based on whether a previous transmural MI is present in a particular myocardial wall, what happens to LV wall motion with an increased heart rate, and a distinct biophysical relationship that if the LV chamber becomes enlarged there is an increase in ST segment elevation. In the setting of a normal heart, as heart rate increases, presumably from sympathetic drive, LV ejection fraction increases and LV volume decreases. In the setting of a wall motion abnormality related to prior MI, however, increased HR and sympathetic drive leads to LV wall expansion in that area of prior MI, EF does not increase (and may even decrease), and LV volume therefore increases. This increase in LV volume leads to ST segment elevation in the areas where the baseline LV wall motion abnormality is located, through this biophysical relationship noted above. That relationship between changes in HR and changes in LV volume is the foundation of the previous clinical use of exercise EF to diagnose CAD by radionuclide ventriculography: if LVEF increased by 5% then CAD was not present, but if LVEF does not increase or actually decreases then CAD is present. This phenomenon of heart-rate associated ST segment elevation is routinely seen during exercise testing in patients with a prior MI and wall motion abnormality in that area (Chahine, et al. Circulation 1976; 54:209). If exercise-induced ST elevation occurs in the area of a prior MI it is of no significance, but if it occurs in the setting of a normal heart the finding is extremely ominous for the presence of severe and extensive CAD. Thank you, Peter -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 22 14:10:34 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 22 Jan 2008 15:10:34 -0200 Subject: [ISCHEMIA-FORUM] 61S Safety/efficacy of antithrombotic/anticoagulation therapy. Dr. Mautner Message-ID: <4796238A.20900@myocardial.ischemia-symposium.org> As a reply to Dr. Pizarro's question, and beyond the accurate quotation by Dr. Magda Heras from our publication: "SOCIO ECONOMIC CRISIS AND MORTALITY. EPIDEMIOLOGICAL TESTIMONY OF THE FINANCIAL COLLAPSE OF ARGENTINA.- Gurfinkel EP, Bozovich GE, Dabbous O, Mautner B, Anderson F. Thrombosis Journal 2005; 3: 22 (Electronic version. doi:10.1186/1477-9560-3-22 ", I have selected from my CV some references about our general contributions, usually linked to the TIMI and GRACE groups (Group 1) and other specific ones from Argentina and neighboring countries (Group 2), evidently and mainly based on our local experience, from which the most important one indicating the basic differences of morbi-mortality and discussing their causes in the different aspects of ACS (in this case without ST elevation) is the following one: 197- INTERNATIONAL COMPARISON OF MORTALITY RATES IN PATIENTS WITH NON-ST ELEVATION ACUTE CORONARY EVENTS.- Gurfinkel EP, Bozovich G, Mautner B.- Heart 2003; 89: 1083-1084 Group 1: 121- MORTALITY, MORBILITY, RESOURCE USE AND QUALITY OF LIFE FOLLOWING Q- vs. NON-Q-WAVE INFARCTION AND THROMBOLYTIC THERAPY: A GUSTO-1 SUBSTUDY.- Barbagelata, A.; Califf, R.M. Sgarbossa, E.B..; Goodman, S.; Knight, D.; Mark, D.B.; Granger, C.B.; Benazzi, M.D.; Calvo, A.; Gates, K.; Agranatti, D.A.; Starr, S.; Song, Q.; Mautner, B.; Wagner, G.S.- J Am Coll Cardiol 1997; 29: 490A (Abstract) 126- A COMPARISON OF LOW MOLECULAR WEIGH HEPARIN WITH UNFRACTIONATED HEPARIN FOR UNSTABLE CORONARY ARTERY DISEASE.- Cohen, M. et al. For the Efficacy and Safety of Suctuaneous Enoxaparin in Non-Q-Wave Coronary Events Study Group (Mautner, B. et al.) N Engl J Med 1997; 337: 447-52 147- RATIONALE FOR THE MANAGEMENT OF CORONARY SYNDROMES WITH LOW MOLECULAR-WEIGH-HEPARINS.- Gurfinkel, E.; Fareed, J.; Antman, E.; Cohen, M.; Mautner, B. Am J Cardiol 1998; 82 (5B): 15L-18L 168- ENOXAPARIN IS SUPERIOR TO UNFRACTIONATED HEPARIN REGARDLESS OF aPTT RANGE ACHIEVED: A TIMI 11B SUBSTUDY.- Bozovich, G.; Gurfinkel, E.; Antman, E.M.; Colorio, C.; McCabe, C.H.; Mautner, B.- J Am Coll Cardiol 1999; 33: 352A (Abstract) 169- TREATMENT BENEFIT WITH ENOXAPARIN IN UNSTABLE ANGINA IS GREATEST IN PATIENTS AT HIGHEST RISK: A MULTIVARIATE ANALYSIS FROM TIMI 11B.- Bernink, P.J.L.M.; Antman, E.M.; McCabe, C.H.; Papuchis, T.H.G.; Mautner, B.; Corbalan, R.; Braunwald, E.- J Am Coll Cardiol 1999; 33: 352A (Abstract) ---- Group 2: 135- NON WEIGH ADJUSTED BOLUS AND INFUSION OF STANDARD HEPARIN REGARDING SAFETY AND EFFICACY DURING THE ESSENCE STUDY.- Gurfinkel, E.; Duronto, E.; Manos, E.; Dos Santos, A.; Mejail, I.; Mautner, B.- Puerto Rico Health Sciences J 1997; 16 (A): 29 (Abstract) 169- REDUCCION DE LA TASA DE REVASCULARIZACION Y COSTOS HOSPITALARIOS EN PACIENTES CON SINDROMES AGUDOS CORONARIOS TIPO NO-Q TRATADOS CON ENOXAPARINA EN COMPARACION CON HEPARINA NO FRACCIONADA EN LA ARGENTIN Y URUGUAY.- Bozovich, G.E.; Gurfinkel, E.P.; Kuster, F.; L?pez, F.; Aon, G,; Belardo, H.; Mautner, B.- Rev Arg Cardiol 1999; 67: 131-36 171- REDUCTION OF HOSPITAL COSTS FOR PATIENTS WITH ACUTE NON-Q-WAVE MYOCARDIAL INFARCTION OR UNSTABLE ANGINA TREATED WITH ENOXAPARIN COMPARED WITH STANDARD HEPARIN.- Bozovich, G.; Gurfinkel, E.; Barreiro, D.; Kuster, F.; L?pez, F.; Mautner,B.- Eur Heart J 1999; (Abstract) 173- LA ENOXAPARINA ES MAS EFICAZ QUE LA HEPARINA NO FRACCIONADA INDEPENDIENTEMENTE DEL RANGO DE ANTICOAGULACION EN EL ESTUDIO TIMI-11B.- Bozovich, G.; Gurfinkel, E.; Colorio, C.; Antman, E.; McCabe, C.; Mautner, B. Rev Arg Cardiol 1999; 67 (SIII): 24 (Abstract)173- 174- RATIONALE FOR THE MANAGEMENT OF CORONARY SYNDROMES WITH LOW- MOLECULAR-WEIGHT HEPARINS.- Gurfinkel, E.; Mautner, B.- Review Series: Cardiology 1999; 3: 2-7 217- SE NECESITAN NUEVOS SCORES PRONOSTICOS EN PACIENTES CON SINDROMES CORONARIOS AGUDOS CON SUPRADESNIVEL DE ST, LUEGO DE LOS AVANCES DEL TRATAMIENTO FARMACOLOGICO Y MECANICO?- Duronto E, Gurfinkel E, Guellroy F, Mautner B . Rev Arg Cardiol 2006; 74:(Supl.3): Abstract 230 As a general comment, I would like to highlight that the local results have been similar but no the same as the international ones, which has different aspects that we have analyzed and discussed in the mentioned publications and in some exchanges with colleagues by means of readers' letters in international journals, which I did not consider necessary to quote here. Sincerely, Prof. Dr. Branco Mautner Jefe Departamento Docencia e Investigaci?n Fundaci?n Favaloro Director de la Carrera de Especialista en Cardiolog?a Universidad Favaloro -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 22 14:05:31 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 22 Jan 2008 15:05:31 -0200 Subject: [ISCHEMIA-FORUM] 63P Revascularization of patients with positive functional tests for ischemia and stable angina. Dr. Souza Message-ID: <4796225B.40801@myocardial.ischemia-symposium.org> Dear colleagues, My gratefulness and congratulations for the organizers of this interesting virtual meeting. My question is for all the participants. I would like to know if the clinical practice of you, my colleagues, has changed after the COURAGE study. It is an interesting study. Below I include the reference and the inclusion and exclusion criteria of the study. Imagine a patient with class II angina according to the Canadian Cardiovascular Society, ejection fraction 40%, lesion of anterior descending branch immediately after the first septal branch and lesion of the right coronary artery in the middle third, both of 75% and where percutaneous revascularization surgery is possible. Scintigraphy with small area of apical ischemia. Would you indicate percutaneous revascularization? Thanks for all of you and congratulations for the event, Marcos Optimal Medical Therapy with or without PCI for Stable Coronary Disease. Boden WE, O'Rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk WJ, Knudtson M, Dada M, Casperson P, N Engl J Med 356:1503, April 12, 2007. Entry criteria included: stenosis of at least 70% in at least one proximal epicardial coronary artery and objective evidence of myocardial ischemia (substantial changes in ST-segment depression or T-wave inversion on the resting electrocardiogram or inducible ischemia with either exercise or pharmacologic vasodilator stress) or at least one coronary stenosis of at least 80% and classic angina without provocative testing. Exclusion criteria included: persistent CCS class IV angina, a markedly positive stress test (substantial ST-segment depression or hypotensive response during stage 1 of the Bruce protocol), refractory heart failure or cardiogenic shock, an ejection fraction of less than 30%, revascularization within the previous 6 months, and coronary anatomy not suitable for PCI. Dr. Marcos R. de Sousa Cardiologista Telefone 3295-6695 e-mail: sousa.mr at uol.com.br home page: http://socios.cardiol.br/visualizar.asp?pasta=mrsousa home page: http://lattes.cnpq.br/8829182259961301 home page: http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4707401P9 AV. DO CONTORNO, 9636, SALA 1607 BAIRRO BARRO PRETO. (31) 3295-6695 CEP 30.110-140 -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 22 14:11:58 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 22 Jan 2008 15:11:58 -0200 Subject: [ISCHEMIA-FORUM] 64S Safety/efficacy of antithrombotic/anticoagulation therapy. Dr. Alvarez Acevedo Message-ID: <479623DE.7090700@myocardial.ischemia-symposium.org> Drs. Pizarro and Heras, Greetings. I inform you that in Cuba, a multicentric study was conducted in more than 20 hospitals, using Cuban recombinant streptokinase as thrombolytic agent in 1996, in Acute Coronary Syndrome, especially in AMI with Q wave, in less than 8 hours with good results. Let me inform you as well, that the Cuban Center of Engineering and Biotechnology manufactures this recombinant thrombolytic agent. Just for your information. Thank you, Prof Eduardo Alvarez Acevedo Cardi?logo -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 22 14:27:50 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 22 Jan 2008 15:27:50 -0200 Subject: [ISCHEMIA-FORUM] 65C: Ventricular False Chordae Tendineae and heart function- Dr Gao Jianxin Message-ID: <47962796.6010908@myocardial.ischemia-symposium.org> Dear Colleagues Does the Ventricular False Chordae Tendineae influence the heart function? Why murmurs could be found for the infant with Ventricular False Chordae Tendineae? Why some youth may feel palpitation when they have Ventricular False Chordae Tendineae? Best regards Gao Jianxin gaojianxin4908 at 126.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 22 14:29:58 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 22 Jan 2008 15:29:58 -0200 Subject: [ISCHEMIA-FORUM] 66S Premature ventricular contraction in the elderly. Dr. Ruiz Message-ID: <47962816.9060407@myocardial.ischemia-symposium.org> Dear friends, This is the chance to send my most sincere and special congratulations for such masterful symposium, which has clarified many doubts and in turn, has updated us in many managements to follow. My concern is: I have a 75-year-old patient that for 20 years has been experiencing premature ventricular contractions, which on occasions reached up to 20-25 per minute, on occasions independent and on others coupled. On a certain occasion, he showed bigeminy and even trigeminy. This anomaly could be corrected perfectly with the administration of propafenone (rytmonorm). I would like to know what could be the etiology of this manifestation, if in fact it could be post-coronary spasms and/or premature contractions by ectopic foci. Of note, none of the studies (stress test, echocardiogram, Holter) showed significant traits as the coronary disease. What could be the management then, and prognosis as well. Thank you very much for your attention, Jorge Ruiz M. D. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 22 18:34:14 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 22 Jan 2008 19:34:14 -0200 Subject: [ISCHEMIA-FORUM] 62R Premature contractions in AMI. Dr. Yabluchansky Message-ID: <47966156.2020001@myocardial.ischemia-symposium.org> Dear Dr. Sidney Campodonico Filho, Please, clarify the following part of your comment on premature contractions: 1. First, you mention that in group H5, 73% of patients had premature contractions; 2. On the other hand, in most patients from the groups from H2 through H5, the incidence of premature contractions did not differentiate from the general population; 3. However, group H5 was included between H2 through H5. What is it then? Kind regards, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 22 19:00:51 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 22 Jan 2008 20:00:51 -0200 Subject: [ISCHEMIA-FORUM] 69E Revascularization of patients with positive functional tests for ischemia and stable angina. Dr. Medeiros Message-ID: <47966793.4020907@myocardial.ischemia-symposium.org> I would like to thank the Organizers the opportunity to participate in this interesting virtual medical event. In relation to the comment of the Dr. MARCOS SOUSA on COURAGE trial effects in the cardiovascular practice around the world, there is no doubts that nothing else will be as it was before. The studies TIME and MASS (multiarterial disease) also came to put a lot of firewood in these debates. Both sides, followers of the optimized clinical treatment or intervencionists, can find in the COURAGE, many arguments to keep their tendencies of conduct. We know that COURAGE used only 3% of pharmacological stents and the patients approached invasively obtained better clinical answer sooner, with less angina, at least for 5 years. Our patients are very pragmatic, and they want immediate clinical improvement. But the high costs of the medical practice in the world of intervencionism leads us to review our cost-benefit paradigms to adapt the better to our patients with the financing of the public and private health. But, at least an unexpected side effect the COURAGE study brought in the stable chronic coronary artery patients' handling in Bras?lia, capital of Brazil. Before COURAGE, many of the patients sent to cineangiocoronariography study returned to their assisting doctors with already implanted stent without any kind of previous consultation and debate with the patient's clinical cardiologist. The decision of implanting or not a stent was taken exclusively by the hemodynamicist, soon after the exam was taken. This brought us many problems and boredom, because a lot of times we didn't agree with the indication. Since 2007, this no more has happened. Nowadays, all the decisions about the cases studied by angiography are based in solid clinical and anatomical evidences in a consensus level, listening to the patient mood. All win with that. Congratulations for all the participants in these event. Dr.? FERNANDO MEDEIROS President - Geriatric Cardiology - Distrito Federal. BRAS?LIA ? BRAZIL. fsm at cardiol.br -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 22 18:57:49 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 22 Jan 2008 19:57:49 -0200 Subject: [ISCHEMIA-FORUM] 68E: Ventricular False Chordae Tendineae and heart function- Dr. Perez Riera Message-ID: <479666DD.9010005@myocardial.ischemia-symposium.org> Dear Dr Gao Jinaxin: Left ventricular false chordae tendinae, false chord or left ventricular false tendon is an anomalous fibrous or fibromuscular band stretching across the LV. It has been implicated as a source of idiopathic left VT (ILVT). ILVT is characterized by QRS complexes with RBBB pattern and left axis deviation is a distinct clinical syndrome that also demonstrates a characteristic response to verapamil and inducibility from the atrium in patients without apparently structural heart disease. However, it is unknown whether pretest bias contributes to an apparent association with disease. The prevalence of LV false chords on autopsy and surgical inspection is approximately 45% among patients without ILVT. Previously reported associations of false chords with ILVT likely underestimated the prevalence of false chords in a normal population (1). The false tendons extend from the septum to the LV free wall or, more rarely, from the septum to a papillary muscle. A false tendon extending from the posteroinferior LV to the septum is a consistent finding in patients with ILVT and probably is responsible for this unique arrhythmia. The mechanism by which the false tendon precipitates tachycardia is speculative, but possibilities include conduction through the false tendon or by producing stretch in the Purkinje network (2). The localization of Left ventricular false tendons from 265 specimens is located in (3) 1) 66% of cases between the posteromedial papillary muscle and the ventricular septum 2) 12% of cases between between the two papillary muscles 3) 11% of cases between between the anterolateral papillary muscle and the ventricular septum 4) 9% of cases between between the free wall and the septum 5) < than 1% between two aspects of the free wall 6) 1% had three or more points of insertion and formed weblike structures. False tendons are common anatomic variants of the normal human left ventricle which may be detected by two-dimensional Echo. A 50-year-old male was first suspected of having a Brugada-type ECG. A drug challenge test with pilsicainide unmasked a typical type 1 Brugada pattern followed by VT with RBBB and left axis deviation pattern. Three years later, he was transferred to the emergency room due to a wide QRS tachycardia with the same QRS morphology as the VT that previously occurred in the drug challenge test. An ECG just after the recorded termination of the VT exhibited a typical Brugada-type 1 ECG. In an electrophysiological study, VF could be easily induced with reproducibility. Since the clinical tachycardia could not be sustained by an isoproterenol infusion, mapping and catheter ablation targeting the pilsicainide-induced VT was performed. The successful ablation site was the left mid-lower septal wall where a Purkinje potential was recorded and a false tendon was attached just to it. (4). Two different patterns of electrophysiological properties of ILVT are described, indicating that this arrhythmia entity does not represent a homogeneous group: 1) The "origin" of the tachycardias as identified by successful RFCA was located in different areas of the LV septum and is distributed from the base to the mid-apical region. RFCA is an effective and safe treatment modality in most of these patients. Here is place left ventricular false chordae tendinae. Verapamil-sensitive left VT with a RBBB pattern and left-axis deviation has been demonstrated to arise from the left posterior fascicle with or without false chordae, and can be cured by RFCA guided by Purkinje potentials. Verapamil-sensitive VT with an RBBB configuration and right-axis deviation is rare, and may originate in the left anterior fascicle. 2) Distinct target site characteristics for successful catheter ablation including polyphasic diastolic activity during tachycardia and fragmented late potentials during sinus rhythm could be identified (6). The prevalence of false tendons in patients with an innocent systolic murmur is 76% in children and 40% in adults, with an overall prevalence of 52%. Furthermore, FT is far more common in subjects with innocent cardiac murmur than in normal subjects. The relationship between FT and murmur thus appears very likely, although not definitely proven (7). False tendons are a common echocardiographic finding of no clinical importance except for their possible role in the genesis of INNOCENT MURMURS and VENTRICULAR ARRHYTHMIAS. The echocardiographic detection of false tendons increases considerably when these structures are specifically sought and in conditions that result in LV chamber dilatation (8). References 1) Gualano SK, Bolling SF, Gordon D, Wilson A, Bach DS. High prevalence of false chordae tendinae in patients without left ventricular tachycardia. Pacing Clin Electrophysiol. 2007 1: 156-159. 2) Thakur RK, Klein GJ, Sivaram CA, Zardini M, Schleinkofer DE, Nakagawa H, Yee R, Jackman WM.Purkinje fiber network on the interventricular septum.Anatomic substrate for idiopathic left ventricular tachycardia. Circulation. 1996; 93:497-501. 3) Luetmer PH, Edwards WD, Seward JB, Tajik AJ.Incidence and distribution of left ventricular false tendons: an autopsy study of 483 normal human hearts. J Am Coll Cardiol. 1986;8:179-183. 4) Ueyama T, Shimizu A, Esato M, Yoshiga Y, Sawa A, Suzuki S, Sugi N, Matsuzaki M. Pilsicainide-induced Brugada-type ECG and ventricular arrhythmias originating from the left posterior fascicle in a case with Brugada syndrome associated with idiopathic left ventricular tachycardia. Europace. 2008; 10:86-90. 5) Nogami A, Naito S, Tada H, Oshima S, Taniguchi K, Aonuma K, Iesaka Y. Verapamil-sensitive left anterior fascicular ventricular tachycardia: results of radiofrequency ablation in six patients. J Cardiovasc Electrophysiol. 1998; 9:1269-1278. 6) Kottkamp H, Chen X, Hindricks G, Willems S, Haverkamp W, Wichter T, Breithardt G, Borggrefe M. Idiopathic left ventricular tachycardia: new insights into electrophysiological characteristics and radiofrequency catheter ablation. Pacing Clin Electrophysiol. 1995; 18:1285-1297. 7) Calabr? MP, De Luca F, Consolo S, Falcone G, Oreto G. Left ventricular false tendon: the most frequent cause of "innocent" murmur in childhood? G Ital Cardiol. 1992; 22: 19-24. 8) Malouf J, Gharzuddine W, Kutayli F. A reappraisal of the prevalence and clinical importance of left ventricular false tendons in children and adults. Br Heart J. 1986; 55: 587-591. All the best for all Andr?s Ricardo P?rez Riera MD Master in Cardiology Area, Santo Andr? S?o Paulo Brasil -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 23 11:00:31 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 23 Jan 2008 12:00:31 -0200 Subject: [ISCHEMIA-FORUM] 67S Indication of ICD. Dr. Conci Message-ID: <4797487F.30103@myocardial.ischemia-symposium.org> Dear colleagues, The score system, based on these five clinical variables (NYHA class 3 or 4, atrial fibrillation, QRS>120 ms, age>70 years old, and BUN>26 mg), correctly stratified the risk of sudden death in the patients from the control group of the MADIT-2 study, in which it was shown that in post-infarction patients with EF lower than 0.30, ICD implanted as primary prevention reduced mortality by 31% at 20 months. The patients with ICD and without it, without any risk factor, had a similar mortality at 2 years (9% and 8%, respectively). The patients with at least one risk factor, had very different mortalities (with ICD 15%, and without ICD 27% at two years; p<0.001). The greatest benefit of ICD was in patients with one or two risk factors. The patients with three or more risk factors had a high nonarrhythmic mortality, so the benefit of ICD was not evident either. The hazard ratio of mortality between patients with ICD vs control patients in the MADIT-2 population (n=1131)? Risk factors n? HR (95% CI) p 0 0.96 (0.44-2.07) 0.91 1 0.51 (0.37-0.70) <0.001 1 0.40 (0.22-0.72) 0.002 2 0.42 (0.25-0.70) <0.001 3 0.80 (0.46-1.40) 0.44 The patients without any of these clinical risk factors did not benefit from ICD, but should be monitored periodically, because these factors are time-dependent and may change and be acquired during follow up. Goldenberg I, Vyas AK, Hall WJ, et al. Risk stratification for primary implantation of a cardioverter-defibrillator in patients with ischemic left ventricular dysfunction. J Am Coll Cardiol 2008:51:288-296. I think that this recently published score system helps us a lot to make a decision on the implantation of ICD. Eduardo Conci Jefe uci del Instituto modelode cardilogia Cordoba Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 23 11:06:20 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 23 Jan 2008 12:06:20 -0200 Subject: [ISCHEMIA-FORUM] 70E Revascularization of patients with positive functional tests for ischemia and stable angina. Dr. P. Stone Message-ID: <479749DC.1020000@myocardial.ischemia-symposium.org> Dear Marcos, Thank you for your very important question. There were a number of other earlier studies that suggested the idea that percutaneous coronary interventions (PCI) improved angina, without an effect on the other, more important, hard outcomes such as death, MI, etc, but the COURAGE Trial was the first investigation to focus attention on this issue in such a large scale manner. I think the study has dramatically altered the balance of decision-making for patients with stable CAD. In Boston many of us have become much more conservative and favor more intensive pharmacologic therapy. The focus of therapy to prevent ACS must be on the typically minor luminal obstructions associated with "vulnerable plaque" since those are the areas that rupture and cause an acute coronary syndrome and death. Our goal of therapy for these areas must be to "passivate" or stabilize the plaques (intensive statins, ACEI, ARB, ASA, beta blockers) and prevent the plaque from becoming more inflamed and likely to rupture. There are still luminal obstructions that cause angina and are a problem requiring PCI, but if our anti-anginal therapies can be improved then the need for widespread PCI for every flow-limiting obstruction becomes much less. I think clinical practice has changed very substantially. Thank you again for your excellent question and I would also be interested in responses from other clinicians from other countries or areas. Best regards, Peter Stone, MD Peter H. Stone, M.D. Cardiovascular Division Brigham & Women's Hospital 75 Francis Street Boston, MA 02115 tel. 617-732-5692 fax 617-732-7134 -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 23 18:37:48 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 23 Jan 2008 19:37:48 -0200 Subject: [ISCHEMIA-FORUM] 71R Lead with greatest deviation of sum of all leads. Dr. Yabluchansky Message-ID: <4797B3AC.9030705@myocardial.ischemia-symposium.org> In my opinion, we have to evaluate ST changes in all leads (where this deviation is observed), since the process of repolarization is not homogeneous. Therefore, a single lead may not reflect accurately the ischemic processes in the myocardium. Kind regards, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 23 14:32:48 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 23 Jan 2008 15:32:48 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASK, EXPERTS ANSWER Message-ID: <47977A40.5000707@myocardial.ischemia-symposium.org> Dr. Alfredo Piombo from Argentina asks - What pathophysiological mechanisms would explain the development of just ST segment depression during coronary spasm? ------------------------------------- Dr. Antoni Bayes deLuna from Spain answers - In coronary spasm the ST elevation is induced because usually the occlusion is total although very transient, and is presented in patients without previous important subendocardial ischemia. If there are crisis in patients with previous subendocardial ischemia, and the occlusion is subtotal, the ECG may present ST depression (see Electrocardiography in ischemic heart diseases by Antoni Bay?s de Luna and M. Fiol-Sala.Blackwell-futura 2007 (p.273). Best regards Antoni -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 23 18:48:46 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 23 Jan 2008 19:48:46 -0200 Subject: [ISCHEMIA-FORUM] 72S 75-year-old patient with prolonged precordial pain. Dr. Pellizzon Message-ID: <4797B63E.8010207@myocardial.ischemia-symposium.org> Dear Dr. Pizarro, You pose an interesting clinico-electrocardiographic case, which will surely allow this symposium's speakers to teach us how they analyze and reason daily clinical issues. My modest point of view before this case is that we should consider: 1) First, interpreting whether chest pain is angor or not; this clinical datum is very important. 2) This history of her cardiologist telling here that she is a coronary patient and that he treated her as such, although she was not taking beta-blockers, is another piece of information to consider. 3) The traumatic stress of her husband's death should also be emphatically considered. 4) In ECG, the ST depression in the leads that you mention is not > 0.5 mm, just as ST elevation in aVR and V1, are not specific diagnostic data. Inferior necrosis is indeed observed (Q in DIII and aVF) and high voltage R waves in V2-V3 that may express dorsal necrosis (of the old classification) and anterior ischemia. Moreover, LA enlargement and incomplete right bundle branch block. Surely Dr. Bayes de Luna or Andres may provide more substantial data. 5) We would manage this patient as ACS without ST elevation (admittance into Coronary Unit, nitroglycerin, ASA, heparin, beta blockers). We should determine troponin at 8-12 hours and evaluate ECG evolution, and determine the risk by TIMI score. 6) Forty eight hours later, if she is asymptomatic, we perform catheterization to determine what arteries are involved. I wouldn't be surprised if she had angiographically normal coronary arteries. The datum on emotional stress should be taken seriously into account. I do have a doubt: the possible residual infero-dorsal necrosis. If she had normal coronary arteries, the ECG tends to normalize and we shouldn't hesitate to conduct a vasospasm test with intracoronary or endovenous ergonovine. I don't think she has trunk or three-vessel lesion, because there is no manifest ST elevation in aVR. Best regards, Dr. Oscar A.Pellizz?n. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 23 18:52:59 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 23 Jan 2008 19:52:59 -0200 Subject: [ISCHEMIA-FORUM] 73S Ventricular extrasystole in elderly people. Dr. Lanzas Rodriguez Message-ID: <4797B73B.1040207@myocardial.ischemia-symposium.org> Dear colleagues, This type of patients sometimes lead clinicians into desperation; even more so than the patient him/herself. Male patient, 75 years of age, asymptomatic, negative stress test (if the arrhythmia disappears with stress, I categorize it as low risk), negative color Echo Doppler (I interpret good ventricular function, without segmentary motility alterations, normal diastolic function, analysis of normal flow), Holter without potentially lethal ventricular arrhythmias, do not imply a significant organic substrate. I would classify the patient now as cardio-angio-sclerotic with "benign" ventricular arrhythmia in a clinical setting. I would like to know the Thyroid Function (sometimes we have concealed hyperthyroidism), mostly in the elderly, serum electrolytes, or "pro-arrhythmic" medication. I would withhold the use or propafenone, since at a given time may be more problematic than beneficial in this case; anyway, if I had to give a medication, in this patient I would lean to a cardioselective beta blocker and I would investigate thoroughly what other risk factors he has, besides age and male gender. Is he hypertensive? Dyslipidemic? Smoker? Then I would control aggressively his risk factors. I will leave my criteria for this case for your consideration. Dr. R?ger A Lanzas Rodr?guez Cardi?logo Clinico Costa Rica. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 23 18:55:42 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 23 Jan 2008 19:55:42 -0200 Subject: [ISCHEMIA-FORUM] 74S AMI and Dengue. Dr. Lugo Message-ID: <4797B7DE.8080405@myocardial.ischemia-symposium.org> Dear professors of the Forum, Now in Venezuela we have frequent cases of Dengue. A few days ago, a male patient presented to the Emergency Room with acute infarction of inferior wall with classical dengue in evolution and 90,000 platelets. I applied conventional medical treatment, because in the center where he is there is no Hemodynamic Lab. I did not administer antiplatelet aggregation agents or heparin. Did I do right??? Does anyone have experience on this? Dr. Adalberto Lugo (Maracaibo-Venezuela) -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 23 18:56:52 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 23 Jan 2008 19:56:52 -0200 Subject: [ISCHEMIA-FORUM] 75S T wave. Dr. Cantu Salinas Message-ID: <4797B824.9030305@myocardial.ischemia-symposium.org> Dr. Andres Ricardo Perez Riera. Congratulations for the magnificent dissertation on ECG components. I hope we can read more on this. Dr J Horacio Cantu Salinas (MEXICO) -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 23 19:41:40 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 23 Jan 2008 20:41:40 -0200 Subject: [ISCHEMIA-FORUM] 76S Vasospasm with myocardial damage? Dr. Espinoza Inga Message-ID: <4797C2A4.7000601@myocardial.ischemia-symposium.org> Dear colleagues, I would like to ask you the following question: a few days ago I received a 41-year-old patient, with no modifiable coronary risk factors, who in the hours of the morning presents oppressive precordial pain with no irradiation that lasts approximately 40 minutes. It yields spontaneously. The episode is repeated after 8 hours, which is when he consults. His ECG shows ST segment elevation in DII, DIII, aVF, and V5, and V6 of 0.5 to 1 mV, seen and measured with a magnifying glass. The pain subsides without any medication after 50 minutes approximately and the ECG "normalizes". In lab tests there are minimal enzymatic changes (CPK, CK-MB, and Troponin T). With all these symptoms, I referred the patient for coronary angiography, which does not show coronary disease. The enzymatic curve was typical, and the ECG did not show evolutionary changes. Was this a case of severe coronary vasospasm with myocardial damage? Sincerely, Diego Espinoza Inga -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 23 19:51:54 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 23 Jan 2008 20:51:54 -0200 Subject: [ISCHEMIA-FORUM] 77S T wave. Dr. Schena Message-ID: <4797C50A.2020003@myocardial.ischemia-symposium.org> For Dr. Perez Riera: Dear Ricardo, I have to congratulate you for your learned explanation on T wave, and I dare, considering our friendship and mutual respect, to ask you a couple of contributions about T wave in Stress Test. I have seen other alterations, not so frequently, that should be taken into account: 1.- If T wave is flattened, or mildly negative, and becomes positive with NEGATIVE HYPERVENTILATION TEST. 2.- If wave voltage increases exaggeratedly, in general if also has symmetrical slopes. 3.- If T wave becomes negative in late recovery. Warm regards and continue with this beautiful Symposium. Dr. Roberto A. Schena -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 24 14:14:08 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 24 Jan 2008 15:14:08 -0200 Subject: [ISCHEMIA-FORUM] 76S Vasospasm with myocardial damage? Dr. P. Stone Message-ID: <4798C760.3000308@myocardial.ischemia-symposium.org> Dear Dr. Inga, Your case is fascinating, and I agree with your assessment that the case probably represented severe vasospasm, most likely of a dominant right coronary artery. It would have been fascinating to have obtained an echo while there was ST segment elevation in the inferolateral leads since there probably would have been reversible inferolateral hypokinesis. Thank you for sharing your case with us. Peter Stone, M.D. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 24 10:23:08 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 24 Jan 2008 11:23:08 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASK, EXPERTS ANSWER Message-ID: <4798913C.40403@myocardial.ischemia-symposium.org> Dr. Ricardo Pizarro from Panama asks - About the New Classification of AMI with Q wave based on cardiac MRI, and that is increasingly better known and accepted by everyone, the AMI of lateral side, with the actual anatomical location of the heart, would generate RS pattern in V1 (I also see ST segment depression), but then, have V7-V8 and V9 leads lost their usefulness with this New Classification, and if not so, what morphology should be expected in this case of lateral AMI? Sincerely, Dr. R. Pizarro Panama ------------------------------------- Dr. Andres Perez Riera from Brazil answers - CLINICAL VALUE OF LEFT POSTEROLATERAL CHEST LEADS: V7, V8, V9 The ECG patterns in posterolateral chest leads (V7, V8, V9 ) in normal subjects were studied in 225 young, normal men (age range 17 to 21 years). The prevalence of 0.5- to 1.0-mm ST-segment elevation in leads V7, V8, and V9 0.08 second after the J point was 8.9%, 5.8%, and 3.1%, respectively. The ST-segment elevation was not >1.0 mm in any subject (1). Occlusion of the left circumflex coronary artery (LCX) may present with either ST elevation typical of inferior or lateral myocardial infarction, ST depression or a normal 12-lead ECG. In patients presenting with ST depression, concomitant ST elevation in the posterolateral chest leads V7, V8, and V9 is believed to reflect ST-elevation MI of the posterior wall. However, to be confident of this diagnosis, it is necessary to know that posterior ST depression does not occur in acute subendocardial ischaemia. Because the posterior wall is faced by none of the 12 standard ECG leads, the ECG diagnosis of posterior myocardial infarction is problematic and has often remained undiagnosed, especially in the acute phase. Acute strictly posterior myocardial infarction wall is very uncommon and predominantly due to occlusion of the LCX. Acute posterior wall MI is challenging to diagnose due to the absence of ST segment elevation on a standard 12-lead ECG even in the setting of total coronary artery occlusion and transmural (Q-wave) infarct (2). The accuracy of the different ECG methods in diagnosing acute ST-elevation MI was studied by Tr?g?rdh et al (3). The study population consisted of 479 patients admitted to Lund University Hospital with acute chest pain. One conventional ECG plus leads V4R, V5R, V7, V8, and V9 were recorded for each patient within 24h of admittance. Biochemical markers were used as the gold standard for diagnosis of AMI. The measured ST-segment elevations in the 12-, 16- and 24-lead postadmission ECGs as well as in the 12-, 19- and 24-lead admission ECGs. The sensitivity for detecting AMI was 28% for the postadmission 12-lead ECG, 33% for the 16-lead ECG and 37% for the 24-lead ECG. The specificities were 97%, 93% and 95%, respectively. For admission ECGs, the sensitivity was 33% for the 12-lead ECG, 45% for the 19-lead ECG and 49% for the 24-lead ECG, with specificities of 97%, 96% and 94%, respectively. The authors conclude that the sensitivity for detecting AMI is higher for the 16-, 19- and 24-lead ECGs than for the conventional 12-lead ECGs. Their specificity, however, is slightly lower. If increased sensitivity for detecting MI is desired, the 24-lead or 19-lead should be used as no additional electrodes are required. Poh et al. (4) have prospectively recorded leads V7, V8, and V9 simultaneously with the standard 12-lead ECG in patients who underwent treadmill stress test. Group A consists of 35 patients who showed ischaemic precordial ST depression in their 12-lead ECGs during treadmill stress test and subsequent angiographic documentation of significant CAD. ST depression was seen in 69% in V7, 31% in V8 and 11% in V9 in the Group A patients at peak exercise. Group B consists of 35 subjects who showed normal ECG findings during treadmill stress test. In none of the Group A or B patients was there ST elevation in leads V7, V8, or V9 either at rest or at peak exercise. The authors conclude that ST elevation in leads V7, V8, and V9 is uncommon in patients presenting with subendocardial ischaemia. Therefore, in patients presenting with acute chest pain and ST depression in the 12-lead ECG, concomitant posterior ST elevation may be a reliable indicator of ST elevation posterior MI. This is likely due to LCX occlusion and may require thrombolytic therapy. Matetzy et al. (5) from 87 patients with a first inferior MI who were treated with recombinant tissue-type plasminogen activator were stratified according to the presence (Group A [46 patients]) or absence (Group B [41 patients]) of concomitant ST segment elevation in posterior chest leads V7, to V9. Patients in Group A had: 1) A higher incidence of posterolateral wall motion abnormalities on radionuclide ventriculography 2) A significative larger infarct area (as evidenced by higher peak creatine kinase levels) 3) A lower LVEF at hospital discharge than those in Group B. Although patency of the infarct-related artery (IRA) in Group A resulted in an improved LVEF at discharge LVEF was unchanged in Group B, regardless of the patency status of the IRA 4) A higher incidence of reinfarction 5) A higher incidence of heart failure or death. The authors conclude that the ST segment elevation in posterolateral cest leads V7 to V9 identifies patients with a larger inferior MI because of concomitant posterolateral involvement. Such patients might benefit more from thrombolytic therapy. ST-segment elevation of?1.0 mm in lead V4R has been shown to be a reliable marker of right ventricular involvement, a strong predictor of a poor outcome in patients with inferior acute myocardial infarction. In patients with Inferior MI caused by the occlusion of the RCA proximal to the first right ventricular branch, no ST-segment elevation in lead V4R can occur because of concomitant posterior involvement. In such patients, the incidence of right ventricular involvement, may be underestimated on the basis of ST-segment elevation in lead V4R (6). According to Chu et al. (7) the features in patients with strictly posterior acute MI are: 1) Typical ST segment elevation in V7, V8, V9 2) V1-V2 R/S ?1 (81.8%); 3) 1 - 2 mm ST depression in V1-V4 (5/11, 45.5%); 4) 0.5 - 1.5 mm ST elevation in I, aVL leads 5) 0.5 - 1.5 mm ST elevation in V5-V6 leads (5/11, 45.5%) 6) LCX was the infarction related artery in a 100% of cases. Acute posterior myocardial infarction should be suspected with V1-V2 R/S ? 1 and V1-V4 ST depression in standard 12 leads ECG. Besides symptoms and cardiac enzyme measurements, recording posterior leads ECG and performing coronary angiography will help to make the correct diagnosis. The sensitivity of the standard 12 ECG leads is less than 50 % in angiographically documented occlusion of the LCX. The extended posterior chest leads V7-V9 improve sensitivity only marginally (by 8 %). Isolated ST-segment depression or no significant ST-segment depression in the standard leads was observed in 26 % and 28 % respectively. The infarct size - as measured by maximum CK-values - did not differ among the respective groups (8). Patients with a LCX artery-related infarct and an abnormal R wave in lead V1 had multivessel disease. An abnormal R wave in lead V1 had a 96% specificity for LCX versus right coronary artery-related infarction but a sensitivity of only 21%. When patients with a LCX-related infarct is stratified according to the presence or absence of abnormal R waves in lead V1 or V2, the abnormal R wave group had more admission ST elevation , a larger infarctand more extensive CAD. Acute ST segment elevation is present in only 48% of patients and 38% of patients with a LCX artery-related infarct had no significant ST changes (elevation or depression) on admission(9). Left posterolateral chest leads (V7, V8, V9) helped distinguish the multiple causes of tall R waves in V1 and/or V2, diagnosed true posterior myocardial infarction when standard leads did not, and identified the presence or absence of posterior injury in patients with inferior infarction (10). The prevalence and clinical significance of ST-segment elevation(STE) in posterior ECG leads during AMI is largely unknown. Bairey et al. (11) obtained posterolateral chest ECG leads (V7, V8, and V9), as well as standard 12-lead and right precordial leads (V4R-V6R), immediately upon admission in 210 consecutive patients with AMI. 19 patients (9% of 210 cases) had STE of ?1 mm in 2 or more posterolateral chest leads, either as an isolated finding (7 cases, 3.3% of 210) or in association with STE at inferior or lateral sites (12 cases, 5.7% of 210). STE in posterior leads was detected in 10.9% (7 of 64) of patients without STE in standard ECG leads. Tall R waves in V1-V2 developed in 5 cases (26.3% of 19). Patients with STE in posterolateral chest leads were significantly older with more frequent cardiovascular risk factors than those without. In-hospital complications were significantly more frequent in these patients compared with matched controls. There was also a trend toward lower EF and increased in-hospital mortality that did not reach statistical significance. The authors conclude that STE in posterior ECG leads is not uncommon among patients with AMI and no STE in standard leads and may portend a worse in-hospital course. Posterolateral chest leads ECG leads have been described for quite a while; however, their use in diagnosing acute posterior wall MI and identifying infarct-related arteries has not been well used. We prospectively studied ECG changes during balloon occlusion of single-vessel RCA and LCX. 34 inflations were performed in RCAs and 38 in LCXs. Analysis of the patients with ECG changes revealed that the most common ECG change during RCA occlusion was inferior ST-segment elevation in leads II, III, and aVF (95%), and the most common change during LCX occlusion was posterior ST elevation in leads V7, V8, and V9 (68%). ST elevation was always seen in inferior leads in the RCA group and in posterior leads in the LCX group. Thus posterolateral chest leads helped identify RCA versus LCX as the infarct-related artery. ST elevation is also noted by posterolateral chest leads in seven (36.8%) additional patients. Thus there is a definite added benefit of posteriolateral leads during LCX occlusion. In the appropriate clinical setting, posterolateral chest leads may help in differentiating LCX occlusion from RCA occlusion (12). References 1) Chia BL, Tan HC, Yip JW, Ang TL. Electrocardiographic patterns in posterior chest leads (V7, V8, V9) in normal subjects. Am J Cardiol. 2000; 85: 911-2, A10. 2) Brown L, Sims J, Conforto A. Posterior myocardial infarction with isolated ST elevations in V8 and V9: Is this an "ST elevation MI"? CJEM. 2003; 5: 115-118. 3) Tr?g?rdh E, Claesson M, Wagner GS, Zhou S, Pahlm O. Detection of acute myocardial infarction using the 12-lead ECG plus inverted leads versus the 16-lead ECG (with additional posterior and right-sided chest electrodes Clin Physiol Funct Imaging. 2007;27:368-374. 4) Poh KK, Chia BL, Tan HC, Yeo TC, Lim YT.Absence of ST elevation in ECG leads V7, V8, V9 in ischemia of non-occlusive etiologies. Int J Cardiol. 2004; 97: 389-392. 5) Matetzky S, Freimark D, Chouraqui P, Rabinowitz B, Rath S, Kaplinsky E, Hod H. Significance of ST segment elevations in posterior chest leads (V7 to V9) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. J Am Coll Cardiol. 1998; 31: 506-511. 6) Kosuge M, Kimura K, Ishikawa T, Hongo Y, Shigemasa T, Sugiyama M, Tochikubo O, Umemura S.Implications of the absence of ST-segment elevation in lead V4R in patients who have inferior wall acute myocardial infarction with right ventricular involvement. Clin Cardiol. 2001; 24: 225-230. 7) Chu G, Zhang GB, Wen QZ, Sun BG.Electrocardiographic and angiographic characteristics of patients with acute solitary posterior myocardial infarction Zhonghua Xin Xue Guan Bing Za Zhi. 2007;35: 645-647. 8) Schmitt C, Lehmann G, Wailersbacher M, Wailersbacher K, Schmieder S, Karch M, Sch?mig A. Problems of electrocardiographic diagnosis of occlusion of the left circumflex coronary artery Dtsch Med Wochenschr. 2001; 126: 1257-1260. 9) Huey BL, Beller GA, Kaiser DL, Gibson RS. A comprehensive analysis of myocardial infarction due to left circumflex artery occlusion: comparison with infarction due to right coronary artery and left anterior descending artery occlusion J Am Coll Cardiol. 1988; 12: 1156-1166. 10) Casas RE, Marriott HJ, Glancy DL.Value of leads V7-V9 in diagnosing posterior wall acute myocardial infarction and other causes of tall R waves in V1-V2. Am J Cardiol. 1997; 80: 508-509. 11) Bairey CN, Shah PK, Lew AS, Hulse S.Electrocardiographic differentiation of occlusion of the left circumflex versus the right coronary artery as a cause of inferior acute myocardial infarction. Am J Cardiol. 1987; 60:456-459. 12) Kulkarni AU, Brown R, Ayoubi M, Banka VS. Clinical use of posterior electrocardiographic leads: a prospective electrocardiographic analysis during coronary occlusion. Am Heart J. 1996;131:736-741. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 24 14:23:46 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 24 Jan 2008 15:23:46 -0200 Subject: [ISCHEMIA-FORUM] 79E Vasospasm with myocardial damage? Dr. Perez Riera Message-ID: <4798C9A2.8010308@myocardial.ischemia-symposium.org> Dear Dr Espinoza Inga: Clinically, patients with Prinzmetal, vasospastic angina or variant angina pectoris and acute myocardial infarction (AMI) usually had their first symptom of vasospastic angina as the severe chest pain of AMI. Approximately 65% of the vasospastic angina patients with AMI had experienced emotional stress before their AMI. The only variable significantly associated with major cardiac events (death, resuscitation from cardiac arrest, AMI) is the detection during angina of ST segment elevation in both anterior and inferior ECG leads. In your case the ECG shows ST segment elevation in inferior leads and apical wall precordial leads (V5, and V6). Patients with diffuse ST segment elevation on ECG are those at the highest risk of mayor cardiac events, independently of angiographic findings (1). Angiographically, the spasm provocation test for vasospastic angina patients with AMI showed more multivessel and diffuse spasm than in vasospastic angina patients without AMI(2). Although the prognosis of variant angina without significant organic stenosis is generally good, the incidence of multivessel spasm, a major prognostic factor, is surprisingly high in provocation tests. Although the prognosis of multivessel spasm is believed to be poor, this may not necessarily be so. Anginal attacks due to sequential and simultaneous multivessel spasm seem to be more dangerous than those involving single-vessel spasm or migratory multivessel spasm (3). Vasospastic angina is associated with ventricular arrhythmias, AMI and sudden arrhythmic death(SAD). The main ischemic mechanism in vasospastic angina is coronary spasm. Because the demonstration of spontaneous coronary spasm is difficult, a number of methods which can provoke spasm in susceptible patients were imagined. Coronary angiography with/without intra-coronary ergonovine testing is necessary in acute coronary syndrome patients to identify the underlying pathology and establish appropriate treatment in these cases. Transient myocardial ischaemia resulting from vasospastic angina induces a significant elevation of serum DNase I activity. Therefore, serum DNase I activity may be applicable as a useful marker for detecting transient myocardial ischaemia. Serum deoxyribonuclease I (DNase I) activity has recently been highlighted as a potential diagnostic marker for detection of AMI (4). Most patients with vasospastic angina who have no significant organic coronary arterial stenosis are well controlled by medical therapy and the prognosis is almost satisfactory. Calcium channel blockers are used as the first choice and effective agents for vasospastic angina. However, they do not always work well. Some uncontrolled coronary vasospasms would happen to cause prolonged occlusion of coronary artery resulting in AMI, life-threatening arrhythmias and SAD. Magnesium deficiency has been observed in patients with variant angina. Intravenous administration of magnesium can suppress exercise-induced coronary spasms in some patients with variant angina, but the degree of magnesium deficiency did not correlate with the suppressions of exercise-induced ST elevation after magnesium administration. Intravenous administration of magnesium had limited efficacy in patients with variant angina and exercise-induced ST segment elevation. In women with variant angina the degree of intracellular magnesium deficiency is closely related to the frequency of chest pain. Attacks of variant angina usually respond promptly to sublingual administration of short-acting nitrates. Calcium antagonists (verapamil, 5 to 10 mg, or diltiazem, 0.15 mg/kg) can be given. Benidipine may be helpful in patients with vasospastic or variant angina pectoris, if diltiazem was not successful. Cardiac events are rather infrequent in patients with vasospastic angina who are receiving treatment with calcium blockers and that the presence of a severe fixed stenosis markedly increases the risk of AMI but not the risk of arrhythmias(5). The mainstay of pharmacologic treatment of coronary artery spasm is calcium channel blocking agents together with nitrates to cover the periods in which spasm is most likely to occur. These powerful vasodilating agents, at their usual doses, are able immediately and completely to control the recurrences of ischemic attacks in as many as 80% of patients (6). Intracoronary stent implantation for persistent coronary spasm refractory to conventional medical therapy can be considered a feasible and attractive treatment modality for the control of symptoms (7). References 1) Lanza GA, Sestito A, Sgueglia GA, Infusino F, Manolfi M, Crea F, Maseri A. Current clinical features, diagnostic assessment and prognostic determinants of patients with variant angina. Int J Cardiol. 2007; 118: 41-47. 2) Kim PJ, Seung KB, Kim DB, Her SH, Shin DI, Jang SW, Park CS, Park HJ, Jung HO, Baek SH, Kim JH, Choi KB.Clinical and angiographic characteristics of acute myocardial infarction caused by vasospastic angina without organic coronary heart disease. Circ J. 2007; 71: 1383-1386. 3) Onaka H, Hirota Y, Shimada S, Kita Y, Sakai Y, Kawakami Y, Suzuki S, Kawamura K. Clinical observation of spontaneous anginal attacks and multivessel spasm in variant angina pectoris with normal coronary arteries: evaluation by 24-hour 12-lead electrocardiography with computer analysis. J Am Coll Cardiol. 1996; 27:38-44. 4) Morikawa N, Kawai Y, Arakawa K, Kumamoto T, Miyamori I, Akao H, Kitayama M, Kajinami K, Lee JD, Takeshita H, Kominato Y, Yasuda T. Serum deoxyribonuclease I activity can be used as a novel marker of transient myocardial ischaemia: results in vasospastic angina pectoris induced by provocation test. Eur Heart J. 2007; 28: 2992-2997. 5) Nakamura M, Takeshita A, Nose Y. Clinical characteristics associated with myocardial infarction, arrhythmias, and sudden death in patients with vasospastic angina. Circulation. 1987; 75: 1110-11106. 6) Lanza GA, Maseri A. Coronary Artery Spasm. Curr Treat Options Cardiovasc Med. 2000; 2: 83-90. 7) K?lt?rsay H, Can L, Payzin S, T?rko?lu C, Altinti? A, Akin M, Akilli A. A rare indication for stenting: persistent coronary artery spasm. Heart Vessels. 1996; 11: 165-168. All the best for all Andr?s Ricardo P?rez Riera MD Master in Cardiology Area, Santo Andr? S?o Paulo Brasil riera at uol.com.br -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 24 14:40:49 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 24 Jan 2008 15:40:49 -0200 Subject: [ISCHEMIA-FORUM] 80E Revascularization of patients with, positive functional tests for ischemia and stable angina. Dr. Souza Message-ID: <4798CDA1.9010208@myocardial.ischemia-symposium.org> Thank you, Dr. Stone, I agree with you. I think it is a landmark trial, in spite of previous evidences. Patients with left ventricular dysfunction (above 30%) and with documented ischemia had had no benefit from revascularization. Our practice in Hospital das Cl?nicas from Universidade Federal de Minas Gerais is similar to yours. Thank you and I would like to hear opinions from other colleagues, Dr. Marcos R. de Sousa Cardiologist -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 24 18:09:36 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 24 Jan 2008 19:09:36 -0200 Subject: [ISCHEMIA-FORUM] 81R Commentaries on Dr. Piombo's question. Dr. Yabluchanski Message-ID: <4798FE90.8040407@myocardial.ischemia-symposium.org> Comments by Dr. Yabluchanski on Dr. Piombo's question. The way I understand this, the foundations of (local) coronary ischemia are metabolic disorders that occur in the myocardial area with irrigation disorders, which reflect on electrophysiologic processes. The kind of electrocardiographic deviation (elevation or depression) is determined by location, dimensions and the phases of the pathological process. Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus , +38(067)5049851 mobile, mydoctorlife at gmail.com my @medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 24 18:11:45 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 24 Jan 2008 19:11:45 -0200 Subject: [ISCHEMIA-FORUM] 82S: False ventricular chordae tendineae and cardiac function- Dr. Solano Message-ID: <4798FF11.1000502@myocardial.ischemia-symposium.org> My most sincere congratulations for Dr. Andres Ricardo Perez Riera MD, Master in Cardiology Area, Santo Andres, Sao Paulo, Brazil, for his magnificent message on chordae tendineae, which I have underestimated due to its high frequency, and it is clear that it is territory to be explored in cases of unexplained dysrrhythmias in patients with this type of anomalies, without having it become the "cause" of many dysrrhythmias. Dr. Yamil Solano Costa Rica Hospital Clinica Labrador. Hospital Escalante Pradilla C.C.S.S.= -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 24 18:12:49 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 24 Jan 2008 19:12:49 -0200 Subject: [ISCHEMIA-FORUM] 83R: False ventricular chordae tendineae and cardiac function. Dr. Yabluchaski Message-ID: <4798FF51.1000500@myocardial.ischemia-symposium.org> If false chordae tendineae are of connective tissue, then they cannot conduct electric impulses. In my opinion, the ectopic impulses are generated by the mechanic tension in the sites where the chords connect. Kind regards, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N . Karazin' National University , Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 25 13:45:11 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 25 Jan 2008 14:45:11 -0200 Subject: [ISCHEMIA-FORUM] 84S Correlatoin of ECG with NMR. Dr. Perez Riera Message-ID: <479A1217.3040606@myocardial.ischemia-symposium.org> Dear friend, Pizarro, I would like to make an addition to my comments. According to the pioneer work of this icon of Electrocardiology, a pride for Latin-Americans, our dear Professor Bayes, the correlation with cardiac magnetic resonance has divided the organ into 7 areas: septal, apical-anterior, anterior-extensive, lateral, inferior, and infero-lateral. The anterior wall no longer exists. The old dorsal wall is today the lateral one, called type B1, which shows RS pattern in V1-V2 and DI, aVL, V6 and/or R wave with low voltage in V6. The sensitivity is 67% and specificity 99% according to the great master. The site of occlusion is the circumflex artery. Traditionally, the term posterior wall was applied to the basal segment of the inferior wall that would finally curve slowly upwards. Currently, the posterior wall is called, according to the consensus of the American Societies of Imaging, as infero-basal portion of the inferior wall. Besides, the infarction of this infero-basal segment (previously called posterior wall) does not cause RS in V1. The pattern occurs in lateral wall infarction. The following arguments are crucial to prove this statement: ? The basal inferior segment is depolarized late, after the first 40 ms of starting the ventricular depolarization (QRS). ? Most of times, this segment does not curve upwardly. ? Spatially, the heart is located in an oblique position, from right to left, and not anterior-posterior. So, in the case of necrosis of the inferior basal segment, the necrosis vector will have its head addressed to the intermediary precordial leads (V3-V4) and not V1. On the other hand, the origin of the necrosis vector (tail of the vector) will be observed in the accessory left latero-dorsal leads V7, V8, and V9. Dear friend, I hope this is clear for you. Best regards for you and all the members of this dynamic Symposium. Andr?s Ricardo P?rez Riera. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 25 14:45:00 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 25 Jan 2008 15:45:00 -0200 Subject: [ISCHEMIA-FORUM] 88E Lead with greatest deviation of sum of all leads. Dr. Singh Message-ID: <479A201C.7080203@myocardial.ischemia-symposium.org> It seems that changes should be present at least in two leads? Dr. R. B. Singh, MD -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 25 14:48:52 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 25 Jan 2008 15:48:52 -0200 Subject: [ISCHEMIA-FORUM] 85S Vasospasm with myocardial lesion? Dr. Pellizzon Message-ID: <479A2104.9070101@myocardial.ischemia-symposium.org> Dear colleague, It is almost certainly a vasospasm. The ECG recorded during pain usually shows significant ST elevation if the vasospasm is occlusive; when it yields the ST elevation decreases and gets leveled, and negative T waves appear. It is possible that ECG you point out is the phase of decreasing ST and out of pain. When there are angiographically normal arteries, we suggest to our hemodynamics specialist to apply intracoronary ergonovine. They are reluctant. We have to insist to know exactly if the vasospasm is focal or diffuse. The therapeutic answers are different. If the hemodynamist does not apply ergonovine, we apply endovenous ergonovine in the Coronary Unit with ECG monitoring. We clarify the doubt. There are many treated vasospasms that are not vasospasms and vice versa. Dr. Oscar A. Pellizz?n Rosario. Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 25 14:51:04 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 25 Jan 2008 15:51:04 -0200 Subject: [ISCHEMIA-FORUM] 86S Primary PCI vs. thrombolysis. Dr. Bonzon Message-ID: <479A2188.2000700@myocardial.ischemia-symposium.org> Dear colleagues, In your excellent lecture with the title: "Significance of a good ECG analysis for decision-making in the catheterization lab. Nikus, Kjell, Eskola, Markku" available at: http://www.myocardial.ischemia-symposium.org/lectures/esp_nikus_eskola/lectu re.php You state: "The superiority of primary PCI over pre-hospital thrombolysis is not proven." My question for both of you is: On which evidence-based publications do you base this statement? On the ones published in cities where the delay in pre-hospital medical care is the rule, or in the cities where primary PCI is the rule, as in our modest hospital, where we have an average "door-balloon" time of less than 40 minutes? Cordially, Dr. Gustavo R. Bonz?n Resistencia, Chaco, Argentina -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 25 15:25:27 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 25 Jan 2008 16:25:27 -0200 Subject: [ISCHEMIA-FORUM] 89E Dr. Wellens presentation. Dr. Madias Message-ID: <479A2997.40201@myocardial.ischemia-symposium.org> This is a response to Dr. Wellens presentation: Dear Dr. Wellens: Greetings to you and all our colleagues (organizers and participants) of this wonderful symposium! I enjoyed immensely your audio presentation (Part I and II), entitled ?The ECG in Acute Coronary Syndromes?. It was a real "treat"! I wanted only to express some reservation about your comments on employing the criterion of ?5 mm of ST-segment elevation in leads V1-V3 to diagnose MI in patients with LBBB. This criterion has a poor specificity for patients with LBBB (1), or patients with LBBB-like ECG patterns due to pacing (2). What prompted this note is that I listened to your presentation this morning, and I saw in consult rounds this afternoon a patient with non-ischemic dilated cardiomyopathy with a chronic LBBB and a stable ST-segment elevation of 6.5 mm in lead V3. This is a frequent encounter in the cardiac clinic, and is found mostly i patients with QRS complexes of very large amplitude (1) . References 1. Madias JE, Sinha A, Ashtiani R, Agarwal H, Win M, Narayan VK. A critique of the new ST-segment criteria for the diagnosis of acute myocardial infarction in patients with left bundle-branch block. Clin Cardiol. 2001;24:652-5. 2. Madias JE. The nonspecificity of ST-segment elevation > or =5.0 mm in V1-V3 in the diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. J Electrocardiol. 2004 ;37:135-9 Wishing everybody a nice week-end, John E. Madias, MD Mount Sinai School of Medicine of the New York University -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 25 17:02:43 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 25 Jan 2008 18:02:43 -0200 Subject: [ISCHEMIA-FORUM] 91S 74S AMI and Dengue. Dr. Lanzas Rodriguez Message-ID: <479A4063.6090107@myocardial.ischemia-symposium.org> Dear colleagues of the Forum, Interesting case that could be very frequent in our Latin-American media. I work in a Regional Hospital of the State of Puerto Limon, Costa Rica, where we have had Dengue epidemics, and at some point as the only cardiologist in this hospital, I had to face the problem of this disease in heart disease patients, with anticoagulation and valve prosthesis, and we take antiplatelet aggregation drugs due to chronic ischemic heart disease. The management that I follow is to suspend antiaggregation and anticoagulation drugs when the platelets in such patients are below 100,000, because of the implicit risk of bleeding. We don't know how Dengue will evolve at a given time, the symptoms are dynamic, and they may vary in a moment to the hemorrhagic type, which implies a shock by decrease of the circulating volume and extravasation to the interstitial space that may put the life of the patient in danger. If I had seen this patient, I would have managed him conventionally too, with strict surveillance of hemodynamic parameters, diuresis, median blood pressure, which is the pressure of tissue perfusion, and daily count of platelets without antiplatelet aggregation agents or heparin. Once the platelet count is recovered to more than 100,000, ideally in 150,000, I would start with antiaggregation platelets or anticoagulation in carriers of valve prosthesis. Sometimes clinical cardiologists in our care centers, lack the appropriate technological resources, and we have to follow managements based on common sense, clinical evidence and the state of the patient. I agree with Dr. Lugo in not administering antiplatelet aggregation drugs or heparin with platelet count below 100,000 in this patient with inferior acute myocardial infarction. I advise that once the platelets are normal, you should begin with aspirin and evidently, if there is no hypotension, a conventional treatment based on atenolol, ACEI, and statins, medications we have available in our institution. Therefore, Dr. Lugo, the way I see it and according to my clinical experience, you acted properly. Dr R?ger A Lanzas Rodr?guez Cardi?logo Cl?nico Puerto Lim?n, Costa Rica. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 25 16:30:38 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 25 Jan 2008 17:30:38 -0200 Subject: [ISCHEMIA-FORUM] 93ECorrelatoin of ECG with NMR. Dr. Perez Riera Message-ID: <479A38DE.5020606@myocardial.ischemia-symposium.org> Dear colleagues of the forum, I have a question that keeps coming round and round to my mind ever since Dr. Pizarro asked his intelligent question and I answered somewhat in a rush. We know that the previously called strict posterior wall, strict dorsal wall, or left infra-atrial wall according to the new nomenclature of ECG/CMR (Cardiac Magnetic Resonance) corresponds to the infero-basal segment of the inferior wall, that finally presents a superior curve (segment 4 in the image "in bulls eye"). This region is depolarized late, always around the initial 40 ms of QRS, and therefore, in theory, it cannot cause Q wave of necrosis (initial 40 ms) in the leads that face the: ACCESSORY LEFT LATERO-DORSAL LEADS V7 through V9. However, these theoretical considerations exist in numerous papers in literature, showing that the infarction in this segment previously and improperly called dorsal wall, causes Q wave of necrosis in these accessory latero-dorsal leads (1,2,3,4,5). The question is: HOW TO EXPLAIN THE CLINICAL FINDING OF Q WAVES APPEARANCE IN THESE ACCESSORY LEADS, V7 THROUGH V9, IF THE INFARCTION IN THIS BASAL REGION DOES NOT MODIFY THE INITIAL 60 ms OF THE QRS COMPLEX? Refer?ncias 1) Melendez LJ, Jones DT, Salcedo JR.Usefulness of three additional electrocardiographic chest leads (V7, V8, and V9) in the diagnosis of acute myocardial infarction. Can Med Assoc J. 1978;119: 745-748. 2) Matetzky S, Freimark D, Chouraqui P, Rabinowitz B, Rath S, Kaplinsky E, Hod H.Significance of ST segment elevations in posterior chest leads (V7 to V9) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. J Am Coll Cardiol. 1998; 31: 506-511. 3) Stoliarov VA, Kolodin MI, Varvarenko VI, Markov VA.Comparative assessment of the left chest EKG leads V7-V9 and bipolar Slapak and Partilla leads in the diagnosis of posterior and posteriobasal myocardial infarction Klin Med (Mosk). 2001; 79:30-33. 4) Casas RE, Marriott HJ, Glancy DL.Value of leads V7-V9 in diagnosing posterior wall acute myocardial infarction and other causes of tall R waves in V1-V2. Am J Cardiol. 1997; 80:508-509. 5) Agarwal JB, Khaw K, Aurignac F, LoCurto A.Importance of posterior chest leads in patients with suspected myocardial infarction, but nondiagnostic, routine 12-lead electrocardiogram. Am J Cardiol. 1999; 83: 323-326. Thanking you in advance, Andr?s Ricardo P?rez Riera MD and Master in Cardiology area -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 25 16:46:49 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 25 Jan 2008 17:46:49 -0200 Subject: [ISCHEMIA-FORUM] 87R Revascularization of patients with positive functional test and stable chronic angina. Dr. Yabluchanski Message-ID: <479A3CA9.6000509@myocardial.ischemia-symposium.org> Excellent answer Dr. Stone! In our clinic we indicate the same treatment with statins (in general with atorvastatin) to all the patients, before or after anticoagulation. Anticoagulation may solve the problem of one or more atherosclerotic plaques transitorily, since atherosclerosis is a systemic process, and new plaques develop in new places; consequently, the management with statins is necessary. Kind regards, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 25 16:51:17 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 25 Jan 2008 17:51:17 -0200 Subject: [ISCHEMIA-FORUM] 94E Correlatoin of ECG with NMR. Dr. Perez Riera MISTAKE Message-ID: <479A3DB5.6020900@myocardial.ischemia-symposium.org> Incorrect There are mistake 7 areas: septal, apical-anterior, anterior-extensive, lateral, inferior, and infero-lateral. The anterior wall no longer exists. The correct is: 7 areas: septal, apical-anterior, anterior-extensive, lateral, inferior, and infero-lateral. The POSTERIOR wall no longer exists. Andr?s. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 25 17:09:47 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 25 Jan 2008 18:09:47 -0200 Subject: [ISCHEMIA-FORUM] 92P: False ventricular chordae tendineae. Dr. Brindeiro (f) Message-ID: <479A420B.10803@myocardial.ischemia-symposium.org> Dear colleagues, In our experience, false ventricular chordae tendineae do not influence the systolic function. Possibly, depending on the site of insertion, they may generate murmur in the left ventricular outflow tract (LVOT), or by preventing a proper coaptation of the mitral valve system, they may cause small reflux toward the left atrium (not only infants, but in children, adolescents, and even adults). Rarely (we have only 2 cases in more than 120,000 tests performed), when the false tendon is inserted into the septum junction with the aorta, a significant obstruction may occur in the LVOT (one of the cases had maximal systolic gradient >100 mmHg and mean gradient 40 mmHg). Possibly, the false chordae tendineae may cause arrhythmia by two probable mechanisms: 1- The traction of the underlying myocardium may work as an ectopic focus, generating premature ventricular contractions, or 2- the false chordae tendineae may work as a means of conduction, generating a reentry phenomenon. Kind regards, Djair Brindeiro Filho Recife - Brasil -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Fri Jan 25 16:57:55 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Fri, 25 Jan 2008 17:57:55 -0200 Subject: [ISCHEMIA-FORUM] =?iso-8859-1?q?90S_Unstable_angina_in_elderly_pa?= =?iso-8859-1?q?tient=2E_Dr=2E_Jir=F3n_Toru=F1o?= Message-ID: <479A3F43.20206@myocardial.ischemia-symposium.org> I have an 80-year-old patient with history of controlled high blood pressure, and presents to the emergency room with precordial pain, 3 episodes over the last 24 hours in rest. In the ECG there is transitory ST depression in the infero-lateral wall with patin, and that gets normal without pain and without treatment. The patient does not have a hemorrhagic background. According to the current studies, in this patient would the following treatment be justified: ASA, clopidogrel, LMWH, etipifibatide and/or tirofiban? Rolando Jir?n Toru?o -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 26 07:24:49 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 26 Jan 2008 08:24:49 -0200 Subject: [ISCHEMIA-FORUM] 96E Vasospasm's aspects. Dr. Singh Message-ID: <479B0A71.9070308@myocardial.ischemia-symposium.org> Dear Dr. Stone, Can you please tell how the biology and biochemistry of vasospasm is? Can vasospasm have a circadian rhythm? Dr. R. B. Singh, MD India -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 26 08:10:29 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 26 Jan 2008 09:10:29 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASK, EXPERTS ANSWER Message-ID: <479B1525.2050509@myocardial.ischemia-symposium.org> Dr. Ricardo Pizarro from Panama asks - Dear Drs. Fiol and Carrillo, About your lecture "Identifying the Culprit Coronary Artery and the Location of Coronary Occlusions in patients with STEMI - A New Algorithm" and in which almost at the end of the excellent presentation, you acknowledge as one of the limitations of the Algorithm and the Study, the "different location of precordial electrodes", reading this reminded me of a magnificent paper by Dr. Andres R. Perez Riera, which he put at the disposal of the Rediris Arrhythmia Forum on December 2007, and that alludes the topic of the "bad placement of precordial electrodes" and compares the % of their good (or bad) placement (in some studies) between ECG technicians, nurses and physicians (cardiologists and noncardiologists), -the latter don't look so good- and where it is emphasized that in order to improve this situation: "The only safe solution is proper precordial electrode placement, which requires training and an environment supporting precision (1)." My question then is: What other opinions you may express about this, to improve this situation? Sincerely, Dr. R. Pizarro Panama 1) Rajaganeshan R, Ludlam CL, Francis DP, et al. Accuracy in ECG lead placement among technicians, nurses, general physicians and cardiologists. Int J Clin Pract. 2007 Aug 31; [Epub ahead of print]) Drs. Miguel Fiol and Andres Carrillo Lopez from Spain answer - The placement of electrodes in the frontal plane does not require a great accuracy, since their more proximal or distal location in a limb will not modify the electrocardiographic tracing. It is not so in precordial leads. An incorrect placement of these electrodes may originate different mistakes in the interpretation of an ECG, more frequently in leads V1, V2 and V3, possibly yielding initial rsr' or rsR' morphology as a false right bundle branch block image, reduction of initial "r" voltage, QS morphology in V1 in horizontal hearts, ascending ramp of ST, alterations in T wave voltage or polarity, presence of negative P wave. The solution to this problem is an appropriate training of the technicians that perform the recording, insisting on its significance in training courses, and a close supervision in daily practice. - Bay?s de Luna A. Texbook of Clinical Electrocardiography. Futura Publishing, Armonk 1998, - Tapia FA and Proudfit WI. Secondary R Waves in Right Precordial Leads in Normal Persons and in Persons with Cardiac Disease, Circulation. 21:28, 1960 - Garc?a Niebla J. Im?genes electrocardiogr?ficas derivadas de una incorrecta colocaci?n de los electrodos. Enfermer?a en Cardiolog?a N.? 32-33; 38-44, 2004; - Fatimah Lateef, Narayan Nimbkar et al. Vertical displacement of the precordial leads alters electrocardiographic morphology. Indian Heart J. 2003; 55:339-343; - Koehler NR. Changes in electrocardiogram in V1 by precordial electrode malposition . Arq Bras Cardiol. 1993 Aug;61(2):99-101. - Wenger W, Kligfield P. Variability of precordial electrode placement during routine electrocardiography. J Electrocardiol. 1996 Jul;29(3):179-84; - Maria Sejersten BS, Olle Pahlm MD, PhD, Jonas Pettersson MD, Peter M. Clemmensen MD, PhD, Farida Rautaharju PhD, Sophia Zhou PhD, Charles Maynard PhD, Charles L. Feldman ScD and Galen S. Wagner MD. The relative accuracies of ECG precordial lead waveforms derived from EASI leads and those acquired from paramedic applied standard leads. Journal of Electrocardiology Volume 36; 2003, 179-185; - Paul Kligfield, Leonard S. Gettes, James J. Bailey, Rory Childers, Barbara J. Deal, E. William Hancock, Gerard van Herpen, Jan A. Kors, Peter Macfarlane, David M. Mirvis, Olle Pahlm, Pentti Rautaharju and Galen S. Wagner Recommendations for the standardization and interpretation of the electrocardiogram: Part I: The electrocardiogram and its technology: A Scientific Statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. Heart Rhythm, Volume 4, Issue 3, March 2007, Pages 394-412 - Bay?s de Luna A. Texbook of Clinical Electrocardiography. Futura Publishing, Armonk 1998, - Tapia FA and Proudfit WI. Secondary R Waves in Right Precordial Leads in Normal Persons and in Persons with Cardiac Disease, Circulation. 21:28, 1960 - Garc?a Niebla J. Im?genes electrocardiogr?ficas derivadas de una incorrecta colocaci?n de los electrodos. Enfermer?a en Cardiolog?a N.? 32-33; 38-44, 2004; - Fatimah Lateef, Narayan Nimbkar et al. Vertical displacement of the precordial leads alters electrocardiographic morphology. Indian Heart J. 2003; 55:339-343; - Koehler NR. Changes in electrocardiogram in V1 by precordial electrode malposition . Arq Bras Cardiol. 1993 Aug;61(2):99-101. - Wenger W, Kligfield P. Variability of precordial electrode placement during routine electrocardiography. J Electrocardiol. 1996 Jul;29(3):179-84; - Maria Sejersten BS, Olle Pahlm MD, PhD, Jonas Pettersson MD, Peter M. Clemmensen MD, PhD, Farida Rautaharju PhD, Sophia Zhou PhD, Charles Maynard PhD, Charles L. Feldman ScD and Galen S. Wagner MD. The relative accuracies of ECG precordial lead waveforms derived from EASI leads and those acquired from paramedic applied standard leads. Journal of Electrocardiology Volume 36; 2003, 179-185; - Paul Kligfield, Leonard S. Gettes, James J. Bailey, Rory Childers, Barbara J. Deal, E. William Hancock, Gerard van Herpen, Jan A. Kors, Peter Macfarlane, David M. Mirvis, Olle Pahlm, Pentti Rautaharju and Galen S. Wagner Recommendations for the standardization and interpretation of the electrocardiogram: Part I: The electrocardiogram and its technology: A Scientific Statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. Heart Rhythm, Volume 4, Issue 3, March 2007, Pages 394-412 -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 26 08:28:16 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 26 Jan 2008 09:28:16 -0200 Subject: [ISCHEMIA-FORUM] 97E Dr. Wellens presentation. Dr. Wellens Message-ID: <479B1950.6020109@myocardial.ischemia-symposium.org> Dear Dr Madias, Thank you very much for your valuable comment. As you have shown in the patient with LBBB a 5 mm or more ST elevation in the leads V1-V3 (Sgarbossa type 3) is not helpful in making the diagnosis of MI. I completely agree with your finding! It stresses that the ECG is often not a reliable source of information in patients with LBBB and chest pain to make the diagnosis of ischemia or MI The clinical impression should play a decisive role in decision making about reperfusion therapy. Thanks again for your comment and a nice weekend! Hein Wellens -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 26 08:50:53 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 26 Jan 2008 09:50:53 -0200 Subject: [ISCHEMIA-FORUM] 98E Amiodarone. Dr. Miyahara Message-ID: <479B1E9D.2060802@myocardial.ischemia-symposium.org> Dear colleagues, What do you think about amiodarone increases mortality in post-MI patients with HF and/or LVSD, according to Dr. Kevin Thomas said (Am Heart J 2008; 155: 87-93)? Dr. K. Miyahara -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 26 17:21:16 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 26 Jan 2008 18:21:16 -0200 Subject: [ISCHEMIA-FORUM] 99S Positive T wave. Dr. Castro Diaz Message-ID: <479B963C.3060807@myocardial.ischemia-symposium.org> Dear Andres, Some have considered that positive T wave in the case of intraventricular blocks with wave jump (as it occurs, for instance, in advanced left bundle branch blocks), may be due to parietal subendocardial ischemia. Some Mexican authors, state about the concept of ischemia: "When there is a parietal subendocardial location, the direction of the repolarization process evidently does not get inverted (which still spreads from the epicardium to the endocardium), but duration increases. This is the cause for positive and symmetrical T waves, or just positive T waves, if the primary change of repolarization is superimposed to a secondary change: for instance, in intraventricular blocks with a wave jump phenomenon, in premature ventricular contractions, and in marked systolic enlargements." De Micheli A, Medrano G, Iturralde P. Diagn?stico Electrovectocardiogr?fico en Cl?nica.M?ndez Editores, S.A. de C.V. M?xico. 1992. P?g 96. Kind regards, Dr. Luis E. Castro D?az. Chitr?, Panam?. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 26 18:16:08 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 26 Jan 2008 19:16:08 -0200 Subject: [ISCHEMIA-FORUM] 100E Primary PCI vs. thrombolysis. Dr. Nikus and Dr. Eskola Message-ID: <479BA318.2080703@myocardial.ischemia-symposium.org> Dear Dr Bonz?n. Thank you for your interest in our presentation. You commented on our statement about lack of data for superiority of primary PCI over pre-hospital thrombolysis. First of all, we think that the most important thing is to have well organized regional STEMI networks to minimize treatment delays as much as possible. We are glad to hear about your short door-to-balloon times. We have organized the local STEMI network in our uptake area together with referring healthcare units and ambulances to include both thrombolysis and primary PCI as alternative reperfusion strategies. The STEMI diagnosis is made through telemedicine by an invasive cardiologist reading the 12-lead (with additional leads if needed) ECG and discussing by cellular phone with the ambulance personnel. The decision about reperfusion therapy is based on clinical and ECG criteria for individual patient risk, and on the stage of the ischemic process. Until recently, we used the patient reported time from symptom onset to diagnosis, to evaluate timing, and tended to use thrombolysis in patients with short delays (less than 2-3h). Now we use the criteria for preinfarction syndrome and evolving MI described in our lecture. The longest transport distances in our STEMI network, where we act as tertiary centre is 300 kilometres, with transport times over 2 hours, and therefore it is not possible to have primary PCI as the only reperfusion therapy. In primary PCI, we always take the patients straight into the cath lab from the ambulance, thereby bypassing the emergency department, and in our centre, the mean "door-to-balloon time" is 29 minutes. When considering choice of reperfusion therapy, we have to take "transport time", including administration of medication like clopidogrel, heparin, aspirin, betablocker, iv nitrates (if needed) on scene, into consideration. If transport time is more than 60-90 minutes, we strongly consider thrombolytic therapy. In that case, the goal is pre-hospital thrombolysis. We aim at having all ambulances administering the thrombolytic agent on scene, but this is not yet possible. Of course there will be time delays if the patient is transported to an emergency department to have the medication. If we choose thrombolytic therapy, we want the patient to be transported to our hospital to be able to do rescue PCI if needed. Most studies have compared primary PCI with "traditional", not pre-hospital, thrombolysis. Kalla et al (Circulation 2006;113:2398) have described their good experience with a central triage in the Viennese Ambulance System. Their system coordinates activities for 5 high-volume interventional centres, and in patients with time from symptom onset less than 2-3 h, they use the fastest available reperfusion strategy, thrombolysis or PCI. We think that we do not have robust data from randomized trials to show superiority of primary PCI over pre-hospital thrombolytic therapy, especially if time from symptom onset to diagnosis is less than 2 or 3 hours. Some retrospective substudies show superiority of thrombolysis, some of pPCI, and some show no difference. Hence, there is, in our opinion, room for individual therapeutic decision making, and the ECG plays a very central role in this. Yours Kjell Nikus and Markku Eskola Heart Centre, Tampere, Finland -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 26 19:26:52 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 26 Jan 2008 20:26:52 -0200 Subject: [ISCHEMIA-FORUM] 103E Positive T wave. Dr. Perez Riera Message-ID: <479BB3AC.1040602@myocardial.ischemia-symposium.org> Dear Dr. Castro Diaz: The ECG diagnosis of CHD is made more difficult in the setting of confounding patterns, including LBBB, ventricular paced rhythm, and LVE. These situations reduce the ability of the ECG to detect ACS change and AMI. The ECG detection of abnormalities arising from acute ischemic cardiac disease in this setting is possible in certain cases, contrary to popular medical opinion. Several strategies are available to assist in the correct interpretation of the ECG with LBBB and potential acute ischemia, including (1): 1) A knowledge of the anticipated ST segment-T wave morphologies of LBBB and, consequently, the ability to recognize ischemic morphologies; This strategy, an awareness of the anticipated ST segment morphologies of LBBB, is the most important and not dependent on additional diagnostic testing or past medical records. 2) The performance of serial ECGs demonstrating dynamic changes encountered in ischemic patients. 3) A comparison with previous ECGs. 4) In patients presenting with ischemic chest pain and complete LBBB, presence of any one of the following ECG criteria is highly specific (90% to 100%) and predictive (85% to 100%) for acute or prior MI(2): 1) Q waves in at least two of leads I, aVL, V5, or V6 2) R wave regression from V1 to V4 3) Notching of the upstroke of the S wave in at least two of leads V3, V4, or V5( Cabrera sign) 4) Primary ST-T wave changes in two or more adjacent leads. Inverted T waves produced by myocardial ischemia are broad and symmetric. T-wave inversion (TWI) associated with an ACS is morphologically characterized by an isoelectric ST segment that is usually bowed upward (ie, concave) and followed by a sharp symmetric downstroke. The terms coronary T wave and coved T wave have been used to describe these ischemic TWIs. A wide and deep inverted T-wave is common in ischaemic heart disease and inflammatory lesions. Focal myocardial lesions (predominantly in the ventricular septum) combined with atrioventricular conductivity disorders in the His-Purkinje system were found to play a definite role in the genesis of the "gigantic" T-wave. In some cases the wide T-wave may develop due to a fusion of T and U-waves. Patients with such ECG alterations suffer severe rhythm disorders in the form of frequent polytopic PVCs, paroxysmal VT/VF. Prominent, deeply inverted, and widely splayed T waves are more characteristic of non-ACS conditions such as: 1) Juvenile T-wave patterns 2) Athlete's heart ECG mimicking hypertrophic cardiomyopathy: deeply inverted T waves (> or = 2 mm in at least three leads) 3) Left ventricular enlargement 4) Asymmetrical apical Hypertrophic cardiomyopathy 5) Acute myocarditis 6) Wolff-Parkinson-White syndrome 7) Wellens's syndrome 8) Acute pulmonary embolism 9) Transient left ventricular ballooning, Takotsubo shaped cardiomyopathy 10) After supraventricular paroxysmal tachycardia 11) Cerebrovascular accident aneurysmal subarachnoid haemorrhage 12) Bundle branch block 13) Later stages of pericarditis 14) After return of normal depolarization in leads where the T waves were normal before pacing: Cardiac memory-persistent T wave changes after ventricular pacing 15) Notched low amplitude, and inverted T waves T waves in female patients with LQT2 (HERG) mutations 16) Large T wave inversion and QT prolongation associated with pulmonary edema The first The Manitoba Follow-Up Study is a longitudinal, prospective study of 3983 originally healthy young men who have been followed with routine medical examinations since 1948. During 56 years of follow-up, sudden unexpected cardiac death (SUCD) occurred in 171 men. This analysis examined 21 possible risk factors for SUCD, including clinical findings, social variables and ECG abnormalities. Excess alcohol consumption and T wave changes were associated with a high short-term risk for SUCD. Arterial hypertension and ST/T changes had sustained excess risk over both the short and long term. Newly developed LBBB was a highly significant short-term risk that diminished with time.(3) Referentes 1) Rosner MH, Brady WJ.The ECG diagnosis of acute myocardial infarction in the presence of left bundle branch block. Am J Emerg Med. 1998;16:697-700. 2) Hands ME,et al.Electrocardiographic diagnosis of myocardial infarction in the presence of complete left bundle branch block. Am Heart J. 1988;116: 23-31. 3) Cuddy TE, Tate RB.Sudden unexpected cardiac death as a function of time since the detection of electrocardiographic and clinical risk factors in apparently healthy men: the Manitoba Follow-Up Study, 1948 to 2004. Can J Cardiol. 2006;22:205-211. ALL THE BEST FOR ALL ANDR?S RICARDO P?REZ RIERA. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sat Jan 26 19:43:28 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sat, 26 Jan 2008 20:43:28 -0200 Subject: [ISCHEMIA-FORUM] 104E Amiodarone. Dr. Perez Riera Message-ID: <479BB790.9060102@myocardial.ischemia-symposium.org> Dear Dr K. Miyahara, Recently Thomas et al (1) using the data from VALIANT trial, a randomized comparison of valsartan, captopril, or both in patients with AMI with HF and/or LV systolic dysfunction. The authors compared baseline characteristics of 825 patients treated with amiodarone at randomization with 13,875 patients not treated with amiodarone. They examined the association of amiodarone use with subsequent mortality during consecutive periods after randomization (days 1-16, 17-45, 46-198, and 199-1096). The authors found that amiodarone group had a significant increase of early and late cardiovascular mortality that patients not treated with amiodarone. These observational findings are in contrast to earlier randomized trials. We speculate that these conflicting dates are consequence that patients treated with amiodarone were older, had higher Killip class, and were more likely to have a history of diabetes mellitus and hypertension. Reference 1) Thomas KL, Al-Khatib SM, Lokhnygina Y, Solomon SD, Kober L, McMurray JJ, Califf RM, Velazquez EJ. Amiodarone use after acute myocardial infarction complicated by heart failure and/or left ventricular dysfunction may be associated with excess mortality. Am Heart J.2008; 155:87-93. All the best Andr?s Ricardo P?rez Riera MD and Master in Cardiology area -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 27 11:48:34 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 27 Jan 2008 12:48:34 -0200 Subject: [ISCHEMIA-FORUM] 108C: False ventricular chordae tendineae and cardiac function. Dr. Qing Zhu Message-ID: <479C99C2.6080602@myocardial.ischemia-symposium.org> I agree with Dr. Yabluchansky Mykola . Best Regards Qing Zhu > > If false chordae tendineae are of connective tissue, then they cannot > > conduct electric impulses. In my opinion, the ectopic impulses are > generated > > by the mechanic tension in the sites where the chords connect. > > > > Kind regards, > > > > Yabluchansky Mykola (Nickolay) -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 27 12:09:25 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 27 Jan 2008 13:09:25 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASK, EXPERTS ANSWER Message-ID: <479C9EA5.5050708@myocardial.ischemia-symposium.org> Dr. Alfredo Piombo from Argentina asks - Do you think that the current evidence is enough to replace low molecular weight heparins by fondaparinux in acute ischemic syndromes without ST elevation? ------------------------------------- Dr. Magda Heras from Spain answers - Reply for Dr. Piombo. The current clinical guidelines for the management of ACS published by the ESC advocate the use of fondaparinux with IA recommendation, while in the ACC guidelines the recommendation is IB. This indicates that the drug is useful, and that it has at least on good randomized study with a big enough sample, on which such recommendation is based. Moreover, one of the important advantages of fondaparinux is the reduction of hemorrhagic events. However, if fondaparinux is used as anticoagulation treatment, and an invasive strategy is sought, we should not forget that the patient should receive nonfractioned heparins at the moment of catheterization, to prevent the catheter thrombotic complications that were observed, although in a small percentage, in the OASIS5 study. For this reason, in the ACC guidelines fondaparinux is preferred when a decision is made on a conservative strategy. Kind regards, Magda Dra. Magda Heras Cap de Secci? de Cardiologia Cl?nica ICT Hospital Cl?nic Villarroel, 170. 08036 Barcelona Tel 34 93 227 9305 Fax 34 93 451 4148 e-mail: mheras at clinic.ub.es -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 27 14:03:40 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 27 Jan 2008 15:03:40 -0200 Subject: [ISCHEMIA-FORUM] 109E Ventricular fibrillation. Dr. Kaan Okyay Message-ID: <479CB96C.4000307@myocardial.ischemia-symposium.org> Dear colleague, Patient who had an episode of VF during thrombolytic therapy and had sinus rhythm after defibrillation does not require permanent intravenous antiarrhythmic therapy. I would prefer to give high dose beta-blocker therapy and intensive anti-aggregant therapy and consider early invasive strategy. A VF or VT, 24 hours after succesfull thrombolytic therapy should make the cardiologist to perform an electrophysiologic study. Sincerely. Dr. Kaan Okyay -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 27 16:51:51 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 27 Jan 2008 17:51:51 -0200 Subject: [ISCHEMIA-FORUM] 110E Vasospasm's aspects. Dr. P. Stone Message-ID: <479CE0D7.3050908@myocardial.ischemia-symposium.org> Dear Dr. Singh, You pose a very interesting and enigmatic question. The cause of the focal coronary vasospasm is not clear. It is likely related to endothelial dysfunction, but this clearly does not explain the focal nature of the vasospasm in a patient with risk factors for CAD in whom the risk factors lead to systemic, diffuse endothelial dysfunction. Focal spasm can also occur in relatively young women without significant CAD or risk factors for CAD. It may be related to focal abnormalities of serotonin metabolism, but that is unclear. It was thought at one time to relate to platelet/endothelial interactions, but episodes of vasospasm are not affected by aspirin treatment. Unfortunately the cause remains quite unknown. It is very clear, though, that coronary vasodilators, such as the calcium channel blockers and nitrates, are very effective to treat and prevent episodes of coronary vasospasm. There is a very clear circadian variation of episodes of coronary vasospasm, with the majority of episodes occurring in the very early morning, such as 2 am-4 am. This is in sharp contrast to episodes of unstable angina or stable angina, which typically occur after 8 am and peak between 8 am - 12 noon. Thank you for your important question. Peter Stone, M.D. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 27 16:55:29 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 27 Jan 2008 17:55:29 -0200 Subject: [ISCHEMIA-FORUM] 111E Unstable angina in elderly patient. Dr. P. Stone Message-ID: <479CE1B1.70007@myocardial.ischemia-symposium.org> Dear Dr. Jiron Toruno, Your question relates to many patients who present to the Emergency Room. If the patient is quite stable and in a place where cardiac catheterization can be done fairly quickly, I would treat with ASA, LMWH (or even UFH), and perhaps a GP IIB/IIIa inhibitor and I would have the patient undergo catheterization to define the anatomy quickly. I would not start the clopidogrel immediately since that will limit the possibility of urgent CABG if the patient has severe and multivessel CAD that is not amenable to PCI. Thank you for your interesting and important question. Peter Stone, MD Peter H. Stone, M.D. Cardiovascular Division Brigham & Women's Hospital 75 Francis Street Boston, MA 02115 tel. 617-732-5692 fax 617-732-7134 -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 27 17:52:52 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 27 Jan 2008 18:52:52 -0200 Subject: [ISCHEMIA-FORUM] 95R Vasospasm with myocardial damage? Dr. Yabluchansky Message-ID: <479CEF24.5040605@myocardial.ischemia-symposium.org> Dear Dr. Diego Espinoza Inga, The age of the patient, the ECG data the coronary angiography support your hypothesis on coronary spasm. Since the main causes of spasm are autonomic nervous system disorders, it would be interesting to obtain more information on the first episode of pain that occurred at dawn. Maybe this episode happened after waking up from the rapid phase of dream? To what is the psychosomatic type of the patient? The information on the cause of the subsequent episodes is also important. Did the patient expect these episodes? I'd like to get more information on this patient. It is known that coronary angiography does not detect mild lesions; however, these lesions could be a "good" substrate for coronary spasm, caused by autonomic nervous system disorders. Sincerely, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 27 17:59:38 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 27 Jan 2008 18:59:38 -0200 Subject: [ISCHEMIA-FORUM] 112E Myocardial ischemia: multiphasic approach. Dr. Shen Message-ID: <479CF0BA.2070504@myocardial.ischemia-symposium.org> Detecting myocardial ischemia needs to be a multiphasic approach. It is essential to look beyond the time domain two dimensional ECG analog plots and its partial or segmental approaches and it is time to look into the new "systems approach" based on a set of computational electrophysiological/mathematical functions and digital databases for better understanding of the link between surface ECG signal and ((and the ability to differentiate) myocardial pathologies: http://www.premierheart.com/webapp/downloads/Grube.pdf http://www.premierheart.com/webapp/downloads/chest.pdf http://www.premierheart.com/webapp/downloads/siegburg.pdf http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11 975826&dopt=AbstractPlus http://www.premierheart.com/webapp/downloads/whitepaper.pdf The future of surface ECG analysis is in front of us, (inspired by http://www.physiome.org/ approach...) Regards, Joseph T. Shen, MD Founder/Managing Member. Premier Heart, LLC 14 Vanderventer Ave., Suite 138 Port Washington, NY 11050 Office: 516-883-3383 Mobile: 516-603-6368 Email: jtshenmd at premierheart.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 27 20:04:23 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 27 Jan 2008 21:04:23 -0200 Subject: [ISCHEMIA-FORUM] 101S Unstable angina in elderly patient. Dr. Vainstein Message-ID: <479D0DF7.3090506@myocardial.ischemia-symposium.org> The patient should have an angiography done immediately - with a quite certain possibility of RCA occlusion. The procedure should be urgent, and subsequently pharmacological management should be administered. Dr. Moises Vainstein - Jerusalem - Israel -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Sun Jan 27 20:40:02 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Sun, 27 Jan 2008 21:40:02 -0200 Subject: [ISCHEMIA-FORUM] =?windows-1252?q?102S_Unstable_angina_in_elderly?= =?windows-1252?q?_patient=2E_Dr=2E_Lanzas_Rodr=EDguez?= Message-ID: <479D1652.9020509@myocardial.ischemia-symposium.org> Dear colleagues of the forum, About this case, an 80-year-old patient with symptoms of unstable angina with pain in rest, and electrocardiographic changes in the infero-lateral wall, three episodes over the last 24 hs, the pain yields spontaneously without treatment, and the ECG is normalized. Such changes suggest circumflex involvement and/or right coronary artery. Initially, I would consider the management of this patient from the medical point of view in an intensive way: 1. Intravenous nitroglycerin for 24-48 hs; 2. cardioselective beta blocker (where I live, atenolol); 3. aspirin; 4. clopidogrel (here the criteria might differ, whether just aspirin or if there is intolerance to it, clopidogrel, or a combination of both). 5. low molecular weight heparins (subcutaneous enoxaparin 1 mg/Kg each 12 hours) (based on the best results with intravenous heparins); 6. risk stratification: serum markers Troponin I stat and repetition after 6 hours, serial ECG, echocardiogram (to assess ventricular function and parietal motility), clinical follow up in ICU, watch for data of ventricular failure, arrhythmias, presence of pain in spite of the medical treatment, apical murmur of recent appearance, pulmonary congestion?. In case of signs of ventricular failure, arrhythmias or persistence of pain, persistent ST depression (poor prognosis), the patients will have to receive intravenous tirofiban and undergo coronary angiography urgently. In conclusion, I think based on the current recommendations: initial intensive medical management, and in case of having indication for coronary angiography, use of tirofiban if we have the medication in the hospital center in which we work; otherwise, refer him to more specialized center for management and coronary angiography. Dr R?ger A. Lanzas Rodr?guez Cardi?logo Cl?nico Puerto Lim?n, Costa Rica. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 28 10:47:21 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 28 Jan 2008 11:47:21 -0200 Subject: [ISCHEMIA-FORUM] 105S 75-year-old female patient with prolonged precordial pain. Dr. Bermudez-Izaguirre Message-ID: <479DDCE9.5060502@myocardial.ischemia-symposium.org> Dear Dr. Pizarro, Dr. Sergio Dubner, and Dr. Edgardo Schapachnik, At the Coronary Unit of the General Hospital of Durango, Mexico, we share the same commentaries and this is the way we approach these patients. Kind regards from Mexico, Dr Tomas Bermudez-Izaguirre Jefe de la UCCI Hosp. Gral de Durango -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 28 10:48:41 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 28 Jan 2008 11:48:41 -0200 Subject: [ISCHEMIA-FORUM] 106S ACS and pacemakers Dr. Pizarro Message-ID: <479DDD39.9020304@myocardial.ischemia-symposium.org> Greetings for everyone, Thus far, the Experts, Faculties, and Participants have dealt with some situations that frequently accompany ACS as diabetes mellitus, CLBBB, ICD, statins, and other medications, but we have not discussed the possible electrocardiographic manifestations associated to ACS in patients with pacemakers (in their different modalities), so I will be very grateful if you could guide me and explain this subject, especially if there are some characteristics or morphologies that could orient me to the diagnosis of ACS prior to the result of cardiac enzymes; i.e. I will be grateful if you could tell me if there are some studies related to this issue, and also about experience-based medicine (or else, evidence-based medicine). Thank you very much for your consideration in answering. Sincerely, Dr. Ricardo Pizarro Panam? -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 28 10:49:59 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 28 Jan 2008 11:49:59 -0200 Subject: [ISCHEMIA-FORUM] 107R Amiodarone. Dr. Yabluchansky Message-ID: <479DDD87.6060703@myocardial.ischemia-symposium.org> I wouldn't trust much the conclusions from the article by Kevin Thomas (Am.Heart J 2008; 155: 87-93). Evidently, the study groups included very different patients: "The patients treated with amiodarone were adults and had a higher degree of Killip; moreover, more patients of this group had diabetes and hypertension in anamnesis." I think that there are more differences between the groups. We have to pay attention too, to the indications of management with amiodarone. It would also be very important to have a control group. According to my own experience, amiodarone is one of the best antiarrhythmic drugs for prolonged use. Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com This is a response to Dr. Pizarro's question: Dear Dr . Pizzaro: Regarding the diagnosis and management of ACS in patients with pacemakers, I would like to point out, that the diagnosis is based on the principles employed for patients with ACS and CLBBB, since the presence of paced rhythms ais associated with CLBBB-like ECG appearance. The diagnostic method has been well described previously (1), although I have reservations about the criterion of ST-segment elvation =/> 5.o mm in the leads V1-V3, where the specificity is very poor (i.e., many patients with stable ST-segment elevation of 6.0, 7.0, 8.0 etc mm in the above leads with paced rhythms may have these features displayed in their ECGs for many years (2). However you can rely on the other 2 criteria described previously (1), namely, 1.0 mm ST-segment depression in leads V1-V3, and 1.0 mm ST-elevation in the lateral precordial leads, for the diagnosis of underlying ACS with ischemic injury ST-elevation (supeimposition mechanism).. For ACS with ischemia producing ST-segment depression supeimposed on a paced rhythm the diagnosis remains problematic, and I would not rely entirely on the ECG. Regarding management of ACS in patients with paced rhythms you should rely on what you do for patients with ACS with intrinsic heart rhythms and normal intraventricular conduction, as advised by the guidelines. References 1 Sgarbossa EB, Pinski SL, Gates KB, Wagner GS. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. GUSTO-I investigators. . Am J Cardiol. 1996;77:423-4. 2. Madias JE. The nonspecificity of ST-segment elevation > or =5.0 mm in V1-V3 in the diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. J Electrocardiol. 2004 ;37:135-9 Sincerely, Greetings and thanks to all organizers and participants, John E. Madias, MD Mount Sinai School of Medicine -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 28 22:29:17 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 28 Jan 2008 23:29:17 -0200 Subject: [ISCHEMIA-FORUM] 115R False chordae tendineae and cardiac function. Dr. Yabluchanski Message-ID: <479E816D.2010704@myocardial.ischemia-symposium.org> Dear Dr. Qing Zhu, I'm very glad to share with you the same insight on this issue. I wish you good luck, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Mon Jan 28 22:32:20 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Mon, 28 Jan 2008 23:32:20 -0200 Subject: [ISCHEMIA-FORUM] 116R Ventricular fibrillation. Dr. Yabluchanski Message-ID: <479E8224.5050706@myocardial.ischemia-symposium.org> I agree with Dr. Kaan Okyay. I have a single comment on the use of beta blockers: using them depends on the clinical situation, and maybe, they are not necessary. In my presentation in the Symposium I discuss about the causes and prophylaxis of VF and other ventricular arrhythmias. Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 10:57:15 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 11:57:15 -0200 Subject: [ISCHEMIA-FORUM] 117E Value of Q in V7 to V 9 in lateral MI. Dr. Bayes de Luna Message-ID: <479F30BB.30402@myocardial.ischemia-symposium.org> Regarding value of Q in V7 to V 9 in lateral MI: The RS in V1 represents MI of mid-apical lateral wall. The MI of only basal part of lateral wall produces "fractioned" QRS (f.i. rsr'). Therefore, this explains the relatively low sensitivity of RS in V1 for lateral MI. Regarding Q in V7 to V9 we are not recording routively these leads but in some cases of lateral MI envolving the posterior part of lateral wall (mid-apical portion) Q may be present, especially in V8-V9, as a mirror patern of RS in V1. Sincerely Dr A Bay?s de Luna -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 14:23:38 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 15:23:38 -0200 Subject: [ISCHEMIA-FORUM] 118E False ventricular chordae tendineae. Dr. Paixao Almeida Message-ID: <479F611A.4020207@myocardial.ischemia-symposium.org> Dear colleagues, with especial attention for Dr. Brindeiro: Excuse-me, Sir. You wrote: "or 2- the false chordae tendineae may work as a means of conduction, generating a reentry phenomenon." Would not be: "or 2-the false chordae tendineae may work as a block of conduction, generating a reentry phenomenon." My Best regards. Dr. Adail P. Almeida ? Cardiologista ? Vit?ria da Conquista ? Bahia - Brasil -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 15:18:52 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 16:18:52 -0200 Subject: [ISCHEMIA-FORUM] 114R Amiodarone. Dr. Yabluchanski Message-ID: <479F6E0C.1030202@myocardial.ischemia-symposium.org> I agree with Dr. Perez Riera's commentaries. Besides, I would like to highlight that the patients that received amiodarone, had an indication for that drug! Consequently, the initial risk was already higher. Sincerely, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 16:13:08 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 17:13:08 -0200 Subject: [ISCHEMIA-FORUM] 119P: False ventricular chordae tendineae and cardiac function. Dr. Brindeiro Message-ID: <479F7AC4.1000107@myocardial.ischemia-symposium.org> Dear Dr. Yabluchansky Mykola and Dr. Qing Zhu, In spite of this conclusion being a hypothesis, please read the article I include below. Cordially, Prof. Dr. Djair Brindeiro Filho Federal University of Pernambuco - Brazil. --------- Anatomic Substrate for Idiopathic Left Ventricular Tachycardia Ranjan K. Thakur, MD; George J. Klein, MD; Chittur A. Sivaram, MD; Marco Zardini, MD; David E. Schleinkofer, MD; Hiroshi Nakagawa, MD; Raymond Yee, MD; Warren M. Jackman, MD From the Arrhythmia Service, University Hospital, London, Canada (R.K.T., G.J.K., M.Z., R.Y.), and the Division of Cardiology, University of Oklahoma Health Sciences Center, Oklahoma City (C.A.S., D.E.S., H.N., W.M.J.). Circulation. 1996;93:497-501 Background: Idiopathic left ventricular tachycardia (ILVT) characterized by QRS complexes with right bundle-branch block (RBBB) morphology and left axis deviation is a distinct clinical syndrome that also demonstrates a characteristic response to verapamil and inducibility from the atrium in patients without structural heart disease. A false tendon has been described in the left ventricle in a patient with ILVT in whom surgical resection of the false tendon resulted in cure. We hypothesized that the false tendon is responsible for the genesis of similar ventricular tachycardia (VT) in others.Conclusions: A false tendon extending from the posteroinferior left ventricle to the septum is a consistent finding in patients with ILVT and probably is responsible for this unique arrhythmia. The mechanism by which the false tendon precipitates tachycardia is speculative, but possibilities include conduction through the false tendon or by producing stretch in the Purkinje fiber network on the interventricular septum. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 19:07:36 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 20:07:36 -0200 Subject: [ISCHEMIA-FORUM] 121S CLBBB and acute ischemia. Dr. Pizarro Message-ID: <479FA3A8.5010201@myocardial.ischemia-symposium.org> Greetings for everyone, and congratulations to the Organizers and Faculties of this magnificent Symposium: I would be very grateful with dear Prof. Dr. Andres Ricardo Perez Riera, if he could elaborate on the topic of: "Several strategies are available to assist in the correct interpretation of the ECG with LBBB and potential acute ischemia, including (1): 1) A knowledge of the anticipated ST segment-T wave morphologies of LBBB and, consequently, the ability to recognize ischemic morphologies; This strategy, an awareness of the anticipated ST segment morphologies of LBBB, is the most important and not dependent on additional diagnostic testing or past medical records." (I have underlined the last sentence). When he answered a commentary from my distinguished fellow countryman, Dr. Luis E. Castro Diaz on the approach (from the prestigious Mexican School) about positive T wave, intraventricular blocks with wave jumps and the concept of ischemia. Thank you very much for your consideration to answer. Sincerely, Dr. R. Pizarro. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 19:09:12 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 20:09:12 -0200 Subject: [ISCHEMIA-FORUM] 122S Sleep phases disorders and coronary spasm. Dr. Pizarro Message-ID: <479FA408.7020206@myocardial.ischemia-symposium.org> Greetings for everyone, About the issue of coronary spasm or coronary artery diseases, the autonomic nervous system and disorders of the phases of sleep about which our distinguished Dr. Mykola (Nickolay) Yabluchansky answered Dr. Diego Espinoza Inga, with his fabulous and interesting (and pathophysiologic) approach, "unknown in English media"; let me ask Dr. Nickolay if just as recently there has been a focus on a certain sleep disorder (slow wave of sleep) as a risk factor for diabetes mellitus II (DM II) making it coincide with hormone changes that affect the regulation of glycose and sensitivity (or resistance) to insulin, and the subsequent reduced tolerance to glycose and increase in the risk of DM II (below I copied 2 abstracts from 2 prestigious journals on the topic); do you have experience or knowledge of some studies on the possible relationship between sleep disorders (as markers of disorders of the autonomic nervous system) as possible risk factors or triggers (in a more acute way) for the generation of ACS? My question is due to the fact that our body works as a whole, and the disorders of an organ or a system will end up affecting, sooner or later, the rest of the other organs and systems, in a sequential way. Thank you very much for you consideration to answer. Sincerely, Dr. R Pizarro. PS: The question is also addressed to the other Faculties and Participants. ------------------------------------------------------- Trastornos del Sue?o como nuevo factor de riesgo para Diabetes mellitas II (?Y para las Cardiopat?as?) http://www.pnas.org/cgi/reprint/105/3/1044.pdf BIOLOGICAL SCIENCES / NEUROSCIENCE Slow-wave sleep and the risk of type 2 diabetes in humans Esra Tasali*, Rachel Leproult, David A. Ehrmann, and Eve Van Cauter Department of Medicine, University of Chicago, Chicago, IL 60637 Edited by Donald F. Steiner, University of Chicago, Chicago, IL, and approved November 9, 2007 (received for review July 10, 2007) Abstract There is convincing evidence that, in humans, discrete sleep stages are important for daytime brain function, but whether any particular sleep stage has functional significance for the rest of the body is not known. Deep non-rapid eye movement (NREM) sleep, also known as slow-wave sleep (SWS), is thought to be the most "restorative" sleep stage, but beneficial effects of SWS for physical well being have not been demonstrated. The initiation of SWS coincides with hormonal changes that affectglucose regulation, suggesting that SWS may be important for normal glucose tolerance. If this were so, selective suppression of SWS should adversely affect glucose homeostasis and increase the risk of type 2 diabetes. Here we show that, in young healthy adults, all-night selective suppression of SWS, without any change in total sleep time, results in marked decreases in insulin sensitivity without adequate compensatory increase in insulin release, leading to reduced glucose tolerance and increaseddiabetes risk. SWS suppression reduced delta spectral power, the dominant EEG frequency range in SWS, and left other EEG frequency bands unchanged. Importantly, the magnitude of the decrease in insulin sensitivity was strongly correlated with the magnitude of the reduction in SWS. These findings demonstrate a clear role for SWS in the maintenance of normal glucose homeostasis.Furthermore, our data suggest that reduced sleep quality with low levels of SWS, as occurs in aging and in many obese individuals, may contribute to increase the risk of type 2 diabetes. Del Journal of Applied Physiology (full text and pdf free) J Appl Physiol 99: 2008-2019, 2005; doi:10.1152/japplphysiol.00660.2005 8750-7587/05 $8.00 http://jap.physiology.org/cgi/content/abstract/99/5/2008? ijkey=0028e6680f7da89f16e7a26e7e448f24b701f469&keytype2=tf_ipsecsha HIGHLIGHTED TOPICS Physiology and Pathophysiology of Sleep Apnea Sleep loss: a novel risk factor for insulin resistance and Type 2 diabetes Karine Spiegel,1 Kristen Knutson,2 Rachel Leproult,2 Esra Tasali,2 and Eve Van Cauter2 1Laboratoire de Physiologie, Centre d'Etude des Rythmes Biologiques (CERB), Universit? Libre de Bruxelles, Belgium; and 2Department of Medicine, University of Chicago, Chicago, Illinois Chronic sleep loss as a consequence of voluntary bedtime restriction is an endemic condition in modern society. Although sleep exerts marked modulatory effects on glucose metabolism, and molecular mechanisms for the interaction between sleeping and feeding have been documented, the potential impact of recurrent sleep curtailment on the risk for diabetes and obesity has only recentlybeen investigated. In laboratory studies of healthy young adults submitted to recurrent partial sleep restriction, marked alterations in glucose metabolism including decreased glucose tolerance and insulin sensitivity have been demonstrated. The neuroendocrine regulation of appetite was also affected as the levels of the anorexigenic hormone leptin were decreased, whereas the levels of the orexigenic factor ghrelin were increased. Importantly, these neuroendocrine abnormalities were correlated with increased hunger and appetite, which may lead to overeating and weight gain. Consistent with these laboratory findings, a growing body of epidemiological evidence supports an association between short sleep duration and the risk for obesity and diabetes. Chronic sleep loss may also be the consequence of pathological conditions such as sleep-disordered breathing. In this increasingly prevalent syndrome, a feedforward cascade of negative events generated by sleep loss, sleep fragmentation, and hypoxia are likely to exacerbate the severity of metabolic disturbances. In conclusion, chronic sleep loss, behavioral or sleep disorder related, may represent a novel risk factor for weight gain, insulin resistance, and Type 2 diabetes. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 19:35:10 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 20:35:10 -0200 Subject: [ISCHEMIA-FORUM] 120S ECG of sportsmen. Dr. Rivero Message-ID: <479FAA1E.1090006@myocardial.ischemia-symposium.org> For the Forum: I frequently see electrocardiograms of sportsmen, for instance, boxers, tennis players, referees. I would like to know your criteria for normalcy and abnormalcy to diagnose these types of ECG, since most are atypical. D. Rosendo Rivero M. Santa Cruz.Bollivia. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 19:37:38 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 20:37:38 -0200 Subject: [ISCHEMIA-FORUM] 124R Amiodarone. Dr. Perez Riera Message-ID: <479FAAB2.6050605@myocardial.ischemia-symposium.org> Dear Dr Yabluchansky Mykola We think that the possible indications of amiodarone in AMI/ACS are: 1) Cardiac Pulmonary Resuscitation: AMI/ACS causes several types of arrhythmia because of its electrical instability and ischemia. The most important arrhythmia is VT which degenerates to VF. Prompt direct current cardioversion will be needed and prevention of VT/VF. In the 2005 CPR guidelines of the European Resuscitation Council IV (300 mg amiodarone is indicated after the third unsuccessful defibrillation attempt. Bolus repetition (150 mg) is possible(1).After prolonged unsuccessful cardiopulmonary resuscitation amiodarone should be preferred over lidocaine, since it may improve short-term survival. 2) Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is a frequent complication of AMI. AF occurs in 5% to 10% of patients who have received fibrinolysis. Post-MI AF is more common in elderly, in patients with CHF, hypotension, third-degree heart block, VF and after more extensive MI. Postinfarction prognosis is worse among patients complicated by AF--indeed, mortality and morbid events including stroke, thromboembolism, and CHF. Despite its frequent occurrence and deleterious influence on outcomes, randomized data regarding management of AF after AMI are scarce. Termination and prevention of AF is another important issue in ACS. Following AMI, AF the choose drugs are beta-blockers. If beta-blockers are contraindicated, the rate can be slowed with digoxin or amiodarone. Aprindine, amiodarone, or bepridil will be the choice to prevent recurrent AF after direct current cardioversion. 3) Electrical storm (ES): There are 3 main clinical circumstances of occurrence: in patients with implanted CDIs, during the AMI, and in Brugada syndrome(BrS). 10 to 15% of patients with ICD are subject to ES in a period of 2 years. The causative arrhythmia is most often VT than VF, especially in secondary prevention and if the initial arrhythmias justifying the device were a VT. Precipitating factors are present in ?30% of cases, mainly acute CHF, electrolyte disturbance and pro-arrhythic effect of drugs. Predictive factors are advanced age, LVEF<35% and renal failure. Arrhythmia reduction is obtained by electrical shock in 50% of cases, antitachycardi stimulation in 30% and in 20% by association of the two. After elimination of inappropriate shocks, is mainly based on beta-blockers and amiodarone, class I antiarrhythmics, lidocaine or bretylium in some cases, and sedation pushed to general anesthesia in some cases. Amiodarone is more effective than sotalol or beta-blockers in preventing inappropriate ICD shocks in patients with AF or CHF, but it has a significant risk of drug-related adverse effects. RFCA and even heart transplantation have been proposed in extreme cases. Isoproterenol, general anesthesia, by-pass, and quinidine have been proved efficient in cases of BrS (2). References 1) Wenzel V, Russo S, Arntz HR, et al; European Resuscitation Council. The new 2005 resuscitation guidelines of the European Resuscitation Council: comments and supplements Anaesthesist. 2006; 55: 958-66, 968-972. 2) Perez Riera AR, Zhang L, Uchida AH, Schapachnik E, Dubner S, Ferreira C. The management of Brugada syndrome patients Cardiology Journal 2007; 14: 97-106. www.cardiologyjournal.org All the best for all Andr?s Ricardo P?rez Riera MD and Master in Cardiology area. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 20:08:16 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 21:08:16 -0200 Subject: [ISCHEMIA-FORUM] =?iso-8859-1?q?125E_Ventricular_fibrillation=2E_?= =?iso-8859-1?q?Dr=2E_Fiol=2C_Carrillo_and_Bay=E9s_de_Luna?= Message-ID: <479FB1E0.4010103@myocardial.ischemia-symposium.org> Answer to Dr. Kaan Okyay In our experience, sustained Ventricular tachycardia in the setting of acute myocardial infarction may be considered a marker of inadequate myocardial perfusion after thrombolysis; therefore, a more agressive revascularization treatment in these patients would be advisable before electrophysiologic study. In a multivariant analysis, the variables related to the occorrence of sustained ventricular tachycardia were CPK-MB peak > 300 UI/L (OR 5.9;95% CI 1.7-21), acute intraventricular conduction disorders (OR 9.02;95% CI 1.7-48), and ischaemia inmediately prior VT (OR 19.64;95% CI 5.3-73). The occurrence of previous myocardial infarction was significative only in the univariate analysis (Fiol M et al Clin Cardiol 2002;25:328) Our results are agree with other authors: Newby KH et al Circulation 1998;98:2567; Huikuri HV et al Heart 1996;75:17-22; Bhaskaran A Clin Cardiol 1995;18:480-483; Wolfe L et al Circulation 1991;84:1543-1551; Mont L et al JACC 1996;28; 1670-1676. Sincerely DR. M Fiol, A Carrillo and A Bay?s de Luna -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 20:38:52 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 21:38:52 -0200 Subject: [ISCHEMIA-FORUM] Closure of activities in the Discussion Forum Message-ID: <479FB90C.1000705@myocardial.ischemia-symposium.org> Dear colleagues, After 15 days of intense activity, we inform you that the Discussion Forum will conclude its activities, permanently on Thursday, January 31st, at 12 hs Buenos Aires time (-2GTM). All the messages that arrive since Wednesday, January 30th at 18 hs Buenos Aires time (20:00GTM) will only be distributed in their original language and will not be translated. Cordially, Sergio and Edgardo -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 20:45:22 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 21:45:22 -0200 Subject: [ISCHEMIA-FORUM] 126E CLBBB and acute ischemia. Dr. Perez Riera Message-ID: <479FBA92.7020106@myocardial.ischemia-symposium.org> Dear friend Dr Pizarro: in uncomplicated complete LBBB the ST-T opposite to a greater deflection of QRS: positive from V1 to V3 and negative in left leads DI, aVL, V5 and V6. These are alterations secondary to ventricular repolarization with wide QRS-ST-T angle and normal ventricular gradient. The QRS/ST-T angle near the 150? 180?. The T wave has asymmetrical limbs with relatively blunt apex. In ACS or AMI the T waves becomes inverted in V1 V2 in anterior MI, the inverted T waves in right precordial leads as well as those in the left precordial leads also tend to become more symmetrical. In AMI or ACS the ST segment is displaced in the same direction as the dominant QRS deflection in the left precordial leads in anterior MI, and in the inferiorly oriented leads in inferior wall MI. The ST segment elevation is exaggerated in the right precordial leads and the ST segment becomes coved to the top. Positive ST Segment displacement in the right precordial lead (V1 and V2) is much more difficult to evaluate, since ST segment elevation in these leads may occur in uncomplicated LBBB alone. With AMI the ST segment elevation is exaggerated (?5 mm) in the right precordial leads and becomes coved, convex-upward. The T wave becomes inverted and/or its limbs tend to become more symmetrical. There is an upward elevation of the ST segment in left leads (V5, V6 DI and aVL.). This constitutes a primary change since the ST segment is normally depressed n these leads in uncomplicated LBBB. In extensive anterior AMI the ST segment elevation is observed from V1 to V6. The ST segment elevation in V1-V2 becomes symmetrically curved and convex to the top blending imperceptibly with the proximal of the T wave The associated T wave is usually inverted with pointed arrow-head configuration. In Horizontal or transverse plane the VCG T loop is counterclockwise recording. The clockwise rotation of T wave in this plane suggests Complete LBBB complicated with MI or LVE. ST/T vector is located in right anterior quadrant opposite to QRS loop Maximal vector of QRS located in the left posterior quadrant (between ?40? to -80?) and of increased magnitude (>2 mV). In frontal plane vectors of ST and T are opposite to QRS (angle around 150? to 180?) and with counterclockwise rotation. Finally in sagittal plane, T loop of location opposite to the QRS loop (anterior) and of clockwise (Right Saggital Plane) or counterclockwise (Left Saggital Plane) rotation. All the best for all Andr?s Ricardo P?rez Riera MD and Master in Cardiology area -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 20:54:21 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 21:54:21 -0200 Subject: [ISCHEMIA-FORUM] 127E ECG of sportsmen. Dr. Perez Riera Message-ID: <479FBCAD.1010306@myocardial.ischemia-symposium.org> Prezado D. Rosendo Rivero: As caracter?sticas mas freq?entes do ECG do atleta s?o: 1) Ritmo: Sinusal, juncional ou raramente ventricular. Marcapasso mut?vel ou ritmo de ?trio esquerdo . O juncional est? presente em 0,31% (na popula??o geral em 0,02%). Arritmia sinusal f?sica ou respirat?ria: presente em 60% (na popula??o no atleta em 2, 4 % ). Pausas sinusais longas: s?o frequentes (> 2 segundos). 2) Freq??ncia Card?aca: Bradicardia sinusal ? mais de 50% dos casos. N?o s?o raras FC de 30 a 40 bpm no repouso. Em atletas altamente treinados h? relatos de FC 25 bpm. Etiologia: a) hipertono vagal; b) decr?ssimo no tono simp?tico de repouso; c) componente intr?nsico para bradicardia. 3) ONDA P: Refere-se aumento da voltagem e entalhes. 4) INTERVALO PR: Bloqueio AV de primeiro grau: 5% e 30% (em n?o atletas, 0,65%). Quando o intervalo PR n?o atinge o valor como crit?rio de Bloqueio AV de primeiro grau ? relativamente prolongado. O intervalo PR se normaliza ou at? encurta-se ap?s o exerc?cio. Bloqueio AV de primeiro grau costuma ser observado por poucos segundos. O Bloqueio AV de primeiro grau observa-se em m?dia entre 10% e 33% dos atletas geralmente em forma fugaz. Em pessoas n?o atletas, ? da ordem de 0,65%. Bloqueio AV de 2o grau: a) Mobitz Tipo I ou Wenckebach: observa-se em 10% (em n?o atletas < 1 em 30000 ou 0,003%), e desaparece invariavelmente durante o exerc?cio e atropina Esta modalidade de dist?rbio drom?tropo observa-se em mais de 20% dos atletas de elite. Na popula??o geral, o Bloqueio AV de 2o Grau Tipo I e II observa-se e 1 em cada 30000 pessoas ou 0,003 %. b) Mobitz Tipo II; Dissocia??o AV. Bloqueio AV completo ou de 3o grau : 5 cada 12000 atletas. 5) QRS: S?QRS: tend?ncia ? posi??o vertical. Eventual presen?a de crit?rios de voltagem para sobrecarga ventricular esquerda: SV1+RV5 > 35mm (?ndice de Sokolow e Lyon). Eventual padr?o de sobrecarga ventricular direita: RV1+SV5 >10.5 mm entre 18% a 69% dos casos. A SVD manifesta-se por um padr?o diast?lico traduzidos por graus m?nimos de BIRD. O BIRD observa-se em 15% dos atletas. Aus?ncia de progress?o do aumento da voltagem da onda r ou R com padrao QR de V1 a V3: padr?o de pseudo infarto em parede anterior. Patente de BCRD: observado em 13.5% dos casos. 6) REPOLARIZA??O VENTRICULAR: SEGMENTO ST Padr?o de s?ndrome de repolariza??o precoce. Descreve-se em quatro padr?es: a) Supra desnivelamento do ponto J e do segmento ST seguida de onda T apiculada de V4 a V6 e na parede inferior ( 2,4% a 44%) b) Infradesnivelamento do ponto J segmento ST (raro); c) Supra desnivelamento do ponto J e do segmento ST seguidos de onda T invertida; d) Desaparecimento do supra desnivelamento do segmento ST ap?s o exerc?cio. 7) REPOLARIZA??O VENTRICULAR: ONDA T Padr?o juvenil da onda T invertida e assim?trica nas deriva??es esquerdas: DI, aVL, V5 e V6, secund?rias a SVE fisiol?gico. Ondas T negativas ou bif?sicas de V1 a V3 e/ou na parede inferior. Frequente ?normaliza??o? da onda T perante o esfor?o. Este tipo de resposta n?o se observa na MH ou na ICo. Cintilo grafia mioc?rdica associada ao TE sempre negativa. Caracter?stica revers?o das ?altera??es? ECG nos casos de interrup??o da atividade competitiva. 8) ECG DE ALTA RESOLU??O Presen?a de potenciais tardios em 10% dos casos contra 1,4% na popula??o atleta. 9) VCG: Aumento das for?as anteriores em quase todos os casos. Deslocamento da al?a QRS para frente e a esquerda no PH. Al?a T discordante com a al?a QRS. Eventualmente, a diferencia??o entre a hipertrofia ventricular fisiol?gica do atleta e a patol?gica (remodelamento ventricular) pode se constituir num desafio. LOCALIZA??O Hipertrofia ventricular fisiol?gica: Sim?trica, por?m pode ser assim?trica. Hipertrofia ventricular patol?gica remodelamento ventricular ISQU?MIA RELATIVA: Hipertrofia ventricular fisiol?gica: Ausente Hipertrofia ventricular patol?gica remodelamento ventricular: Presente RELA??O COMPONENTE MIOC?TICO/N?O MIOC?TICO: Hipertrofia ventricular fisiol?gica: Conservado. Hipertrofia ventricular patol?gica remodelamento ventricular: Perda do equil?brio em favor do componente n?o mioc?tico (fibrose). CICLO ENERG?TICO: Hipertrofia ventricular fisiol?gica: Aerobiose. Hipertrofia ventricular patol?gica remodelamento ventricular: Anaerobiose. MECANISMO RENINA-ANGIOTENSINA ALDOSTERONA OREPINEFRINA Hipertrofia ventricular fisiol?gica: Normal. Hipertrofia ventricular patol?gica remodelamento ventricular: Incrementado. PEPT?DIO NATRIUR?TICO ATRIAL Hipertrofia ventricular fisiol?gica: Normal. Hipertrofia ventricular patol?gica remodelamento ventricular: Pode estar aumentado. FUN??O DE BOMBA Hipertrofia ventricular fisiol?gica: Normal. Hipertrofia ventricular patol?gica remodelamento ventricular: Deprimida. FREQU?NCIA CARD?ACA: Hipertrofia ventricular fisiol?gica: Tend?ncia a bradiarritmia sinusal por vagotonia. Hipertrofia ventricular patol?gica remodelamento ventricular: Freq?ente taquiarritmia e simpaticotonia. Pd2 VE: Hipertrofia ventricular fisiol?gica: Normal. Hipertrofia ventricular patol?gica remodelamento ventricular: Aumentada. Abra?o a todos Andr?s Ricardo P?rez Riera MD and Master degree in Cardiology ?rea. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 09:03:25 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 10:03:25 -0200 Subject: [ISCHEMIA-FORUM] 127E ECG of sportsmen. Dr. Perez Riera Message-ID: <47A0678D.7080300@myocardial.ischemia-symposium.org> Dear Dr. Rosendo Rivero, The most frequent features of ECG in athletes are: 1) Rhythm: sinus, junctional, or rarely ventricular. Mutable pacemaker or left atrium rhythm. The junctional one is present in 0.31% (in the general population in 0.02%). Phasic or respiratory sinus arrhythmia: present in 60% (in the athlete population in 2.4%). Prolonged sinus pauses: frequent (>2 seconds). 2) Heart rate: sinus bradycardia is more than 50% of the cases. A HR of 30 to 40 bpm is not rare in rest. In highly trained athletes there are reports of HR of 25 bpm. Etiology: a) vagal hypertone; b) decrease of sympathetic tone in rest; c) intrinsicoid component for bradycardia. 3) P wave: increase in voltage and notches are referred. 4) PR interval: first degree AV block: 5% and 30% (in nonathletes, 0.65%). 2nd degree AV block. A) Mobitz type I or Wenckebach: it is observed in 10% (in nonathletes <1 in 30,000 or 0.003%), and it always disappears during exercise and with atropine. This modality of dromotropic disorder is observed in more than 20% of elite athletes. In the general population, type I and II 2nd degree AV block is observed in 1 each 30,000 or 0.003%); b) Mobitz type II, AV dissociation. Complete or 3rd degree AV block: 5 each 12,000 athletes. 5) QRS: SAQRS: tendency to vertical position. Possible presence of voltage criteria for left ventricular enlargement: SV1+RV5 > 35 mm (Sokolow-Lyon index). Possible pattern of right ventricular enlargement: RV1+SV5>10.5 mm between 18% and 69% of the cases. RVE manifests by a diastolic pattern translated by minimal degrees of IRBBB. IRBBB is observed in 15% of athletes. Absence of progression of r or R wave voltage increase with QR pattern from V1 through V3: pattern of pseudo infarction in anterior wall. CRBBB pattern: observed in 13.5% of cases. 6) Ventricular repolarization: ST segment: early repolarization syndrome pattern. It is described in four patterns: a) J point and ST segment elevation followed by apiculate T wave from V4 through V6 an in inferior wall (2.4% to 44%); b) J point and ST segment depression (rare); c) J point and ST segment elevation followed by inverted T wave; d) disappearance of ST segment elevation after exercise. 7) Ventricular repolarization: T wave: juvenile pattern of inverted and asymmetric T wave in left leads: DI, aVL, V5 and V6, secondary to physiologic LVE. Negative or biphasic T waves from V1 through V3 and/or in inferior wall. Frequent "normalization" of T wave with strain. This type of response is not observed in HCM or in coronary insufficiency. Myocardial scintigraphy associated to TE is always negative. Characteristic reversion of ECG "alterations" in the cases of interruption of competitive activities. 8) High resolution ECG: presence of late potentials in 10% of the cases vs. 1.4% in athlete population. 9) VCG: increase of anterior forces in nearly all the cases. QRS loop shift to the front and left in the HP. T loop not matching the QRS loop. Possibly, the differentiation between physiologic ventricular hypertrophy in athletes and the pathological one (ventricular remodeling) could constitute a challenge. Location: Physiologic ventricular hypertrophy: symmetric; however it could be asymmetric. Pathologic ventricular hypertrophy: ventricular remodeling. Relative ischemia: Physiologic ventricular hypertrophy: ventricular hypertrophy absent. Pathologic ventricular remodeling: present. Myocytic/nonmyocytic component ratio: Physiologic ventricular hypertrophy: preserved. Pathologic ventricular hypertrophy, ventricular remodeling: loss of balance in favor of the nonmyocytic component (fibrosis). Energetic cycle: Physiologic ventricular hypertrophy: aerobiosis. Pathologic ventricular hypertrophy, ventricular remodeling: anaerobiosis. Renin-angiotensin aldosterone norepinephrine mechanism: Physiologic ventricular hypertrophy: normal. Pathologic ventricular hypertrophy, ventricular remodeling: increased. Atrial natriuretic peptide: Physiologic ventricular hypertrophy: normal. Pathologic ventricular hypertrophy, ventricular remodeling: it may be increased. Pump function: Physiologic ventricular hypertrophy: normal. Pathologic ventricular hypertrophy, ventricular remodeling: depressed. Heart rate: Physiologic ventricular hypertrophy: tendency to sinus bradyarrhythmia by vagotonia. Pathologic ventricular hypertrophy, ventricular remodeling: frequent tachyarrhythmia and sympathicotonia. LVEDP: Physiologic ventricular hypertrophy: normal. Pathologic ventricular hypertrophy, ventricular remodeling: increased. Regards for everyone, Andr?s Ricardo P?rez Riera MD and Master degree in Cardiology ?rea. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Tue Jan 29 22:38:24 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Tue, 29 Jan 2008 23:38:24 -0200 Subject: [ISCHEMIA-FORUM] Thank you the MI-Forum Organizers and Congratulations for the Great Success! Message-ID: <479FD510.1010702@myocardial.ischemia-symposium.org> Dear Dr. Stone and the MI-Forum Organizers: For several months you have done a lot of prep work in organizing the symposium. Your hard work has led to the great success in delivering this CAD-symposium world wide with a record high participation. Congratulations! In our Chinese team I'm only a small facilitator. Dr. Yunlong Xia and Dr. Susan Dong have worked hardest along with many Chinese translation team members, cardiology colleagues and lecturers we are supported by Drs. Dayi Hu, Yanzong Yang and a group of leading Chinese cardiologists under Chinese Society of Cardiology and Chinese Heart Rhythm Society. And we are grateful to you for your sincere friendship, superior professional skills and the efforts for bringing the innovative ideas/technology and rich clinical experience to this unique online platform so the front line cardiologists, CAD specialists can exchange their opinions with the experts in one-on-one basis. Although most of participants are far apart around the globe physically, in this cyber space we are all only one click away from each other! Some people take the advantage of Internet for bad. By totally opposite, we take a whole lot of online advantage for good, for knowledge and life-saving. It is absolutely wonderful. Many thanks again to you Dr. Stone, Dr. Luna, and to all the organizers and lecturers! VERY SPECIAL THANKS to the three online education masters: Drs. Edgardo Schapachink, Andres Recardo Perez Riera and our ISHNE President Dr. Segio Dubner. Congratulations!!! Li Zhang, MD On behalf of Chinese MI-Forum participants -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 09:06:24 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 10:06:24 -0200 Subject: [ISCHEMIA-FORUM] 128R: Flase tendinous chords and cardiac function. Dr. Yabluchanski Message-ID: <47A06840.6010409@myocardial.ischemia-symposium.org> It means: "A false tendon extending from the posteroinferior left ventricle to the septum is a consistent finding in patients with ILVT and probably is responsible for this unique arrhythmia. The mechanism by which the false tendon precipitates tachycardia is speculative, but possibilities include conduction through the false tendon or by producing stretch in the Purkinje fiber network on the interventricular septum." The mechanism of arrhythmia is "speculative" because it is not clear. I think that if tension ends in the contact sites of the chords with the myocardial wall, the arrhythmia disappears. On the other hand, to show the hypothesis posed in this article, we would have to show at least 2 things: 1) that the chords have muscular fibers; 2) that reentry circuit is really generated. Best regards, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 09:14:55 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 10:14:55 -0200 Subject: [ISCHEMIA-FORUM] Acknowledgement by Dr.Yabluchanski Message-ID: <47A06A3F.10201@myocardial.ischemia-symposium.org> Time goes by very fast, we have to admit it. For me, participating in this wonderful Symposium was a very nice experience. We have to seize it to the most. I would like to thank Drs. Sergio Dubner and Edgardo Schapachnik for the impeccable organization of the Symposium. Best regards, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 09:17:18 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 10:17:18 -0200 Subject: [ISCHEMIA-FORUM] 130S Vasospasm with myocardial damage? Dr. Espinoza Inga Message-ID: <47A06ACE.1030902@myocardial.ischemia-symposium.org> Dear Dr. Yabluchansky Mykola: Thank you for your comments and let me clarify some doubts you pose in this case. The pain appeared in the first hours of the morning, more or less 8:30 hs/9:00 hs with the patient awake in rest and no triggering cause. It lasted 40 minutes and yielded spontaneously. The patient is very stressed because of his job (coach of a soccer team). His biotype is normal, with discrete overweight. The second episode for which he consulted, appeared in the same way. He did not expect to have an episode; much less a second one. All these symptoms appeared for the first time in his life. During coronary angiography, the ventriculogram did not show any alteration. An echocardiogram was made next day (completely asymptomatic), which was absolutely normal. In our lab, cardiac enzymes have the following normal values: CPK: 24 to 190 UI CK-Mb up to 25 UI Troponin T less than 0.100 nanograms/ml, and the enzymatic peak for the patient was CPK 657 CK-Mb 138 and Troponin T 1. Once again, thank you for your valuable reply. Sincerely, Diego Espinoza Inga Cardi?logo del Hospital Monte Sina? Cuenca Ecuador -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 09:10:18 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 10:10:18 -0200 Subject: [ISCHEMIA-FORUM] 129R ECG in athletes. Dr. Yabluchansky Message-ID: <47A0692A.7050607@myocardial.ischemia-symposium.org> Each human being is individual; guidelines are static, and many of them are within the limits of normal, and at times, outside normal. For this reason in the world of medicine we deal with indeterminate sets, but we understand that not everyone has the same measure. This includes sportsmen, who live in a world of significant physical stress and have guidelines of their own, adapted to this type of stress. Such guidelines have deficiencies. Therefore, in the cases of sportsmen we have to follow our own experience and common sense, multiplied by a good knowledge of medicine. Bernard Shaw said it best: "The golden rule is that there are no golden rules." I wish you the best of luck, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 13:00:03 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 14:00:03 -0200 Subject: [ISCHEMIA-FORUM] 131P False ventricular tendinous chords. Dr. Brindeiro Filho Message-ID: <47A09F03.3090900@myocardial.ischemia-symposium.org> Dear Dr. Adail P. Almeida, Thank you for your message. Below I include the hypothetic mechanism according to the published article (I have highlighted a phrase with inverted commas) that I sent to the Forum yesterday (Tuesday, January 29th, 2008, 16 hs 17 min). Sincerely, Djair Brindeiro Filho Conclusions: A false tendon extending from the posteroinferior left ventricle to the septum is a consistent finding in patients with ILVT and probably is resposible for this unique arrhythmia. The mechanism by which the false tendon precipitates tachycardia is speculative, but possibilities include "conduction through the false tendon" or by producing stretch in the Purkinje fiber network on the interventricular septum. Circulation. 1996;93:497-501 -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 14:28:17 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 15:28:17 -0200 Subject: [ISCHEMIA-FORUM] Acknowledgement. Dr. Lanzas Rodriguez Message-ID: <47A0B3B1.8060604@myocardial.ischemia-symposium.org> I would like to express my gratefulness and congratulations to the organizers of this magnificent event, which once again gathers the international cardiological community, updating knowledge with the excellent and renowned experts and authors. Congratulations to all the participants and kind regards and a friendly embrace to all the colleagues that with their comments and experience have enriched us. Let's not ever forget in the practice of our profession, the humanism that should characterize us in the care of our patients. I express a though from the Master Chavez from Mexico: "The physician is not as a mechanic that should fix a sick organism as if it was a broken machine; instead he is a human being approaching another human being, offering whatever he has?a bit of science and a LOT OF EMPATHY AND AFFECTION" Regards for everyone, Dr. R?ger A Lanzas Rodr?guez Cardi?logo Cl?nico Puerto Lim?n Costa Rica. drlanzas at yahoo.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 15:21:04 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 16:21:04 -0200 Subject: [ISCHEMIA-FORUM] 132R Inferior AMI and AV block. Dr.Yuriy Kosolapov Message-ID: <47A0C010.2020603@myocardial.ischemia-symposium.org> Greetings for all the colleagues! I would like to thank the organizers of this excellent Symposium and all the participants, who answered my question on VF during thrombolysis. Let me ask another question: A patient is admitted with inferior AMI, 6 hs of evolution, with complete AV block and clinical signs of cardiogenic shock. What do we do? Do we administer thrombolytic agents, waiting for a good clinical response and recovery of conduction, or do we place a transitory pacemaker and not thrombolytic, since central venous puncture is a relative contraindication (we do not have electrodes available for peripheral venous access). In our clinic, we do not have hemodynamics; moreover, moving the patient to a center with it is not always possible. What would be the right management? Yuriy Kosolapov; Russia. Novosibirsk. Emergency Hospital Number 2. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 15:33:27 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 16:33:27 -0200 Subject: [ISCHEMIA-FORUM] EXPERTS ASK, EXPERTS ANSWER Message-ID: <47A0C2F7.4000505@myocardial.ischemia-symposium.org> Dr. Andriy Vorotniak from Russia and Argentina asks - For Drs. Nikus, Kjell/Eskola, Markku, About the training of a good "electrocardiologist." To optimize the management of ACS, the opinion of a good specialist in ECG is often needed. Currently, most young cardiologists interpret ECGs by criteria and algorithms. Since vectocardiography, regrettably, is no longer used, it is very hard to interpret ECGs by vectors. How a good "electrocardiologist" should be trained nowadays? ------------------------------------- Dr. Kjell Nikus and Dr. Markku Eskolaq from Finland answers - First of all, we think that instead of learning by criteria and algorithms, it is important to understand what is going on in the myocardium and in the coronary tree when studying individual cases. A good electrocardiologist dealing with acute coronary syndrome should, of course, have basic knowledge about mechanisms behind changes in the ST segment, the T wave and the QRS complex in acute myocardial ischemia, but it is also important to be familiar with invasive/interventional cardiology. In that way one can follow cases from the first ECG through the first therapeutic steps to the catheterization laboratory and during the hospital stay. Cases should be shared between electrocardiologists and interventional cardiologists. In addition, there should be vivid communication between those involved in patient care and some experienced "master", to whom clinical data and ECGs can be easily shown or, alternatively sent by internet, even for immediate telemedicine consultation. Cases may also presented at lectures, but it is important to show all the data, not only the ECGs, but clinical, angiographic and sometimes echo- or other available data. We think that sound self-criticism is important - at least in our experience, the ECG never lies, but the interpreter may be on the wrong track. This is the point where one should go through all data (ECGs, angio, laboratory tests and other) afterwards, consult the literature and discuss with colleagues. Every case is unique and has something to teach us. Yours Kjell Nikus & Markku Eskola -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 16:12:51 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 17:12:51 -0200 Subject: [ISCHEMIA-FORUM] Thank you very much. Dr. Espinoza Inga Message-ID: <47A0CC33.90403@myocardial.ischemia-symposium.org> Thank you very much and congratulations to all the participants of this excellent virtual forum, and very particularly to those who organized it, and thank you for the chance you gave me to participate in it, and be able to nourish from your knowledge. Sincerely, Diego Espinoza Inga Cardi?logo Hospital Monte Sina? Cuenca - Ecuador -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 16:26:55 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 17:26:55 -0200 Subject: [ISCHEMIA-FORUM] 133R Sleep disorders and coronary spasm. Dr. Yabluchansky Message-ID: <47A0CF7F.3050307@myocardial.ischemia-symposium.org> Dear Dr. R. Pizarro, You brought up a very interesting topic, and it would be impossible to answer your question briefly. Very often, the answers are not in the guidelines, but in the book by the famous cardiologist Lown, "The Lost Art of Healing." It is worth remembering a clinical case, described by the author, about a patient with episodes of nocturnal arrhythmias: then, Dr. Lown advised waking up 2 hours earlier than the usual time of appearance of arrhythmia, taking a double dose of medication, and then continue resting. As a result of such advice, the patient completely forgot about his arrhythmia. All processes are related; for this reason, I totally agree with the relationship between glycose metabolism and the autonomic nervous system. Well, we have to start researching. I don't know the studies related to the topic, so you could go first. The abstracts submitted were very interesting, and I would also start investigating this interesting issue, which is possible nowadays. Thank you very much for your interest and appreciation of my hypothesis, and also for the new ideas for my research team. Next, I invite you to read my presentation in the symposium: http://www.myocardial.ischemia-symposium.org/lectures/ing_yabluchansky_nykol a/lecture.php Precisely "unknown to the English media" was a reference to this presentation. Best regards, Yabluchansky Mykola (Nickolay) Head and Professor of Internal Diseases Dept. of School of Fundamental Medicine Kharkiv V.N. Karazin' National University, Chief editor of medical newspaper Medicus Amicus, +38(067)5049851 mobile, mydoctorlife at gmail.com my at medicusamicus.com www.medicusamicus.com -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 17:01:21 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 18:01:21 -0200 Subject: [ISCHEMIA-FORUM] 135P False tendinous chord Dr. Paixao Almeida Message-ID: <47A0D791.3060705@myocardial.ischemia-symposium.org> Dear Prof. Dr. Djair Brindeiro, Thank you for your attention and by the clarification. Based on the work, you are completely right. But the "atrocious doubt that torments and frigthens" is conduction by fibrous tissue. This is why I thought of (and quite a lot) on arrhythmogenesis by block. Regards, Dr. Paixao Almeida -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 18:51:06 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 19:51:06 -0200 Subject: [ISCHEMIA-FORUM] 138E VCG. Dr. Perez Riera Message-ID: <47A0F14A.1020509@myocardial.ischemia-symposium.org> Dear Dr. Andriy Vorotniak from Russia and Argentina I agree wit you that is regrettably, that VCG is no longer used. Until the middle 80s, it was believed that the VCG presented a greater specificity, sensitivity and accuracy in comparison to the conventional ECG, in the diagnosis of the different heart diseases. However, more recent studies revealed that both methods present similar diagnostic abilities. The VCG still is superior to the ECG in very specific situations, such as in the evaluation of electrically inactive areas, in intraventricular conduction disorders combined and/or in association to inactive areas, in the identification and location of ventricular pre-excitation, in the differential diagnosis of patterns varying from normal of electrical axis deviation, in the evaluation of particular aspects of Brugada Syndrome, and in the estimation of the severity of some enlargements, among others. With the advent of computerized vectocardiography, a technology that improves the determination of the onset and the end of loops, establishes a ratio between the length and width of the T waves and the spatial areas of the vectors; a future still promising is expected for this methodology. In the fields of education and research, VCG provided a better and more rational insight into the electrical phenomena that occur spatially, and represented an important impact on the progress of ECG. Although a few medical centers still use the method as a routine, we hope that the use of this resource will not get lost over time, sinceVCG still represents a source to enrich science by enabling a better morphological interpretation of the electrical phenomena of the heart. The advantages of the VCG compared to the ECG are: 1) The VCG provides three-dimensional information of the electric activity of the atria and the ventricles, showing in a clearer way than the ECG, the spatial orientation and the magnitude of the vectors at every moment1. 2) The VCG has a greater sensitivity than the ECG in detecting atrial enlargements2 and greater sensitivity and specificity than the ECG in the diagnosis of left ventricular enlargement (LVE). Abbott-Smith et al., made vectocardiograms in 100 patients carriers of left ventricular enlargement (LVE) confirmed in the necropsy2 and concluded that the VCG was capable of diagnosing 50% of the cases, with 11.7% of false positives. These figures point out a greater sensitivity of the VCG over the ECG in the diagnosis of LVE; 3) The VCG may clear doubts in the cases of suspicion of electrically inactive area in the septal or antero-septal wall of the left ventricle (LV), when the LVE of the systolic type is present, observed in ECG with QS pattern in V1; V1 and V2 or V1, V2 and V3. In absence of electrically inactive area, the "dashes" of the initial 10 to 20 ms of the QRS loop, are recorded without delay, while in the presence of electrically inactive area, the dashes of the initial 40 ms are very close to each other3. 4) The VCG presents a greater correlation with the echocardiogram, when compared with the ECG, in determining the left ventricular mass4, and it appears as superior to ECG and echocardiogram in the diagnosis of chamber enlargement, associated to electrically inactive areas5 5) The VCG presents a greater diagnostic sensitivity in comparison to the ECG in acute myocardial infarction (AMI), when associated to left anterior fascicular block (LAFB). In the presence of AMI of the LV inferior wall, the VCG may bring additional information, which the ECG does not reveal, such as the association with LAFB6. 6) The VCG presents a greater sensitivity and specificity than the ECG in the diagnosis of lateral infarction (old strict dorsal AMI), and it enables a more appropriate differentiation with other causes of prominent anterior forces, such as normal hearts with counterclockwise rotation of the longitudinal axis and shift to the right of the transition area in precordial leads, right ventricle enlargement, complete right bundle branch block (CRBBB), hypertrophic cardiomyopathy both in its obstructive and non-obstructive form (increase in the magnitude of the septal vector), diastolic enlargement of the left ventricle with dislocation of the transition area to the right, ventricular pre-excitation of the Wolff-Parkinson-White type with anomalous bundle, in a parallel way to posterior location (WPW type A), Duchenne-Erb myopathy or malignant in childhood and other causes9; 10 7) The VCG has more sensitivity than the ECG for the diagnosis of multiple infarctions, associated to LAFB11. 8) The VCG has a greater accuracy than the ECG in the diagnosis of inferior infarction12, however, about this topic, there is no consensus since there are studies that concluded that the VCG is not superior to the ECG in the diagnosis of isolated diaphragmatic infarction12. Edenbrandt et al, compared the diagnostic value of both methods in 65 patients with inferior AMI proven by hemodynamic study and gammagraphy with Thallium 201. The authors observed that the sensitivity of the VCG was 69%, and the ECG was 43%, with this difference being statistically significant (p<0.001). In the control group, only three false positives occurred13. 9) The method improves sensitivity in the diagnosis of inferior infarction extended to the LV anterior wall14(called deep septal infarction). 10) The VCG is of great significance for the diagnosis of the left septal fascicular block (LSFB)15; 16; 17. This type of left fascicular block was shown in numerous publications and, in an unexplainable way, the Anglo-Saxon literature does not acknowledge it. 11) The VCG is superior to the ECG in the cases of atypical CRBBB associated to LAFB (bifascicular block) called by Rosenbaum "standard masquerading bundle branch block". In these cases, in the presence of CRBBB associated to a high degree of LAFB, the DI lead presents small or non-existent s wave, with a pure R wave appearing in this lead, characteristic of CLBBB (pseudo CLBBB). This situation translates the presence of CRBBB associated to LAFB, LVE and block located in the left ventricle18. In some cases, a CRBBB pattern is observed in the right precordial leads and CLBBB in the left precordial leads. This situation was called "masquerading bundle branch block". This pattern defines the presence of CRBBB associated to severe LVE, a block located in the antero-lateral wall of the left ventricle and usually LAFB19. 12) The VCG is very useful to differentiate the rare CLBBB with extreme deviation of SAQRS to the right in the FP (to the right of +90?). According to the location of SAQRS in the FP, the CLBBB was divided into 4 types: 1) CLBBB with SAQRS not deviated: between ?30? and +60?. It represents 65% to 70% of the cases; 2) CLBBB with SAQRS with extreme deviation to the left: beyond ?30?. It represents 5% of the total; 3) CLBBB with SAQRS deviated to the right between +60? and +90?. It represents 4% of the total; 4) CLBBB with SAQRS presenting extreme deviation to the right: >+90?. This group represents less than 1% of the total of CLBBB and was called "paradoxical type" by Lepeschkin. CLBBB with SAQRS located to the right of +90? in the FP, may have SAQRS located in the right inferior or right superior quadrant. Lepeschkin called them "paradoxical CLBBB" or type IV (SAQRS between +90? and +135?). We could add a type V when SAQRS is located to the right of +135? (CLBBB of congenital heart diseases). In these cases, the VCG is superior to ECG in determining the possible cause: 1) If CLBBB is associated to severe RVE; 2) If fascicular CLBBB (LAFB + LPFB) by a higher degree of block in the left posterior fascicle; 3) If the CLBBB is associated to lateral electrically inactive area. 13) The technique known as Continuing Vectocardiography Monitoring (CVM) carried out during elective angioplasty, proved to be a promising tool to detect patients with an increased risk of developing AMI related to the procedure. Guo et al20, used the method in 169 patients, which started 5 minutes before the procedure and was interrupted 30 minutes after the first insufflation of the angioplasty balloon. Considering the ST segment elevation to determine the AMI, the sensitivity of the CVM to detect increased risk of acute myocardial infarction related to the procedure was 93%, the specificity was 56% and the negative predictive value 99%. 14) The VCG presents a greater diagnostic sensitivity than ECG to determine the severity of congenital aortic valve stenosis. Thus, the presence of the maximal vector in the horizontal plane to the left (LMSV) with a voltage greater than 4 mV, heading to the left and backward around ?56?, represents a significant marker of severe aortic stenosis (left intraventricular pressure > 200 mmHg); the presence of the maximal vector to the left with a voltage near 2.2 mV and around ?19?, indicates mild congenital aortic stenosis20. 15) In patients carriers of congenital pulmonary valve stenosis, the VCG has a good correlation between the value of the systolic pressure of the right ventricle and the presence of the maximal spatial vector to the right of the HP: "Maximal Spatial Voltage directed to the Right" (RMSV). Thus, a right intraventricular pressure >100 mmHg has a RMSV >2.3 mV21. 16) The VCG is superior to the ECG to identify and locate the anomalous bundle in pre-excitation of the Wolff-Parkinson-White. The method presents a high sensitivity and accuracy. This fact is relevant to guide the electrophysiologist, pointing the most appropriate site to apply radiofrequency energy22. The diagnostic specificity is not increased when compared to an ECG in this case1. 17) The VCG presents greater sensitivity and specificity than ECG in the diagnosis of end conduction delay by the fascicles of the right branch (blocks of the right branch: fascicular, zonal or of the free wall). The VCG enables to rule out or confirm the cases where the ECG presents a doubt when there is association of end delay through the right branch with electrically inactive areas, both of the inferior and the anterior walls23. 18) The VCG optimizes the differential diagnosis of right fascicular blocks with left fascicular blocks24. 19) The VCG is very useful in the diagnosis of Brugada syndrome when the ECG shows extreme deviation of SAQRS to the left in the FP (9.5% of the cases)25. We showed that in this entity, the extreme deviation of SAQRS to the left might be the consequence of LAFB and of end conduction delay through the superior or subpulmonary fascicle of the right branch, which goes through the right ventricle outflow tract, the area affected in this entity26. 20) The VCG has a great value in the analysis of electrical modifications that are the consequence of septal percutaneous ablation of the obstructive form of severe hypertrophic cardiomyopathy, not responsive to drugs and with incapacitating symptoms (functional class II and IV), by injection of absolute alcohol. The result of septal or antero-septal infarction generates a pattern of CRBBB in almost all cases, unlike myotomy/myectomy surgery, which promotes CLBBB in approximately 80% of the cases28. References 1. Chou TC. Value and limitations of vectorcardiography in cardiac diagnosis. Cardiovasc Clin 1975;6:163-178. 2. Chou TC. When is the vectorcardiogram superior to the scalar electrocardiogram? J Am Coll Cardiol 1986;8:791-799. 3. Abbott-Smith CW, Chou T; Vectorcardiographic criteria for the diagnosis of left ventricular hypertrophy. Am Heart J. 1970;79:361-369. 4. Pipberger HV, Goldman MJ, Littmann D, et al, Correlations of the orthogonal electrocardiogram and vectorcardiogram with constitutional variablesin 518 normal men. Circulation; 1967;35: 536-551. 5. Vine DL, Finchum RN, Dodge HT, et al. Comparison of the vectorcardiogram with the electrocardiogram in the prediction of left ventricular size. Circulation. 1971;43:547-558. 6. Benchimol A, Desser KB, Schumacher J. left anterior hemiblock from inferior infarction with left axis deviation. Chest 1972;61:74-76. 7. Hurd HP 2nd, Starling MR, Crawford MH, et al. Comparative accuracy of electrocardiographic and vectorcardiographic criteria for inferior myocardial infarction. Circulation 1981;63:025-1029. 8. Brisse B. Clinical vectorcardiography: the Fritz-Schellong commemorative lecture Z Kardiol. 1987;76:65-71. 9. Hoffman I, Taymor RC, Morris MH Kittell I. Quantitative criteria for the diagnosis of dorsal infarction using the Frank Vectorcardigram .Am Heart J. 1965;70:295-304. 10. Benchimol A, Desser KB. Advances in clinical vectorcardiography. Am J Cardiol 1975;36:76-86. 11. Lui CY, Ornato JP, Buell JC, et al. Lack of superiority of the vectorcardiogram over the electrocardiogram in detecting inferior wall myocardial infarction regardless of time since infarction. J Electrocardiol 1987;20:241-246. 12. Edenbrandt L, Pahlm O, Lyttkens K, et al.Vectorcardiogram more sensitive than 12-lead ECG in the detection of inferior myocardial infarction. Clin Physiol 1990;10:551-559. 13. Mehta J, Hoffman I, Smedresman P, et al. Vectorcardiographic, electrocardiographic, and angiographic correlations in apparently isolated inferior wall myocardial infarction. Am Heart J 1976;91:699-704. 14. Tranchesi J, Moffa PJ, Pastore CA, et al. Block of the antero-medial division of the left bundle branch of His in coronary diseases. Vectrocardiographic characterization. Arq Bras Cardiol 1979;32:355-360. 15. Nakaya Y, Hiraga T. Reassessment of the subdivision block of the left bundle branch. Jpn Circ J 1981;45:503-516. 16. 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;47:1179-1189. 17. Rosenbaum MB, Yesuron J, Lazzari JO, Elizari MV. Left anterior hemiblock obscuring the diagnosis of right bundle branch block. Circulation. 1973;48:298-303. 18. Rosenbaum MB, Elizari MV, Lazzari JO, Halpern MS, Nau GJ. Bilateral bundle branch block: its recognition and significance. Cardiovasc Clin. 1971; 2:151-179. 19. Guo X, Jue X, Ruan Y, et al. Model TJ-IV computer-assisted vectorcardiogram analysis system. J Tongji Med Univ. 2001;21:21-22,81. 20. Ellison RC and Restieaux NJ, Vectorcardiography in congenital Heart disease. A method for Estimating severity. Chapter 5 pp: 44, 1972 W.B. Saunders Company Philadelphia ? London-Toronto. 21. Ellison RC, and Restieaux NJ. Vectorcardiography In Congenital Heart Disease. A Method for Estimating Severity, Valvular Pulmonic Stenosis Chapter 6 pp: 60-74 1972 W.B. Saunders Company Philadelphia ? London-Toronto. 22. Giorgi C, Nadeau R, Primeau R, et al. Comparative accuracy of the vectorcardiogram and electrocardiogram in the localization of the accessory pathway in patients with Wolff-Parkinson-White syndrome: validation of a new vectorcardiographic algorithm by intraoperative epicardial mapping and electrophysiologic studies. Am Heart J 1990;119:592-598. 23. Pastore CA, Moffa PJ, Tobias NM, de Moraes AP, Nishioka SA, Chierighini JE, Cruz Mdo C, Del Nero Junior E, Bellotti G, Pileggi F.Segmental blocks of the right bundle-branch and electrically inactive areas. Differential electro-vectorcardiographic diagnosis. Arq Bras Cardiol. 1985;45:309-17. 24. Pastore CA, Moffa PJ, Spiritus MO, et al. Fascicular blocks of the right branch. Standardization of vectorelectrocardiographic findings. Arq Bras Cardiol. 1983;41:161-166. 25. Atarashi H, Ogawa S, Harumi K, et al. Idiopathic VentricularFibrillation Investigators. Three-year follow-up of patients with right bundle branch block and ST segment elevation in the right precordial leads:Japanese Registry of Brugada Syndrome. Idiopathic Ventricular Fibrillation Investigators. J Am Coll Cardiol 2001;37:1916-1920. 26. P?rez Riera AR, Ferreira C, Schapachnik E. Value of 12 lead electrocardiogram and //derived methodologies in the diagnosis of Brugada disease?. Chapter 7; pp: 87-110. In The Brugada Syndrome From Bench to Bedside. Editor Charles Antzelevich With Associate Editors Pedro Brugada, Joseph Brugada e Ram?n Brugada ? 2005 - Blackwell ? Futura. 27. Riera AR, de Cano SJ, Cano MN, et al. Vector electrocardiographic alterations after percutaneous septal ablation in obstructive hypertrophic cardiomyopathy. Possible anatomic causes. Arq Bras Cardiol. 2002;79:466-475. All the best for all and congratulations to all the participants of this fantastic virtual symposium, and very particularly to my dearest friends Edgardo Schapachnik, Sergio Dubner and the fantastic Prof. Antoni Bayes de Luna. Andr?s Ricardo P?rez Riera MD and Master in cardiology area. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 18:58:38 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 19:58:38 -0200 Subject: [ISCHEMIA-FORUM] 139E Infarction heart. Dr. Serafinovich Message-ID: <47A0F30E.4050507@myocardial.ischemia-symposium.org> Dear colleagues. The present letter consists the new conception of ?Infarction heart?. We suggest that today the term ?myocardial infarction? is not enough to explain all peculiarities of origin, development, course, classification, terminology, diagnosis, management and prognosis of this disease. If myocardial infarction is a local process, how can we mark and interpret myocardium changes beyond it borders? Why is infarction (even transmural) often invisible on ECG? Is the troponin level coincident to clinical perception of the disease? Is the myocardial infarction necrosis or aseptic inflammation? Does the posterior infarction really exist? What does the myocardial infarction mean? Why and how do diffused processes (left ventricle remodeling and secondary cardiomyophathy) develop? It is possible to percept the myocardial infarction by the term ?Infarction heart?. "Infarction heart" is the aggregate of morphological and functional abnormalities in various heart segments, cavities size and form changes, valves condition and blood flow directions, developed due to significant reduction of coronary perfusion with cardiomyocytes necrosis and aseptic inflammation. Request for collaboration. To our sorrow, the technology resources of clinic cannot allow us to realize ourselves all investigations according this conception. We will grateful for any offers of collaboration. Best regards, Dr. Serafinovich I., PhD Grodno, Belarus E-mail: drserafinovich at mail.ru drserafinovich at grsmu.by -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 19:07:03 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 20:07:03 -0200 Subject: [ISCHEMIA-FORUM] 134R Question by Dr. Pizarro on ACS triggers. Dr. Saveliev Message-ID: <47A0F507.9080107@myocardial.ischemia-symposium.org> Dear colleagues! Probably, speaking about nocturnal vasospasm triggers, it is worth remembering the acetylcholine mechanism in this process. The relationship could be this: endothelial dysfunction ---> increase of nocturnal acetylcholine ---> hyperreactivity of the vascular smooth muscle. In these processes, the calcium plays a significant role, and for this reason the management with calcium blockers is usually effective. Sincerely, Dr. Saveliev, Russia -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Wed Jan 30 20:26:11 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Wed, 30 Jan 2008 21:26:11 -0200 Subject: [ISCHEMIA-FORUM] Acknowledgement. Dr. Conci Message-ID: <47A10793.5040906@myocardial.ischemia-symposium.org> JUST THANK YOU. Dr Eduardo Conci (I.M.C.CBA ARGENTINA) -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 31 09:40:34 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 31 Jan 2008 10:40:34 -0200 Subject: [ISCHEMIA-FORUM] 144E Ventricular fibrillation. Dr. Okyay Message-ID: <47A1C1C2.8050800@myocardial.ischemia-symposium.org> Dear colleague, Patient who had an episode of VF during thrombolytic therapy and had sinus rhythm after defibrillation does not require permanent intravenous antiarrhythmic therapy. I would prefer to give high dose beta-blocker therapy and intensive anti-aggregant therapy and consider early invasive strategy. A VF or VT, 24 hours after succesfull thrombolytic therapy should make the cardiologist to perform an electrophysiologic study. Sincerely. Dr. Kaan Okyay -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 31 10:29:35 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 31 Jan 2008 11:29:35 -0200 Subject: [ISCHEMIA-FORUM] Congratulations. Dr. Mautner Message-ID: <47A1CD3F.9040800@myocardial.ischemia-symposium.org> Congratulations to all the people in charge of this virtual event, both for the success and the scientific quality achieved. Best regards, Prof. Dr. Branco Mautner Ex- Presidente de ISHNE -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 31 10:41:31 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 31 Jan 2008 11:41:31 -0200 Subject: [ISCHEMIA-FORUM] 136S Inferior AMI and AV block. Dr. Pellizzon Message-ID: <47A1D00B.5050302@myocardial.ischemia-symposium.org> Dear Yuri, Your question is very interesting, because often the answers are not in books or papers, but in our experience and the art of medicine. Most information always comes from developed areas of the world, where access to technology or the sanitary organization is very different from developing countries or from large population centers. Currently, in my service we stop asking ourselves this question, because we have a swift access to the hemodynamics, but it did exist in the thrombolytic era?And we solved it in the following way: First, we implanted the pacemaker because initially we didn't know if the hemodynamic failure was related to bradyarrhythmia, to the extension of AMI, or to RV involvement, since when this happens, the occlusion of the right coronary artery is generally proximal. Moreover, we did not have problem of bleeding in post-thrombolysis puncture. Later, we administered streptokinase and we evaluated if there was reperfusion or not. Let's remember that reperfusion with thrombolysis is 50-65%, so it is unlikely for complete AVB to be solved after reperfusion and even more when the injury has been prolonged. Solving a conduction disorder occurs within days, and as we know, we have to solve the bradyarrhythmia that generates ventricular tachyarrhythmia. Back then we would always apply thrombolysis, because this drug changed the history of AMI. I hope this commentary is helpful. Warm regards, Dr. Oscar A. Pellizz?n Jefe Unidad Coronaria, H. P. del Centenario Rosario, Argentina. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 31 13:27:35 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 31 Jan 2008 14:27:35 -0200 Subject: [ISCHEMIA-FORUM] 146E Inferior AMI and AV block. Dr. Madias Message-ID: <47A1F6F7.6090805@myocardial.ischemia-symposium.org> This is a message for Dr. Yuriy Kosolapov; Russia. Novosibirsk. Emergency Hospital Number 2. Dear Dr. Kosolapov: I would go ahead and give thrombolysis, while I apply the external pacemaker electrodes to the patients chestwall, for prophylactic demand pacemaking, in case the idioventricular or AV junctional subsidiary pacemaker rate is too low. Warmest Regards to all John E. Madias, MD, FACC, FAHA Mount Sinai School of Medicine -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 31 14:54:45 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 31 Jan 2008 15:54:45 -0200 Subject: [ISCHEMIA-FORUM] Closing remarks. Dr. Stone Message-ID: <47A20B65.40102@myocardial.ischemia-symposium.org> Dear Friends and Colleagues, On behalf of ISHNE and ISCP, as well as my internet symposium Co-Directors, Drs. Antoni Bayes de Luna, Juan-Carlos Kaski, and Richard Verrier, I would like to thank you for your participation in this unique international symposium. We have had many excellent presentations covering a broad range of topics in the diagnosis and management of patients with coronary artery disease, and a large number of insightful and thought-provoking questions and discussions from our many participants from around the world. We are all extremely pleased with your participation and we hope that the symposium has been helpful to you in your care of coronary patients. We look forward to interacting closely with you again in the future. We encourage you to take part in as many activities of ISHNE and ISCP as possible, since these organizations are created to help in the understanding of the management of patients with cardiac disease, and to disseminate new and valuable educational information. We will be organizing many other internet symposia in the future and we look forward to seeing you then! Best regards and thank you again for your participation, Peter H. Stone, M.D. -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia From info at myocardial.ischemia-symposium.org Thu Jan 31 14:56:13 2008 From: info at myocardial.ischemia-symposium.org (MYOCARDIAL.ISCHEMIA-INFO) Date: Thu, 31 Jan 2008 15:56:13 -0200 Subject: [ISCHEMIA-FORUM] Closing remarks. Dr. Bayes de Luna and Dr. Dubner Message-ID: <47A20BBD.80702@myocardial.ischemia-symposium.org> Dear friends, The symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia 2008 has come to an end, in spite of the ceaseless exchange of questions and answers that still goes on although it has already ended. This was the first experience that we have realized jointly between 2 scientific societies, ISHNE and ISCP, and the result is nothing less than surprising: we could gather the largest audience in our history of virtual symposia. This response encourages us to organize new scientific events and generates new challenges for us. We would like to thank everyone who has collaborated with this event; the directors of the Symposium, Drs. P. Stone, A. Bayes de Luna, JC Kaski, and R. Verrier; the authors that have presented lectures with an exceptional scientific level, and all of you, the 15,893 registrants, who have generated a discussion framework hardly ever seen before. We would also like to thank the companies that accompanied us in this symposium, without which help this event would have been impossible (GE Healthcare platinum sponsor, CV Therapeutics, Servier, and the Uriach Group, silver sponsors), the Directors of the Organizing Committee, Drs. E. Schapachnik and S. Dubner, the technical and operative group, the translators, who will receive out gratefulness personally in due time, due to their great efforts and care so that this symposium could be ready on time, in spite of numerous setbacks. We would like to make a special mention to the Chinese team in general, and Drs. Li Zhang and Yunlong Xia for their particular care and their close relationship to the organizers of the www.365heart page, with whom we have made an agreement of collaboration for a greater dissemination of our Internet activities in China. To all of you, thank you very much, and we will be waiting for you in our next scientific event: an update on arrhythmogenic right ventricular dysplasia, chaired by Drs. F. Marcus, W. Zareba, and G. Fontaine. Best regards, Dr. Antoni Bayes de Luna Dr. Sergio Dubner President of ICSP President of ISHNE -- Dr. Sergio Dubner Dr. Edgardo Schapachnik ------------------------------- Coordinators Steering Committees of the ISHNE/ISCP Internet Symposium on Current Approaches for the Assessment and Management of Myocardial Infarction and Ischemia