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ST elevation and emergency decision making
EDITORIAL COMMENTARY
ST elevation and emergency decision making Mark G. Hoogendijk, MD From the Heart Failure Research Center, Department of Experimental Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. ST elevation identifies myocardial infarction patients most likely to benefit from reperfusion strategies and plays a central role in the therapeutic decision-making process for suspected myocardial infarction.1 However, ST elevation is not specific for myocardial infarction,2 and conditions mimicking the ECG features of myocardial infarction have challenged the diagnostic skills of physicians for almost a century. Retrospectively, the first ST-elevation myocardial infarction (STEMI) was presented in 1920 by Pardee.3 The threelead ECG recorded 4 hours after the onset of complaints showed “. . . large mounds in leads II and III which must correspond to those waves in lead I which are marked R and T.” This observed ST elevation was thought to be reliable evidence of a recent myocardial infarction in the twenties of the last century. Consequently, ST elevation on the first reported ECG of a patient with pericarditis by Scott at al4 prompted the diagnosis of myocardial infarction despite suspected pericardial effusion, and the diagnosis of pericarditis was not made until autopsy. In contrast with ECGs of patients with myocardial infarction, Scott et al4 noticed the absence of reciprocal ST depression. Nowadays, increased knowledge of the ECG characteristics of pericarditis (diffuse concave ST elevation and PR depression) usually enables electrocardiographic differentiation from acute myocardial infarction.5 Nonetheless, pericarditis still is one of the most common diagnoses in patients with a normal coronary angiogram after referral for primary percutaneous coronary intervention.6,7 In an elegant experimental study reported in this issue of Heart Rhythm, Wiegerinck et al8 tested whether QRS duration and morphology may further help differentiate pericarditis from coronary occlusion. Subepicardial injury by pericarditis was simulated by application of high potassium concentrations to the epicardium and compared with 5 minutes of left anterior descending coronary artery (LAD) occlusion in the same pig. Similar to epicardial application of potassium, creation of ischemia by LAD occlusion leads to regionally increased extracellular potassium concentration Address reprint requests and correspondence: Dr. Mark G. Hoogendijk, Heart Failure Research Center, Academic Medical Center, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. E-mail address: m.g.hoogendijk@ amc.uva.nl.
and depolarization of the resting membrane potential.9 This in turn causes ST elevation on the ECG.10 Besides causing ST elevation, regional depolarization of the resting membrane potentials also reduces cardiac excitability.10 LAD occlusion, but not epicardial application of potassium, resulted in activation delay because activation spreads from the subendocardium to the subepicardium11 and therefore needs to transverse the injured area. As a result, 5 minutes of LAD occlusion caused QRS prolongation and increased R-wave amplitudes in leads with ST elevation, but subepicardial injury did not. Although scientifically interesting, extrapolating the findings of this study to patients is difficult. The main difference with STEMI patients is that the presentation delay usually exceeds the 5 minutes of coronary occlusion used in the study, and the ECG appearance of an evolving STEMI can change markedly over time.12 After 5 minutes of coronary occlusion, extracellular potassium concentration reaches its maximum and, at least in the ischemic border zone, decreases thereafter.9 Furthermore, after about 15 minutes of ischemia, cardiomyocytes start to uncouple electrically, which will reduce the contribution of the ischemic myocardium to the ECG.13 Therefore, the effect of transmural ischemia on QRS duration and R-wave amplitude is likely to reach its maximum during the early stages of STEMI and is unlikely to persist throughout the time frame in which reperfusion strategies are effective. The persisting diagnostic uncertainties and the fact that the risk of withholding reperfusion therapy often outweighs the risk of a coronary angiogram make the referral of some patients without coronary disease for percutaneous coronary intervention imperative. Nevertheless, increased insight into the mechanisms underlying the ECG features of ischemia, as provided here by Wiegerinck et al,8 may aid future differentiation from other conditions.
References 1. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction— executive summary: a report of the American College of Cardiology/American Heart Association task force on practice guidelines (writing committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). Circulation 2004;110:588 – 636. 2. Wang K, Asinger RW, Marriott HJL. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003;349:2128 –2135.
1547-5271/$ -see front matter © 2010 Heart Rhythm Society. All rights reserved.
doi:10.1016/j.hrthm.2010.07.021
Hoogendijk
Editorial Commentary
3. Pardee HEB. An electrocardiographic sign of coronary artery obstruction. Arch Intern Med 1920;24:244 –257. 4. Scott RW, Feil HS, Katz LN. The electrocardiogram in pericardial effusion: I. Clinical. Am Heart J 1929;5:68 –76. 5. Spodick DH. Acute pericarditis: current concepts and practice. JAMA 2003; 289:1150 –1153. 6. Gu Y, Svilaas T, van der Horst I, Zijlstra F. Conditions mimicking acute ST-segment elevation myocardial infarction in patients referred for primary percutaneous coronary intervention. Neth Heart J 2008;16:325–331. 7. Prasad SB, Richards DAB, Sadick N, Ong ATL, Kovoor P. Clinical and electrocardiographic correlates of normal coronary angiography in patients referred for primary percutaneous coronary intervention. Am J Cardiol 2008;102:155–159. 8. Wiegerinck RF, Gálvez-Monton C, Jorge E, Martínez R, Ricart E, Cinca J. Changes in QRS duration and R-wave amplitude in ECG leads with ST-segment elevation differentiate epicardial and transmural myocardial injury. Heart Rhythm 2010;7:1667–1673.
1675 9. Coronel R, Fiolet JW, Wilms-Schopman FJ, et al. Distribution of extracellular potassium and its relation to electrophysiologic changes during acute myocardial ischemia in the isolated perfused porcine heart. Circulation 1988;77:1125–1138. 10. Kleber AG, Janse MJ, van Capelle FJ, Durrer D. Mechanism and time course of S-T and T-Q segment changes during acute regional myocardial ischemia in the pig heart determined by extracellular and intracellular recordings. Circ Res 1978;42:603– 613. 11. Durrer D, van Dam R, Freud G, Janse M, Meijler F, Arzbaecher R. Total excitation of the isolated human heart. Circulation 1970;41:899 –912. 12. Cinca J, Janse MJ, Moréna H, Candell J, Valle V, Durrer D. Mechanism and time course of the early electrical changes during acute coronary artery occlusion. Chest 1980;77:499 –505. 13. Kleber AG, Riegger CB, Janse MJ. Electrical uncoupling and increase of extracellular resistance after induction of ischemia in isolated, arterially perfused rabbit papillary muscle. Circ Res 1987;61:271–279.
ST elevation and emergency decision making Mark G. Hoogendijk, MD From the Heart Failure Research Center, Department of Experimental Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. ST elevation identifies myocardial infarction patients most likely to benefit from reperfusion strategies and plays a central role in the therapeutic decision-making process for suspected myocardial infarction.1 However, ST elevation is not specific for myocardial infarction,2 and conditions mimicking the ECG features of myocardial infarction have challenged the diagnostic skills of physicians for almost a century. Retrospectively, the first ST-elevation myocardial infarction (STEMI) was presented in 1920 by Pardee.3 The threelead ECG recorded 4 hours after the onset of complaints showed “. . . large mounds in leads II and III which must correspond to those waves in lead I which are marked R and T.” This observed ST elevation was thought to be reliable evidence of a recent myocardial infarction in the twenties of the last century. Consequently, ST elevation on the first reported ECG of a patient with pericarditis by Scott at al4 prompted the diagnosis of myocardial infarction despite suspected pericardial effusion, and the diagnosis of pericarditis was not made until autopsy. In contrast with ECGs of patients with myocardial infarction, Scott et al4 noticed the absence of reciprocal ST depression. Nowadays, increased knowledge of the ECG characteristics of pericarditis (diffuse concave ST elevation and PR depression) usually enables electrocardiographic differentiation from acute myocardial infarction.5 Nonetheless, pericarditis still is one of the most common diagnoses in patients with a normal coronary angiogram after referral for primary percutaneous coronary intervention.6,7 In an elegant experimental study reported in this issue of Heart Rhythm, Wiegerinck et al8 tested whether QRS duration and morphology may further help differentiate pericarditis from coronary occlusion. Subepicardial injury by pericarditis was simulated by application of high potassium concentrations to the epicardium and compared with 5 minutes of left anterior descending coronary artery (LAD) occlusion in the same pig. Similar to epicardial application of potassium, creation of ischemia by LAD occlusion leads to regionally increased extracellular potassium concentration Address reprint requests and correspondence: Dr. Mark G. Hoogendijk, Heart Failure Research Center, Academic Medical Center, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. E-mail address: m.g.hoogendijk@ amc.uva.nl.
and depolarization of the resting membrane potential.9 This in turn causes ST elevation on the ECG.10 Besides causing ST elevation, regional depolarization of the resting membrane potentials also reduces cardiac excitability.10 LAD occlusion, but not epicardial application of potassium, resulted in activation delay because activation spreads from the subendocardium to the subepicardium11 and therefore needs to transverse the injured area. As a result, 5 minutes of LAD occlusion caused QRS prolongation and increased R-wave amplitudes in leads with ST elevation, but subepicardial injury did not. Although scientifically interesting, extrapolating the findings of this study to patients is difficult. The main difference with STEMI patients is that the presentation delay usually exceeds the 5 minutes of coronary occlusion used in the study, and the ECG appearance of an evolving STEMI can change markedly over time.12 After 5 minutes of coronary occlusion, extracellular potassium concentration reaches its maximum and, at least in the ischemic border zone, decreases thereafter.9 Furthermore, after about 15 minutes of ischemia, cardiomyocytes start to uncouple electrically, which will reduce the contribution of the ischemic myocardium to the ECG.13 Therefore, the effect of transmural ischemia on QRS duration and R-wave amplitude is likely to reach its maximum during the early stages of STEMI and is unlikely to persist throughout the time frame in which reperfusion strategies are effective. The persisting diagnostic uncertainties and the fact that the risk of withholding reperfusion therapy often outweighs the risk of a coronary angiogram make the referral of some patients without coronary disease for percutaneous coronary intervention imperative. Nevertheless, increased insight into the mechanisms underlying the ECG features of ischemia, as provided here by Wiegerinck et al,8 may aid future differentiation from other conditions.
References 1. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction— executive summary: a report of the American College of Cardiology/American Heart Association task force on practice guidelines (writing committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). Circulation 2004;110:588 – 636. 2. Wang K, Asinger RW, Marriott HJL. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003;349:2128 –2135.
1547-5271/$ -see front matter © 2010 Heart Rhythm Society. All rights reserved.
doi:10.1016/j.hrthm.2010.07.021
Hoogendijk
Editorial Commentary
3. Pardee HEB. An electrocardiographic sign of coronary artery obstruction. Arch Intern Med 1920;24:244 –257. 4. Scott RW, Feil HS, Katz LN. The electrocardiogram in pericardial effusion: I. Clinical. Am Heart J 1929;5:68 –76. 5. Spodick DH. Acute pericarditis: current concepts and practice. JAMA 2003; 289:1150 –1153. 6. Gu Y, Svilaas T, van der Horst I, Zijlstra F. Conditions mimicking acute ST-segment elevation myocardial infarction in patients referred for primary percutaneous coronary intervention. Neth Heart J 2008;16:325–331. 7. Prasad SB, Richards DAB, Sadick N, Ong ATL, Kovoor P. Clinical and electrocardiographic correlates of normal coronary angiography in patients referred for primary percutaneous coronary intervention. Am J Cardiol 2008;102:155–159. 8. Wiegerinck RF, Gálvez-Monton C, Jorge E, Martínez R, Ricart E, Cinca J. Changes in QRS duration and R-wave amplitude in ECG leads with ST-segment elevation differentiate epicardial and transmural myocardial injury. Heart Rhythm 2010;7:1667–1673.
1675 9. Coronel R, Fiolet JW, Wilms-Schopman FJ, et al. Distribution of extracellular potassium and its relation to electrophysiologic changes during acute myocardial ischemia in the isolated perfused porcine heart. Circulation 1988;77:1125–1138. 10. Kleber AG, Janse MJ, van Capelle FJ, Durrer D. Mechanism and time course of S-T and T-Q segment changes during acute regional myocardial ischemia in the pig heart determined by extracellular and intracellular recordings. Circ Res 1978;42:603– 613. 11. Durrer D, van Dam R, Freud G, Janse M, Meijler F, Arzbaecher R. Total excitation of the isolated human heart. Circulation 1970;41:899 –912. 12. Cinca J, Janse MJ, Moréna H, Candell J, Valle V, Durrer D. Mechanism and time course of the early electrical changes during acute coronary artery occlusion. Chest 1980;77:499 –505. 13. Kleber AG, Riegger CB, Janse MJ. Electrical uncoupling and increase of extracellular resistance after induction of ischemia in isolated, arterially perfused rabbit papillary muscle. Circ Res 1987;61:271–279.