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Electrocardiographic J waves as a hyperacute sign of Takotsubo syndrome
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Journal of Electrocardiology 45 (2012) 353 – 356 www.jecgonline.com
Electrocardiographic J waves as a hyperacute sign of Takotsubo syndrome☆ Alessandro Zorzi, MD, Federico Migliore, MD, Martina Perazzolo Marra, MD, PhD, Giuseppe Tarantini, MD, PhD, Sabino Iliceto, MD, Domenico Corrado, MD, PhD⁎ Division of Cardiology, Department of Cardiac, Thoracic and Vascular sciences, University of Padova, Italy Received 28 February 2012
Abstract
Typical electrocardiographic (ECG) signs of acute Takotsubo syndrome (TTS) consist of STsegment elevation and/or T wave inversion. We report an unusual case of a 62-year-old woman with TTS who acutely exhibited on 12-lead ECG transient J waves preceding ST-T abnormalities. In the experimental model of myocardial ischemia, the appearance of J waves represents an early ECG abnormality and is followed by ST-segment elevation. Because of the similar ECG time course observed in TTS and myocardial ischemia, we speculate that common electrophysiologic mechanisms may account for J waves appearance in these 2 clinical conditions. Our case report shows that recording of ECG J waves in postmenopausal women presenting for acute chest pain may be a sign of an ongoing TTS and suggests a similarity to myocardial ischemia as the pathologic basis. © 2012 Elsevier Inc. All rights reserved.
Keywords:
J wave; Early repolarization; Electrocardiogram; Takotsubo cardiomyopathy; Action potential
Introduction Takotsubo syndrome (TTS) is characterized by reversible left ventricular (LV) dysfunction in the absence of obstructive coronary artery disease usually after an emotional or physical stress. Although several mechanisms have been proposed, the precise pathophysiologic bases of the syndrome remain to be fully elucidated. 1 The usual electrocardiographic (ECG) changes of the acute phase of TTS consist of mild ST-segment elevation extending beyond the distribution of a single coronary artery, which is followed, in the subacute phase, by transient T wave inversion and QTc prolongation. 2 We report an unusual case of a patient admitted for hyperacute TTS who exhibited transient J waves preceding ST-segment elevation and T wave inversion. The potential electrophysiologic mechanisms responsible for such a sequence of ECG changes that resembled those observed in experimental myocardial ischemia are discussed. Case presentation A 62-year-old woman was admitted to the emergency department very early (≈30 minutes) since the onset of chest ☆ Conflicts of interest and financial disclosures: none. ⁎ Corresponding author. Inherited Arrhythmogenic Cardiomiopathy Unit, Department of Cardiac Thoracic and Vascular Sciences, University of Padua Medical School, Via N. Giustiniani 2 35121 Padova, Italy. E-mail address: [email protected]
0022-0736/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2012.04.004
pain after an emotional stress. Her blood pressure was 140/ 90 mm Hg, and the physical examination was unremarkable. On admission, ECG revealed the presence of prominent J waves in leads L1, L2, aVF, and V4 throughV6 (Fig. 1). The first troponin I sample on admission was negative, whereas a second, obtained 3 hours later, showed an enzyme raise to 0.43 μg/L (normal value b0.045 μg/L). At this time, a new ECG tracing showed diffuse ST-segment elevation in place of J waves, and an echocardiogram revealed diffuse akinesia of mid-apical LV segments with moderate ejection fraction reduction (37%). Urgent cardiac catheterization with coronary arteriography and LV angiography showed LV apical ballooning in the absence of coronary artery disease consistent with TTS (Fig. 2A and B). Over the following days, repolarization abnormalities evolved to T wave inversion associated with QTc interval prolongation. Troponin I values peaked at 6.52 μg/L on day 2. A contrast-enhanced cardiac magnetic resonance (1.5-T scanner, Magnetom Avanto; Siemens Medical Solutions, Erlangen, Germany) revealed on T2-weighted sequences the presence of transmural myocardial edema localized to the LV mid-apical segments in the absence of late gadolinium enhancement on T1 inversion recovery postcontrast sequences (Fig. 2C and D). According to clinical and instrumental findings, a diagnosis of TTS was achieved. 3 The subsequent hospital stay was uneventful, and the patient was discharged at day 8. She was prescribed home therapy with β-blockers, angiotensin-
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A. Zorzi et al. / Journal of Electrocardiology 45 (2012) 353–356
Fig. 1. Electrocardiogram recorded at admission showing J waves in leads L1, L2, aVF, and V4 through V6, and no significant ST-segment elevation.
converting enzyme inhibitors, and benzodiazepine. One month after, the woman was asymptomatic, and both ECG and echocardiogram completely normalized. Discussion The J wave, also referred to as the Osborn wave, is a slow, positive ECG deflection at the R-ST junction with a dome or hump morphology. It was initially described as a result of hypothermia and subsequently became a recognized ECG marker of the benign “early repolarization.” Recently, this
ECG pattern has gained interest because of its reported association with idiopatic ventricular fibrillation (VF) and increased risk of cardiovascular death. 4,5 The electrogenesis of the ECG J waves has been explained by transmural differences in myocyte action potentials. At baseline, the opening of the Ito potassium repolarizing channels gives rise to a prominent “notch” in the phase 1 of the epicardial myocyte action potential but not in endocardial layers. This mechanism generates a transmural voltage gradient, which results in the physiologic J-point elevation at ECG. Increase of the ITO current by
Fig. 2. Left ventriculography, right anterior oblique view, performed few hours after admission showing normal left-ventricle end-diastolic volume (A) and typical apical ballooning with hypercontractile basal segments in systole (B). Cardiac magnetic resonance performed the same day, 2-chamber view, revealing myocardial edema (increased signal intensity on T2-weighted sequences) in the LV mid anterior wall, apical segments and mid inferior wall (arrows) (C). No discrete (N5 standard deviations) late-enhancement suggestive of myocardial necrosis was detected on T1 inversion recovery postcontrast sequences (D).
A. Zorzi et al. / Journal of Electrocardiology 45 (2012) 353–356
355
Fig. 3. Time course of ECG repolarization abnormalities in the lateral precordial leads V4 through V6. J waves observed at admission were amalgamated into elevated ST segment after 3 hours and substituted by T wave inversion in the subacute phase. No ST-T changes were present at a follow-up ECG performed 1 month after.
modulating factors such as hypothermia or acetylcholine accentuates the voltage gradient leading to augmentation of the J-point elevation or appearance of a discrete “J wave.” 5 The same mechanism has been advocated to explain J waves observed in a patient with acute myocardial infarction of the posterior LV wall. Indeed, in experimental myocardial ischemia of arterially perfused canine wedge preparations, accentuation of the phase 1 epicardial action potential notch occurs shortly after coronary ligation. 6 Afterward, the ischemia-induced outward shift in repolarizing currents caused by a decrease in Na + or Ca ++ and an increase in K + ion currents results in a loss of the action potential dome in the epicardium but not in the endocardium and gives rise to ST-segment elevation at ECG. 7 In experimental druginduced models and in genetically proven channelopathies such as Brugada syndrome, the reduction of the INa current, the increase of the ITO current, or the activation of the adenosine triphosphate–sensitive potassium current (IK-ATP) generates a J wave predisposing to VF. 8 It is noteworthy that this ECG pattern is also associated with the development of VF in patients with acute myocardial infarction. 9,10 Takotsubo syndrome is increasingly diagnosed in postmenopausal women complaining acute chest pain. 1 Our patients had an unusual ECG presentation with prominent J
waves preceding by few hours the occurrence of ST-segment elevation and T wave inversion. Clinical manifestations of TTS show many similarities with those of transient myocardial ischemia, including reversible LV systolic dysfunction and time course of ECG abnormalities (Fig. 3). 1,2 The pathogenesis of TTS remains to be elucidated; however, proposed mechanisms focus on ischemic myocardial damage as a result of multivessel epicardial spasm, coronary microvascular dysfunction, or cathecolamine storm. 11 Our report of J waves as an acute ECG sign of TTS further supports the concept of a common pathophysiologic mechanism underlying both TTS and acute myocardial ischemia. Conclusions We reported for the first time the appearance of prominent J waves in the hyperacute phase of TTS. The J waves have been reported in clinical acute myocardial infarction and experimentally reproduced in the hyperacute phase of myocardial ischemia. Based on the parallel time course and similarities of repolarization changes dynamics including J waves, it is attractive to speculate on common pathophysiology of TTS and myocardial ischemia. The knowledge that J waves may be an hyperacute ECG marker of
356
A. Zorzi et al. / Journal of Electrocardiology 45 (2012) 353–356
TTS may help early diagnosis and proper clinical management in this syndrome. Appendix A. Supplementary data Supplementary data to this article can be found online at doi:10.1016/j.jelectrocard.2012.04.004. References 1. Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J 2008;155:408. 2. Kurisu S, Inoue I, Kawagoe T, et al. Time course of electrocardiographic changes in patients with Tako-Tsubo syndrome—comparison with acute myocardial infarction with minimal enzymatic release. Circ J 2004;68:77. 3. Madhavan M, Prasad A. Proposed Mayo Clinic criteria for the diagnosis of Tako-Tsubo cardiomyopathy and long-term prognosis. Herz 2010; 35:240.
4. Haïssaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med 2008;358:2016. 5. Tikkanen JT, Anttonen O, Junttila MJ, et al. Long-term outcome associated with early repolarization on electrocardiography. N Engl J Med 2009;361:2529. 6. Yan Gx, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation 1996;93:372. 7. Rituparna S, Suresh S, Chandrashekhar M, et al. Occurence of “J waves” in 12-lead ECG as a marker of acute ischemia and their cellular basis. Pacing Clin Electrophysiol 2007;30:817. 8. Di Diego JM, Fish JM, Antzelevitch C. Brugada syndrome and ischemia-induced ST-segment elevation. Similarities and differences. J Electrocardiol 2005;38:14. 9. Jastrzebski M, Kukla P. Ischemic J wave: novel risk marker for ventricular fibrillation? Heart Rhythm 2009;6:829. 10. Aizawa Y, Jastrzebski M, Ozawa T, et al. Characteristics of electrocardiographic repolarization in acute myocardial infarction complicated by ventricular fibrillation. J Electrocardiol 2012. In press. 11. Lukas A, Antzelevitch C. Differences in the electrophysiological response of canine ventricular epicardium and endocardium to ischemia. Role of the transient outward current. Circulation 1993;88:2903.
Journal of Electrocardiology 45 (2012) 353 – 356 www.jecgonline.com
Electrocardiographic J waves as a hyperacute sign of Takotsubo syndrome☆ Alessandro Zorzi, MD, Federico Migliore, MD, Martina Perazzolo Marra, MD, PhD, Giuseppe Tarantini, MD, PhD, Sabino Iliceto, MD, Domenico Corrado, MD, PhD⁎ Division of Cardiology, Department of Cardiac, Thoracic and Vascular sciences, University of Padova, Italy Received 28 February 2012
Abstract
Typical electrocardiographic (ECG) signs of acute Takotsubo syndrome (TTS) consist of STsegment elevation and/or T wave inversion. We report an unusual case of a 62-year-old woman with TTS who acutely exhibited on 12-lead ECG transient J waves preceding ST-T abnormalities. In the experimental model of myocardial ischemia, the appearance of J waves represents an early ECG abnormality and is followed by ST-segment elevation. Because of the similar ECG time course observed in TTS and myocardial ischemia, we speculate that common electrophysiologic mechanisms may account for J waves appearance in these 2 clinical conditions. Our case report shows that recording of ECG J waves in postmenopausal women presenting for acute chest pain may be a sign of an ongoing TTS and suggests a similarity to myocardial ischemia as the pathologic basis. © 2012 Elsevier Inc. All rights reserved.
Keywords:
J wave; Early repolarization; Electrocardiogram; Takotsubo cardiomyopathy; Action potential
Introduction Takotsubo syndrome (TTS) is characterized by reversible left ventricular (LV) dysfunction in the absence of obstructive coronary artery disease usually after an emotional or physical stress. Although several mechanisms have been proposed, the precise pathophysiologic bases of the syndrome remain to be fully elucidated. 1 The usual electrocardiographic (ECG) changes of the acute phase of TTS consist of mild ST-segment elevation extending beyond the distribution of a single coronary artery, which is followed, in the subacute phase, by transient T wave inversion and QTc prolongation. 2 We report an unusual case of a patient admitted for hyperacute TTS who exhibited transient J waves preceding ST-segment elevation and T wave inversion. The potential electrophysiologic mechanisms responsible for such a sequence of ECG changes that resembled those observed in experimental myocardial ischemia are discussed. Case presentation A 62-year-old woman was admitted to the emergency department very early (≈30 minutes) since the onset of chest ☆ Conflicts of interest and financial disclosures: none. ⁎ Corresponding author. Inherited Arrhythmogenic Cardiomiopathy Unit, Department of Cardiac Thoracic and Vascular Sciences, University of Padua Medical School, Via N. Giustiniani 2 35121 Padova, Italy. E-mail address: [email protected]
0022-0736/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2012.04.004
pain after an emotional stress. Her blood pressure was 140/ 90 mm Hg, and the physical examination was unremarkable. On admission, ECG revealed the presence of prominent J waves in leads L1, L2, aVF, and V4 throughV6 (Fig. 1). The first troponin I sample on admission was negative, whereas a second, obtained 3 hours later, showed an enzyme raise to 0.43 μg/L (normal value b0.045 μg/L). At this time, a new ECG tracing showed diffuse ST-segment elevation in place of J waves, and an echocardiogram revealed diffuse akinesia of mid-apical LV segments with moderate ejection fraction reduction (37%). Urgent cardiac catheterization with coronary arteriography and LV angiography showed LV apical ballooning in the absence of coronary artery disease consistent with TTS (Fig. 2A and B). Over the following days, repolarization abnormalities evolved to T wave inversion associated with QTc interval prolongation. Troponin I values peaked at 6.52 μg/L on day 2. A contrast-enhanced cardiac magnetic resonance (1.5-T scanner, Magnetom Avanto; Siemens Medical Solutions, Erlangen, Germany) revealed on T2-weighted sequences the presence of transmural myocardial edema localized to the LV mid-apical segments in the absence of late gadolinium enhancement on T1 inversion recovery postcontrast sequences (Fig. 2C and D). According to clinical and instrumental findings, a diagnosis of TTS was achieved. 3 The subsequent hospital stay was uneventful, and the patient was discharged at day 8. She was prescribed home therapy with β-blockers, angiotensin-
354
A. Zorzi et al. / Journal of Electrocardiology 45 (2012) 353–356
Fig. 1. Electrocardiogram recorded at admission showing J waves in leads L1, L2, aVF, and V4 through V6, and no significant ST-segment elevation.
converting enzyme inhibitors, and benzodiazepine. One month after, the woman was asymptomatic, and both ECG and echocardiogram completely normalized. Discussion The J wave, also referred to as the Osborn wave, is a slow, positive ECG deflection at the R-ST junction with a dome or hump morphology. It was initially described as a result of hypothermia and subsequently became a recognized ECG marker of the benign “early repolarization.” Recently, this
ECG pattern has gained interest because of its reported association with idiopatic ventricular fibrillation (VF) and increased risk of cardiovascular death. 4,5 The electrogenesis of the ECG J waves has been explained by transmural differences in myocyte action potentials. At baseline, the opening of the Ito potassium repolarizing channels gives rise to a prominent “notch” in the phase 1 of the epicardial myocyte action potential but not in endocardial layers. This mechanism generates a transmural voltage gradient, which results in the physiologic J-point elevation at ECG. Increase of the ITO current by
Fig. 2. Left ventriculography, right anterior oblique view, performed few hours after admission showing normal left-ventricle end-diastolic volume (A) and typical apical ballooning with hypercontractile basal segments in systole (B). Cardiac magnetic resonance performed the same day, 2-chamber view, revealing myocardial edema (increased signal intensity on T2-weighted sequences) in the LV mid anterior wall, apical segments and mid inferior wall (arrows) (C). No discrete (N5 standard deviations) late-enhancement suggestive of myocardial necrosis was detected on T1 inversion recovery postcontrast sequences (D).
A. Zorzi et al. / Journal of Electrocardiology 45 (2012) 353–356
355
Fig. 3. Time course of ECG repolarization abnormalities in the lateral precordial leads V4 through V6. J waves observed at admission were amalgamated into elevated ST segment after 3 hours and substituted by T wave inversion in the subacute phase. No ST-T changes were present at a follow-up ECG performed 1 month after.
modulating factors such as hypothermia or acetylcholine accentuates the voltage gradient leading to augmentation of the J-point elevation or appearance of a discrete “J wave.” 5 The same mechanism has been advocated to explain J waves observed in a patient with acute myocardial infarction of the posterior LV wall. Indeed, in experimental myocardial ischemia of arterially perfused canine wedge preparations, accentuation of the phase 1 epicardial action potential notch occurs shortly after coronary ligation. 6 Afterward, the ischemia-induced outward shift in repolarizing currents caused by a decrease in Na + or Ca ++ and an increase in K + ion currents results in a loss of the action potential dome in the epicardium but not in the endocardium and gives rise to ST-segment elevation at ECG. 7 In experimental druginduced models and in genetically proven channelopathies such as Brugada syndrome, the reduction of the INa current, the increase of the ITO current, or the activation of the adenosine triphosphate–sensitive potassium current (IK-ATP) generates a J wave predisposing to VF. 8 It is noteworthy that this ECG pattern is also associated with the development of VF in patients with acute myocardial infarction. 9,10 Takotsubo syndrome is increasingly diagnosed in postmenopausal women complaining acute chest pain. 1 Our patients had an unusual ECG presentation with prominent J
waves preceding by few hours the occurrence of ST-segment elevation and T wave inversion. Clinical manifestations of TTS show many similarities with those of transient myocardial ischemia, including reversible LV systolic dysfunction and time course of ECG abnormalities (Fig. 3). 1,2 The pathogenesis of TTS remains to be elucidated; however, proposed mechanisms focus on ischemic myocardial damage as a result of multivessel epicardial spasm, coronary microvascular dysfunction, or cathecolamine storm. 11 Our report of J waves as an acute ECG sign of TTS further supports the concept of a common pathophysiologic mechanism underlying both TTS and acute myocardial ischemia. Conclusions We reported for the first time the appearance of prominent J waves in the hyperacute phase of TTS. The J waves have been reported in clinical acute myocardial infarction and experimentally reproduced in the hyperacute phase of myocardial ischemia. Based on the parallel time course and similarities of repolarization changes dynamics including J waves, it is attractive to speculate on common pathophysiology of TTS and myocardial ischemia. The knowledge that J waves may be an hyperacute ECG marker of
356
A. Zorzi et al. / Journal of Electrocardiology 45 (2012) 353–356
TTS may help early diagnosis and proper clinical management in this syndrome. Appendix A. Supplementary data Supplementary data to this article can be found online at doi:10.1016/j.jelectrocard.2012.04.004. References 1. Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J 2008;155:408. 2. Kurisu S, Inoue I, Kawagoe T, et al. Time course of electrocardiographic changes in patients with Tako-Tsubo syndrome—comparison with acute myocardial infarction with minimal enzymatic release. Circ J 2004;68:77. 3. Madhavan M, Prasad A. Proposed Mayo Clinic criteria for the diagnosis of Tako-Tsubo cardiomyopathy and long-term prognosis. Herz 2010; 35:240.
4. Haïssaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med 2008;358:2016. 5. Tikkanen JT, Anttonen O, Junttila MJ, et al. Long-term outcome associated with early repolarization on electrocardiography. N Engl J Med 2009;361:2529. 6. Yan Gx, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation 1996;93:372. 7. Rituparna S, Suresh S, Chandrashekhar M, et al. Occurence of “J waves” in 12-lead ECG as a marker of acute ischemia and their cellular basis. Pacing Clin Electrophysiol 2007;30:817. 8. Di Diego JM, Fish JM, Antzelevitch C. Brugada syndrome and ischemia-induced ST-segment elevation. Similarities and differences. J Electrocardiol 2005;38:14. 9. Jastrzebski M, Kukla P. Ischemic J wave: novel risk marker for ventricular fibrillation? Heart Rhythm 2009;6:829. 10. Aizawa Y, Jastrzebski M, Ozawa T, et al. Characteristics of electrocardiographic repolarization in acute myocardial infarction complicated by ventricular fibrillation. J Electrocardiol 2012. In press. 11. Lukas A, Antzelevitch C. Differences in the electrophysiological response of canine ventricular epicardium and endocardium to ischemia. Role of the transient outward current. Circulation 1993;88:2903.