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THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA Developments in Cardiovascular Medicine 232 A Bayés de Luna, F Furlanello, B.J Maron and D.P Zipes (eds.): ISBN: 0-7923-6337-X Arrhythmias and Sudden Death in Athletes 2000 233 J-C Tardif and M.G Bourassa (eds): Antioxidants and Cardiovascular Disease 2000 ISBN: 0-7923-7829-6 234 J Candell-Riera, J Castell-Conesa, S Aguadé Bruiz (eds): Myocardium at Risk and Viable Myocardium Evaluation by SPET 2000.ISBN: 0-7923-6724-3 235 M.H Ellestad and E Amsterdam (eds): Exercise Testing: New Concepts for the New Century 2001 ISBN: 0-7923-7378-2 236 Douglas L Mann (ed.): The Role of Inflammatory Mediators in the Failing Heart 2001 ISBN: 0-7923-7381-2 237 Donald M Bers (ed.): Excitation-Contraction Coupling and Cardiac Contractile Force, Second Edition 2001 ISBN: 0-7923-7157-7 238 Brian D Hoit, Richard A Walsh (eds.): Cardiovascular Physiology in the Genetically Engineered Mouse, Second Edition 2001 ISBN 0-7923-7536-X 239 Pieter A Doevendans, A.A.M Wilde (eds.): Cardiovascular Genetics for Clinicians 2001 ISBN 1-4020-0097-9 240 Stephen M Factor, Maria A.Lamberti-Abadi, Jacobo Abadi (eds.): Handbook of Pathology and Pathophysiology of Cardiovascular Disease 2001 ISBN 0-7923-7542-4 241 Liong Bing Liem, Eugene Downar (eds): Progress in Catheter Ablation 2001 ISBN 1-4020-0147-9 242 Pieter A Doevendans, Stefan Kääb (eds): Cardiovascular Genomics: New Pathophysiological Concepts 2002 ISBN 1-4020-7022-5 243 Antonio Pacifico (ed.), Philip D Henry, Gust H Bardy, Martin Borggrefe, Francis E Marchlinski, Andrea Natale, Bruce L Wilkoff (assoc eds): Implantable Defibrillator Therapy: A Clinical Guide 2002 ISBN 1-4020-7143-4 244 Hein J.J Wellens, Anton P.M Gorgels, Pieter A Doevendans (eds.): The ECG in Acute Myocardial Infarction and Unstable Angina: Diagnosis and Risk Stratification 2002 ISBN 1-4020-7214-7 Previous volumes are still available THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA Diagnosis and Risk Stratification by Hein J.J Wellens Anton P.M Gorgels Academic Hospital, Maastricht The Netherlands and Pieter A Doevendans, MD Interuniversity Cardiology Institute of The Netherlands Utrecht, The Netherlands KLUWER ACADEMIC PUBLISHERS NEW YORK, BOSTON, DORDRECHT, LONDON, MOSCOW eBook ISBN: Print ISBN: 0-306-48202-9 1-4020-7214-7 ©2002 Kluwer Academic Publishers New York, Boston, Dordrecht, London, Moscow Print ©2003 Kluwer Academic Publishers Dordrecht All rights reserved No part of this eBook may be reproduced or transmitted in any form or by any means, electronic, mechanical, recording, or otherwise, without written consent from the Publisher Created in the United States of America Visit Kluwer Online at: and Kluwer's eBookstore at: http://kluweronline.com http://ebooks.kluweronline.com CONTENTS Chapter Introduction Chapter Determining the size of the area at risk, the severity of ischemia, and identifying the site of occlusion in the culprit coronary artery A The ST segment deviation score B The terminal QRS-ST segment pattern 11 C Specific ECG patterns indicating the site of coronary artery occlusion: I Infero-posterior myocardial infarction with or without right ventricular infarction II Anterior wall myocardial infarction Chapter Chapter 13 13 24 Conduction disturbances in acute myocardial infarction 43 A The sino-atrial region 45 B The AV nodal conduction system 49 C The sub-AV nodal conduction system 53 Myocardial infarction in the presence of abnormal ventricular activation 65 A Left bundle branch block 68 B 76 Paced ventricular rhythm C Pre-excitation 79 Chapter Arrhythmias in acute myocardial infarction: Incidence and prognostic significance 85 A Supraventricular arrhythmias 87 B Ventricular arrhythmias 91 Chapter The electrocardiographic signs of reperfusion 99 Chapter The electrocardiogram in unstable angina 117 Recognition of multivessel and left main disease Recognition of critical narrowing of the left anterior descending coronary artery Index 127 ERRATA The ECG in Acute Myocardial Infarction and Unstable Angina: Diagnosis and Risk Stratification by: Hein J.J Wellens, Anton P.M Gorgels and Pieter A Doevendans ISBN: 1-4020-7214-7 The publisher regrets that due to a publishing error, the incorrect series number appears on the series page and the back cover The correct series number is DICM245 The corrected series page appears below Kluwer Academic Publishers Developments in Cardiovascular Medicine 232 233 234 235 236 237 238 239 240 241 242 243 244 245 A Bayés de Luna, F Furlanello, B.J Maron and D.P Zipes (eds.): Arrhythmias and Sudden Death in Athletes 2000 ISBN: 0-7923-6337-X J-C Tardif and M.G Bourassa (eds): Antioxidants and Cardiovascular Disease 2000 ISBN: 0-7923-7829-6 J Candell-Riera, J Castell-Conesa, S Aguadé Bruiz (eds): Myocardium at Risk and Viable Myocardium Evaluation by SPET 2000.ISBN: 0-7923-6724-3 M.H Ellestad and E Amsterdam (eds): Exercise Testing: New Concepts for the New Century 2001 ISBN: 0-7923-7378-2 Douglas L Mann (ed.): The Role of Inflammatory Mediators in the Failing Heart 2001 ISBN: 0-7923-7381-2 Donald M Bers (ed.): Excitation-Contraction Coupling and Cardiac ISBN: 0-7923-7157-7 Contractile Force, Second Edition 2001 Brian D Hoit, Richard A Walsh (eds.): Cardiovascular Physiology in the Genetically Engineered Mouse, Second Edition 2001 ISBN 0-7923-7536-X Pieter A Doevendans, A.A.M Wilde (eds.): Cardiovascular Genetics for Clinicians 2001 ISBN 1-4020-0097-9 Stephen M Factor, Maria A.Lamberti-Abadi, Jacobo Abadi (eds.): Handbook of Pathology and Pathophysiology of Cardiovascular Disease 2001 ISBN 0-7923-7542-4 Liong Bing Liem, Eugene Downar (eds): Progress in Catheter Ablation 2001 ISBN 1-4020-0147-9 Pieter A Doevendans, Stefan Kääb (eds): Cardiovascular Genomics: New ISBN 1-4020-7022-5 Pathophysiological Concepts 2002 Daan Kromhout, Alessandro Menotti, Henry Blackburn (eds.): Prevention of Coronary Heart Disease: Diet, Lifestyle and Risk Factors in the Seven Countries Study 2002 ISBN 1-4020-7123-X Antonio Pacifico (ed.), Philip D Henry, Gust H Bardy, Martin Borggrefe, Francis E Marchlinski, Andrea Natale, Bruce L Wilkoff (assoc eds): Implantable Defibrillator Therapy: A Clinical Guide 2002 ISBN 1-4020-7143-4 Hein J.J Wellens, Anton P.M Gorgels, Pieter A Doevendans (eds.): The ECG in Acute Myocardial Infarction and Unstable Angina: Diagnosis and Risk Stratification 2002 ISBN 1-4020-7214-7 Previous volumes are still available Authors Pieter A Doevendans, M.D Associate Professor of Cardiology, Department of Cardiology Academic Hospital Maastricht University of Maastricht, the Netherlands Anton P Gorgels, M.D Associate Professor of Cardiology Department of Cardiology Academic Hospital Maastricht University of Maastricht, the Netherlands Hein J.J.Wellens, M.D Professor of Cardiology Medical Director of the Interuniversity Cardiology Institute of the Netherlands (ICIN) Utrecht, the Netherlands Acknowledgements Over the years the cardiologists, residents, fellows and nursing staff, working at the Department of Cardiology of the Academic Hospital of Maastricht, have carefully collected the electrocardiograms published in this book We are very much indebted to them for their enthusiasm and willingness to donate those pearls to us! To have the electrocardiograms perfectly reproduced we had the good fortune to have Adrie van den Dool working for us She and the medical photography group of the hospital did a perfect job, demonstrating again their ability to make beautiful illustrations Excellent secretarial assistance was provided by Birgit van den Burg, Miriam Habex, Vivianne Schellings and Willemijn Gagliardi We greatly appreciated their pleasant, never complaining way of helping us again and again! Manja Helmers played an important role in the final phase by expertly producing the layout of the manuscript Hein J.J Wellens Anton P.M Gorgels Pieter A Doevendans 118 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA ST segment depression on admission identifies a high risk group of patients with unstable coronary artery disease Magnitude and distribution of ST segment depression should determine invasive versus conservative management strategy In patients with acute myocardial ischemia continuous 12 lead ECG or serial ECG’s recordings may be needed to diagnose unstable angina or non ST-segment elevation myocardial infarction Determine troponin level to document recent loss of myocardial tissue In left main or vessel disease ST segment changes in or more ECG leads develop during chest pain In critical LAD narrowing precordial T wave negativity develops after chest pain has subsided THE ELECTROCARDIOGRAM IN UNSTABLE ANGINA An unstable plaque in a coronary artery may lead to critical narrowing or complete occlusion resulting in acute ischemia and/or necrosis of the myocardium The resulting clinical entities are called acute coronary syndromes and include unstable angina and acute myocardial infarction Initially it may not be clear which of the two is present, and the determination of biochemical cardiac markers such as troponin requires time and may have a low sensitivity in the early phase of myocardial ischemia The importance of ST segment depression In unstable angina and non-ST-segment elevation myocardial infarction, the 12 lead surface electrocardiogram (ECG) on admission can give important information about the site and the extent of ischemia Antman et al (1) showed that in those patients the number of leads showing ST depression and the amount of ST depression indicate size and severity of the ischemic area This was recently confirmed by Kaul et al (2) It was also shown that patients with ST segment depression may have a poorer long-term prognosis than patients with an acute myocardial infarction (3,4) Magnitude and distribution of ST depression should determine which patient will profit from an invasive versus a conservative management strategy (5) Recent data from the FRISC II study indicate that the presence of ST depression on admission is already sufficient evidence to propose early invasive treatment to the patient (6) The ECG also allows identification of high-risk syndromes such as unstable angina due to a lesion proximal in the left anterior descending (LAD) branch of the left coronary artery or due to either vessel disease or left main stem stenosis Recognizing these entities is important in the decision making to re-open the culprit artery, either pharmacologically or invasively using a percutaneous coronary intervention or bypass surgery These strategies have led to a marked improved in-hospital and post discharge prognosis of unstable angina during the last decade (7) The value of serial ECG’s Diagnosing unstable angina and also non-ST-segment elevation myocardial infarction can be particularly difficult both in relation to the presence or absence of chest pain and the changes on the ECG At the time of recording the ECG the chest pain may have already subsided In that situation it is very important to look for the development of postischemic T wave changes They may occur within a few hours Ideally they should be picked up by a continuous recording of the 12-lead ECG (8) The importance of this was recently shown by Akkerhuis et al (9) who used continuous multilead ST-T segment monitoring to identify patients with acute coronary syndromes at high risk of adverse cardiac events They especially recommended this approach in patients not showing on admission either clear ST elevation pointing to acute MI or definite ST segment depression In those patients diagnostic ST-T segment changes may occur during continuous multilead ECG monitoring and can be helpful to identify patients that will profit from an early invasive 119 120 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA intervention When continuous ECG monitoring is not possible, it is recommended to keep the patient in the emergency room, to wait for the troponin value and to record at least one more ECG before deciding to send the patient home Occasionally the ECG findings are not specific even during chest pain, especially in case of a circumflex coronary artery narrowing or occlusion Also in that situation it is very helpful to record sequential ECG’s during the observation period, to demonstrate ischemia Keep in mind that a single normal ECG in a patient with a typical syndrome of chest pain is insufficient to exclude myocardial ischemia The ECG in vessel or left main stem disease Unstable angina, such as angina at rest carries an increased risk for myocardial infarction or sudden death It is important to record the ECG during chest pain, not only to document the ischemic nature of the complaints, but also to assess the site and the extent of ischemia Typically, high-risk situations are proximal LAD involvement (10,11) 3-vessel disease and left main stem stenosis (12) (fig 7.1) The latter conditions result in a typical ECG pattern during chest pain (figure 7.2) with generalized, often marked ST-segment depression combined with ST-segment elevation in lead AVR and frequently in In a study of 120 patients with rest angina we found that the larger the number of leads with and the greater the amount of ST segment depression, the higher the risk of 3-vessel disease or main stem stenosis: A 75% positive predictive accuracy of vessel disease or a left main stenosis was present when leads or more showed ST-segment changes during chest pain (11), with leads AVR and showing ST-elevation! These ECG findings are also valid for determining the extent of ischemia when they are observed during exercise (figure 7.3) The unstable nature of the syndrome is confirmed by the persistence of changes during the recovery phase (figure 7.3C) The proximal LAD syndrome During chest pain: Peaked T-waves in the precordial leads Changes in the ST segment and the T-wave are important to diagnose both acute and subacute ischemia During acute ischemia predominant T-wave changes can be found, without marked changes in the ST-segment Typically, the T-waves become peaked, more symmetric and shorter in duration (figure 7.4) These changes reflect ischemia rather than injury and are probably explained by shortening of the subendocardial repolarization phase with intact duration of repolarization in the subepicardial layers (13) The coronary perfusion is not completely blocked either because there is a subtotal stenosis or a complete occlusion but with collateral circulation THE ELECTROCARDIOGRAM IN UNSTABLE ANGINA 121 122 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA THE ELECTROCARDIOGRAM IN UNSTABLE ANGINA After chest pain: T wave negativity in the precordial leads Recording the development of negative T waves in at least the precordial leads to following the episode of chest pain has been very useful to identify a subgroup of patients with unstable angina having an increased risk of subsequent MI or sudden cardiac death (figure 7.5) Coronary angiographic correlations invariably showed severe proximal stenosis in the left anterior descending (LAD) branch or total LAD occlusion in the presence of collateral circulation (10,14,15) LAD obstruction will lead to MI of the anterior wall as shown in fig 7.5, which was recorded before the advent of thrombolytic therapy Recognition of the ECG pattern of a critical LAD stenosis is important because vessel occlusion will lead to a large anterior wall myocardial infarction and early death may occur due to pump failure or high degree sub-AV nodal block Ventricular tachycardia may appear later during the subacute and the chronic phase and can be prevented by prompt measures to restore flow (16) After an acute coronary syndrome in the anterior wall occasionally giant T wave negativity can be observed (figure 7.6) This latter phenomenon has recently been described to predict good prognosis, as evidenced by recovery of R-waves and preservation of left ventricular function (17) 123 124 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA Recovery of T wave abnormalities following ischemia In patients having unstable angina because of a proximal LAD stenosis and surviving for at least months after the ischemic event, our group found normalization of the ST-T-segment within weeks in half of the population, and in 80% within months (16) Similar findings were reported in another study after balloon angioplasty, revealing normalization of the T wave in 90% of patients after 28 weeks (14) A more recent study also confirmed the rapid resolution of postischemic T wave inversion (within 3-21 days of presentation in 75% of cases) Persistence of T wave inversion was related to a worse outcome: More new events were found during follow-up of these patients, when compared with an unstable angina group without postischemic T wave abnormalities (14) Conclusion While Troponin determination will document loss of myocardial tissue in unstable angina the standard 12 lead ECG gives important information about the site and extent of ischemia It is possible to identify high risk situations such as unstable angina due to a proximal LAD lesion or caused by either vessel disease or left main stem stenosis Recognizing these entities is important for decision making to restore adequate patency in the culprit vessel(s) THE ELECTROCARDIOGRAM IN UNSTABLE ANGINA References Antman EM, Cohen M, Bernink PJ et al The TIMI risk score for unstable angina from ST elevation MI: a method for prognosticitation and therapeutic decision making JAMA 2000; 284:835-842 Kaul P, Fu Y, Shang WC, et al Prognostic value of ST segment depression in acute coronary syndromes : insights from PARAGON-A applied to GUSTO-II b J Am Coll Cardiol 2001;38:64-71 Savonitto S, Ardissino D, Granger CB, et al Prognostic value of the admission electrocardiogram in acute coronary syndromes JAMA 1999;281:707-713 Hyde TA, French JK, Wong CK, et al Four-year survival of patients with acute coronary syndromes without ST-segment elevation and prognostic significance of 0,5 mm STsegment depression Am J Cardiol 1999;84:379-385 Solomon DH, Stone PH, Glynn RJ, et al Use of risk stratification to identify patients with unstable angina likeliest to benefit from an invasive versus conservative management strategy J Am Coll Cardiol 2001;38:969-976 Didenholm E, Andren B, Frostfeldt G, et al ST depression in ECG at entry indicates severe coronary lesions and large benefits of an early invasive treatment strategy in unstable coronary artery disease Eur Heart J 2002;23:41-49 Widdershoven JW, Gorgels AP, Vermeer F, et al Changing characteristics and in-hospital outcome of patients admitted with acute myocardial infarction Observations from 19821994 Eur Heart J 1997;1073-1080 Klootwijk P, Mey S, Van Es GA, et al Comparison of usefulness of computer-assisted continuous hour 3-lead with 12-lead ECG-ischemia monitoring for detection and quantification of ischemia in patients with unstable angina Eur Heart J 1997; 18: 931-940 Akkerhuis KM, Klootwijk PAJ, Lindeboom W, et al Recurrent ischemia during continuous multilead ST-segment monitoring identifies patients with acute coronary syndromes at high risk of adverse cardiac events Eur Heart J 2001; 22:1997-2006 10 De Zwaan C, Bar FW, Wellens HJ Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction Am Heart J 1982;103:730-735 11 De Zwaan C, Bar FW, Gorgels AP, Wellens HJ Unstable angina: are we able to recognize high-risk patients? Chest 1997;112:224-50 12 Gorgels APM, Vos MA, Mulleneers R, de Zwaan C, Bar FW, Wellens HJ Value of the electrocardiogram in diagnosing the number of severely narrowed coronary arteries in rest angina pectoris Am J Cardiol 1993;72:999-1003 13 Fozzard HA, Makielski JC.The electrophysiology of acute myocardial ischemia Annual review of medicine 1985;36:275-280 14 Simon K, Hackett D, Szelier A, et al The natural history of postischemic T wave inversion: a predictor of poor short-term prognosis? Coronary Artery Disease 1994;5:937-942 125 126 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA 15 Shawl FA, Velasco CE, Goldbaum TS, Forman BM Effect of coronary angioplasty on electrocardiographic changes in patients with unstable angina secondary to left anterior descending coronary artery disease J Am Coll Cardiol 1990;16:325-331 16 De Zwaan C, Bar FW, Janssen JH, et al Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery Am Heart J 1989;117:657-666 17 Agetsuma H, Hirai M, Hirayama H, et al Transient giant negative T-wave in acute anterior wall infarction predicts R-wave recovery and preservation of left ventricular dysfunction Heart 1996;75:229-234 Index A Abnormal ventricular activation, myocardial infarction with, 65–83 left bundle branch block, 68–75 intermittent, 72–73 practical approach, 74–75 serial ECG’s, 74 paced ventricular rhythm, 76–79 ventricular pre-excitation, 79–81 Accelerated idiopathic ventricular rhythm, 106–109 Acute myocardial infarction arrhythmias in, 85–98 AV-nodal conduction system, 49–53 atrio-ventricular nodal level ECG findings, 49–51 incidence, 52–53 left bundle branch block, inferior wall myocardial infarction, 51–52 conduction abnormalities, atrio-ventricular nodal level, 49–53 management, 53 conduction abnormalities, sub-AV-nodal level, 53–63 ECG findings, 53–59 incidence, 60–61 management, 61–62 conduction disturbances, 43–64 sino-atrial region, 45–49 atrio-ventricular conduction system, 45–46 blood supply of sinus node, atrio-ventricular conduction system, 45 ECG findings, 46 incidence, 47 management, 48–49 sino atrial block, sinus arrest, 47–48 sinus bradycardia, 46 sinus node, sino-atrial region, 45 slow rhythms, conduction abnormalities, sinus nodal, sino-atrial level, 46 sinus arrest, sino-atrial block, 44 sub-AV nodal conduction disturbances, 44 supraventricular arrhythmias, 87–90 atrial fibrillation, 88–90 sinus tachycardia, 87–88 ventricular arrhythmias, 91–94 ventricular fibrillation, 93–94 ventricular premature beats, 91–92 ventricular tachycardia, 92–93 Angina, unstable, ECG in, 117–126 chest pain peaked T-waves in precordial leads, 120–122 T wave negativity in precordial leads, 123 ischemia, recovery of T wave abnormalities following, 124 left main stem disease, 120 proximal LAD syndrome, 120–124 serial ECG’s, 119–120 ST segment depression, 119 Anterior wall infarction, coronary artery occlusion, 24–37 distal LAD occlusion, 28–29 LAD occlusion distal to first diagonal branch, proximal to first septal branch, 31–32 distal to first septal branch, proximal to first diagonal branch, 30 proximal to first septal, first diagonal branch high risk, 26–28 left main occlusion, 33–34 new infarction in presence of old one, 36 site of occlusion in, criteria to identify, 33 ST deviation score, location, coronary artery occlusion, 34–36 ST segment vector, to localize site of ischemia, 25–26 Anterior wall myocardial infarction, coronary artery occlusion, grades of ischemia, 12 Arrhythmias in acute myocardial infarction, 85–98 supraventricular arrhythmias, 87–90 atrial fibrillation, 88–90 sinus tachycardia, 87–88 ventricular arrhythmias, 91–94 ventricular fibrillation, 93–94 128 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA ventricular premature beats, 91–92 ventricular tachycardia, 92–93 Atrial fibrillation, 88–90 Atrial tachycardia, 106 Atrio-ventricular conduction system acute myocardial infarction, 45 conduction disturbances, 45 acute myocardial infarction, sino-atrial region, 45–46 sino-atrial region, 45 sinus node, blood supply of, 45 Atrio-ventricular nodal level acute myocardial infarction, ECG findings, 49–51 AV-nodal conduction system, conduction disturbances, 49–51 AV nodal conduction disturbances, conduction disturbances, acute myocardial infarction, 44 AV-nodal conduction system, conduction disturbances, acute myocardial infarction, 49–53 atrio-ventricular nodal level ECG findings, 49–51 incidence, 52–53 left bundle branch block, inferior wall myocardial infarction, 51–52 conduction abnormalities, atrio-ventricular nodal level, 49–53 management, 53 B Blood supply of sinus node, 45 Brady arrhythmias, 111–112 ECG findings, 111 incidence, 111 mechanism, 111 prognosis, 111 C Chest pain peaked T-waves in precordial leads, 120–122 T wave negativity in precordial leads, 123 Conduction abnormalities acute myocardial infarction, sub-AV-nodal level, 53–63 ECG findings, 53–59 incidence, 60–61 management, 61–62 AV-nodal conduction system, acute myocardial infarction, atrio-ventricular nodal level, 49–53 Conduction disturbances, acute myocardial infarction, 43–64 AV-nodal conduction system, 49–53 atrio-ventricular nodal level ECG findings, 49–51 incidence, 52–53 left bundle branch block, inferior wall myocardial infarction, 51–52 mechanism, 52–53 prognostic significance, 52–53 conduction abnormalities, atrio-ventricular nodal level, 49–53 management, 53 conduction abnormalities, sub-AV-nodal level, 53–63 ECG findings, 53–59 incidence, 60–61 management, 61–62 mechanism, 60–61 prognostic significance, 60–61 sino-atrial region, 45–49 atrio-ventricular conduction system, 45–46 blood supply of sinus node, atrio-ventricular conduction system, 45 ECG findings, 46 incidence, 47 management, 48-49 mechanisms, 47 prognostic significance, 47 sino atrial block, sinus arrest, 47–48 sinus bradycardia, 46 sinus node, sino-atrial region, 45 slow rhythms, conduction abnormalities, sinus nodal, sino-atrial level, 46 sinus arrest, sino-atrial block, 44 sub-AV nodal conduction disturbances, 44 Coronary artery anterior wall infarction, 24–37 distal LAD occlusion, 28–29 LAD occlusion distal to first diagonal branch, proximal to first septal branch, 31–32 distal to first septal branch, proximal to first diagonal branch, 30 proximal to first septal, first diagonal branch high risk, 26–28 left main occlusion, 33–34 new infarction in presence of old one, 36 site of occlusion in, criteria to identify, 33 ST deviation score, location of coronary artery occlusion, 34–36 ST segment vector, to localize site of ischemia, 25–26 anterior wall myocardial infarction, grades of ischemia, 12 INDEX coronary artery, infero-posterior wall infarction, 13–24 identification of, 5–42 anterior wall infarction, 8–9 distal LAD occlusion, 8–9 LAD occlusion distal to first diagonal, proximal to first septal branch, distal to first septal, proximal to first diagonal branch, proximal to first septal, first diagonal branch, ECG patterns, 7–9 infero posterior infarction, 7–8 atrial infarction, lateral wall involvement, posterior wall involvement, ST depression in precordial leads, proximal, distal RCA, RCA, CX, infero posterior myocardial infarction, grades of ischemia, 12 infero-posterior wall infarction atrial infarction, 24 AV nodal block, 24 coronary patho-anatomy, 13–15 CX occlusion, diagnosing, difficulties in, 24 dominance, 15 inferior wall myocardial infarction, RCA, CX occlusion in, 15–17 isolated RV infarction, 22–23 lateral wall involvement, 17 posterior wall involvement, 17 RV infarction, 18–21 mortality, clinical, ECG variables, 10 severity of ischemia, 5–42 site of occlusion, coronary artery, ECG patterns, 13–37 size of area at risk, 5–42 ST segment deviation score, 7, 9–11 terminal QRS-ST segment pattern, severity of cardiac ischemia, 11–13 Coronary artery occlusion, severity of ischemia, 5–42 129 atrial, 88–90 ventricular, 93–94 I Inferior wall myocardial infarction, left bundle branch block, atrio-ventricular nodal level, 51–52 Infero posterior myocardial infarction, coronary artery occlusion, grades of ischemia, 12 Infero-posterior wall infarction, coronary artery occlusion atrial infarction, 24 AV nodal block, 24 coronary patho-anatomy, 13–15 CX occlusion, diagnosing, difficulties in, 24 dominance, 15 inferior wall myocardial infarction, RCA, CX occlusion in, 15–17 isolated RV infarction, 22–23 lateral wall involvement, 17 posterior wall involvement, 17 RV infarction, 18–21 L Left bundle branch block, 68–75 acute myocardial infarction, 51–52 AV-nodal conduction system, conduction disturbances, 51–52 inferior wall myocardial infarction, atrio-ventricular nodal level, 51–52 intermittent, 72–73 practical approach, 74–75 serial ECG’s, 74 Left main stem disease, 120 M Myocardial infarction, with abnormal ventricular activation, 65–83 left bundle branch block, 68–75 intermittent, 72–73 practical approach, 74–75 serial ECG’s, 74 paced ventricular rhythm, 76–79 ventricular pre-excitation, 79–81 E Ectopic activity, 105 ECG findings, 105 N Non-sustained ventricular tachycardia, 106, 109 F O Fibrillation Occlusion, coronary artery 130 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA anterior wall infarction, 24–37 distal LAD occlusion, 28–29 LAD occlusion distal to first diagonal branch, proximal to first septal branch, 31–32 distal to first septal branch, proximal to first diagonal branch, 30 proximal to first septal, first diagonal branch high risk, 26–28 left main occlusion, 33–34 new infarction in presence of old one, 36 site of occlusion in, criteria to identify, 33 ST deviation score, location of coronary artery occlusion, 34–36 ST segment vector, to localize site of ischemia, 25–26 anterior wall myocardial infarction, grades of ischemia, 12 infero posterior myocardial infarction, grades of ischemia, 12 infero-posterior wall infarction atrial infarction, 24 AV nodal block, 24 coronary patho-anatomy, 13–15 CX occlusion, diagnosing, difficulties in, 24 dominance, 15 inferior wall myocardial infarction, RCA, CX occlusion in, 15–17 isolated RV infarction, 22–23 lateral wall involvement, 17 posterior wall involvement, 17 RV infarction, 18–21 mortality, clinical, ECG variables, 10 site of, identification, 5–42 site of occlusion coronary artery ECG patterns, 13–37 infero-posterior wall infarction, 13–24 identification of anterior wall infarction, 8–9 distal LAD occlusion, 8–9 LAD occlusion distal to first diagonal, proximal to first septal branch, distal to first septal, proximal to first diagonal branch, proximal to first septal, first diagonal branch, ECG patterns, 7–9 infero posterior infarction, 7–8 atrial infarction, lateral wall involvement, posterior wall involvement, ST depression in precordial leads, proximal, distal RCA, RCA, CX, size of area at risk, 5–42 ST segment deviation score, 7, 9–11 terminal QRS-ST segment pattern, severity of cardiac ischemia, 11–13 P Pre-excitation, ventricular, 79–81 Premature beats, ventricular, 91–92 R Reperfusion, ECG signs of, 99–116 accelerated idiopathic ventricular rhythm, 106 atrial tachycardia, 106 brady arrhythmias, 111–112 ECG findings, 111 incidence, 111 ectopic activity, 105 ECG findings, 105 non-sustained ventricular tachycardia, 106, 109 reperfusion arrhythmias, defined, 106 sinus bradycardia, 106 ST-T segment behavior, 101–105 incidence, 104–105 ST segment changes, 101–103 T wave changes, 103–104 supraventricular arrhythmias, 110 ECG findings, 110 incidence, 110 ventricular premature beats, 106–109 increase in, 106 Reperfusion arrhythmias, defined, 106 S Sino-atrial block conduction disturbances, acute myocardial infarction, sinus arrest, 44 sino-atrial region, conduction disturbances, acute myocardial infarction, sinus arrest, 47–48 Sino-atrial region conduction disturbances, acute myocardial infarction, 45–49 atrio-ventricular conduction system, 45–46 blood supply of sinus node, atrio-ventricular conduction system, 45 INDEX ECG findings, 46 incidence, 47 management, 48–49 sino atrial block, sinus arrest, 47–48 sinus bradycardia, 46 sinus node, sino-atrial region, 45 slow rhythms, conduction abnormalities, sinus nodal, sino-atrial level, 46 sinus node, conduction disturbances, acute myocardial infarction, sino-atrial region, 45 Sinus arrest sino atrial block, sino-atrial region, conduction disturbances, acute myocardial infarction, 47–48 sino-atrial block, conduction disturbances, acute myocardial infarction, 44 Sinus bradycardia, 106 sino-atrial region, conduction disturbances, acute myocardial infarction, 46 Sinus node blood supply of, atrio-ventricular conduction system, conduction disturbances, acute myocardial infarction, sino-atrial region, 45 sino-atrial region, conduction disturbances, acute myocardial infarction, sino-atrial region, 45 Sinus tachycardia, 87–88 Site of occlusion coronary artery coronary artery occlusion ECG patterns, 13–37 infero-posterior wall infarction, 13–24 identification of, 5–42 identification of, coronary artery occlusion anterior wall infarction, 8–9 distal LAD occlusion, 8–9 LAD occlusion, proximal to first septal, first diagonal branch, ECG patterns, 7–9 infero posterior infarction, 7–8 atrial infarction, lateral wall involvement, posterior wall involvement, ST depression in precordial leads, proximal, distal RCA, RCA, CX, Size of area at risk, coronary artery occlusion, 5–42 131 Slow rhythms conduction disturbances, acute myocardial infarction, sino-atrial region, conduction abnormalities, sinus nodal, sino-atrial level, 46 sinus nodal, sino-atrial level, conduction disturbances, acute myocardial infarction, sino-atrial region, 46 ST segment deviation score, coronary artery occlusion, 7, 9–11 ST-T segment behavior, 101–105 incidence, 104–105 mechanism, 104–105 prognastic implications, 104–105 ST segment changes, 101–103 T wave changes, 103–104 Sub-AV nodal conduction disturbances, conduction disturbances, acute myocardial infarction, 44 Supraventricular arrhythmias, 87–90, 110 atrial fibrillation, 88–90 ECG findings, 110 incidence, 110 mechanism, 110 prognosis, 110 sinus tachycardia, 87–88 T Tachycardia sinus, 87–88 ventricular, 92–93 Terminal QRS-ST segment pattern coronary artery occlusion, severity of cardiac ischemia, coronary artery occlusion, 11–13 U Unstable angina, ECG in, 117–26 chest pain peaked T-waves in precordial leads, 120–122 T wave negativity in precordial leads, 123 ischemia, recovery of T wave abnormalities following, 124 left main stem disease, 120 proximal LAD syndrome, 120–124 serial ECG’s, 119–120 ST segment depression, 119 V Ventricular activation, abnormal, myocardial infarction with, 65–83 132 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA left bundle branch block, 68–75 intermittent, 72–73 practical approach, 74–75 serial ECG’s, 74 paced ventricular rhythm, 76–79 ventricular pre-excitation, 79–81 Ventricular arrhythmias, 91–94 ventricular premature beats, 91–92 ventricular tachycardia, 92–93 Ventricular fibrillation, 93–94, 109 Ventricular pre-excitation, 79–81 Ventricular premature beats, 91–92, 106–109 increase in, 106 Ventricular tachycardia, 92–93 [...]... occlusion(20) 3) The sinoatrial branch This vessel originates in 60% from the RCA, and in about 40% from the CX (11 in fig 2.3) 13 14 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA and rarely from both arteries Involvement of this vessel may lead to sinus node ischemia with sinus bradycardia, sino-atrial block and atrial infarction and may favor the occurrence of atrial fibrillation 4) The right... in table 2.2 27 28 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA Distal LAD occlusion Low risk Figure 2.17 shows an example of an acute anterior wall infarction due to a distal LAD occlusion (behind the major proximal septal and diagonal branches) Typical findings are the presence of Q waves in leads and and the absence of ST depression in the inferior leads (53,54) In this situation there... needed to use the right precordial leads for determining the site of coronary artery occlusion 19 20 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA In a minority of cases of RV involvement the precordial lead shows STelevation The sensitivity of ST elevation in lead is 24% but the specificity 100% Figure 2.10 shows an acute inferior wall infarction due to RCA occlusion In lead the ST segment... OCCLUSION 23 24 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA Atrial infarction Atrial infarction may occur when a RCA or CX occlusion is proximal to the sinoatrial branch An example is given in figure 2.6 It shows slight elevation of the baseline following the P wave, best seen in lead II This Pta segment elevation reflects the repolarization phase of the P wave The presence of atrial infarction. .. important in decision making on reperfusion therapy and the type of intervention is to look for markers indicating a higher mortality rate from myocardial infarction The ECG is a reliable, inexpensive, non-invasive instrument to obtain that information Recently it has become clear that both in anterior and inferior myocardial infarction, the ECG frequently allows not only to identify the infarct related... more ST elevation in III than in II leading to ST depression in lead I In case of CX occlusion the vector will point towards lead II, leading to ST elevation or an isoelectric ST segment in lead I When the vector points towards AW, the ST vector is perpendicular to lead I, resulting 15 16 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA in an iso-electric ST segment in lead I In our experience... ischemia leads to these findings because of ischemia of the relatively thin RV anterior wall This is confirmed by the positive right precordial leads (right panel) SIZE OF AREA AT RISK, SEVERITY OF ISCHEMIA, AND SITE OF CORONARY OCCLUSION 21 22 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA Isolated RV infarction Rarely the ECG shows only minor or no changes in the inferior leads and ST elevation... block (46) The clinical picture may include heart failure and in the subacute phase ventricular tachycardia and fibrillation may occur, leading to increased in- hospital and one year mortality (47,48) Anterior wall infarction is diagnosed by the presence of ST elevation in the precordial leads to The challenge in anterior wall infarction is to recognize the size of the area at risk and the site of the occlusion... Therefore the identification of the patient with left main stenosis, severe three vessel disease or proximal narrowing of the left anterior descending branch is of obvious importance Again, also under 3 4 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA these circumstances the ECG allows us to select those patients who need invasive diagnostic studies Chapter 2 Determining the size of the area... positive T wave in lead Distal RCA Iso electric ST with positive T wave in lead Posterior wall involvement? ST depression in precordial leads 7 8 THE ECG IN ACUTE MYOCARDIAL INFARCTION AND UNSTABLE ANGINA Lateral wall involvement? ST elevation in leads I, AVL, and Atrial infarction? Pta segment elevation in lead II II Anterior wall infarction LAD occlusion proximal to first septal and first diagonal