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ScienceDirect Journal of Electrocardiology xx (2014) xxx – xxx www.jecgonline.com

Electrocardiographic findings of takotsubo cardiomyopathy as compared with those of anterior acute myocardial infarction☆ Masami Kosuge, MD,⁎ Kazuo Kimura, MD Division of Cardiology, Yokohama City University Medical Center, Yokohama, Japan

Abstract

Takotsubo cardiomyopathy (TC) is a recently recognized novel cardiac syndrome characterized by transient left ventricular dysfunction without obstructive coronary disease, electrocardiographic (ECG) changes (ST-segment elevation and/or negative T wave) or elevated cardiac enzymes. Because the clinical features and ECG findings of TC mimic those of anterior acute myocardial infarction (AMI) with occlusion of the left anterior descending coronary artery, differential diagnosis has an important role in selecting the most appropriate treatment strategy. Especially in the acute phase, differential diagnosis is essential for deciding whether reperfusion therapy is required. Although it has been suggested that ECG does not allow reliable differentiation between TC and anterior AMI, several ECG criteria distinguishing TC from anterior AMI have been proposed. In this review, we discuss ECG findings of TC, especially in the acute phase, compare them with those of anterior AMI, and identify ECG features that may facilitate early recognition of this disease. © 2014 Elsevier Inc. All rights reserved.

Keywords:

Electrocardiogram; Takotsubo cardiomyopathy; Myocardial infarction

Introduction Takotsubo cardiomyopathy (TC) is a recently recognized novel cardiac syndrome defined as follows: (1) transient hypokinesis, akinesis, or dyskinesis of the left ventricular mid segments with or without apical involvement; the regional wall motion abnormalities extend beyond a single epicardial vascular distribution; a stressful trigger is often, but not always present; (2) absence of obstructive coronary artery disease or angiographic evidence of acute plaque rupture; (3) new electrocardiographic (ECG) abnormalities (either ST-segment elevation and/or T wave inversion) or modest elevation in cardiac troponin; and (4) absence of pheochromocytoma and myocarditis [1–5]. Because the clinical features and ECG findings of TC mimic those of anterior acute myocardial infarction (AMI) with occlusion of the left anterior descending (LAD) coronary artery, differential diagnosis has an important role in selecting the most appropriate treatment strategy. Especially in the acute phase, differential diagnosis is essential for deciding whether reperfusion therapy is required. Fibrinolytic therapy in ☆

There are no relationships with industry and financial disclosure. ⁎ Corresponding author at: The Division of Cardiology, Yokohama City University Medical Center, 4-57 Urafune-cho, Minami-ku, Yokohama 232-0024, Japan. E-mail address: [email protected] http://dx.doi.org/10.1016/j.jelectrocard.2014.03.004 0022-0736/© 2014 Elsevier Inc. All rights reserved.

patients with TC is associated with an increased risk of bleeding, which is particularly problematic because most cases occur in postmenopausal elderly women who are prone to bleed [6,7]. In contrast to patients with anterior AMI, those with TC have complete resolution of left ventricular dysfunction within several days to weeks, accompanied by a generally good prognosis [1–5]. Early (i.e., before angiography), accurate, and noninvasive differentiation of TC from anterior AMI is thus a major clinical issue with important prognostic and therapeutic implications. The 12-lead ECG is the simplest, most widely available, initial clinical diagnostic test. To date, ECG characteristics of TC remain to be well defined. In this review article, we discuss ECG findings of TC, especially in the acute phase when ST-segment elevation is observed, compare them with ECG findings in anterior AMI, and identify ECG features that may facilitate early recognition of this disease. Common ECG abnormalities: ST-segment elevation and negative T waves Although recent review articles and other reports propose that ECG findings in TC are heterogeneous, the most common abnormality on initial ECG is ST-segment elevation or negative T waves [1–5]. However, the frequencies of ST-segment elevation (11%–100%) and of

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negative T waves (17%–100%) have varied considerably in previous studies assessing ECG findings in TC [2,3,8]. The results of previous studies must be interpreted with caution because the elapsed time from symptom onset to recording ECG widely varied among studies and was not specified in some articles [2,8]. Mitsuma et al. [9] and Kurisu et al. [10] examined detailed ECG changes in TC and showed that TC was characterized by 4 ECG phases: phase 1, initial ST-segment elevation immediately after symptom onset; phase 2, initial T-wave inversion after resolution of ST-segment elevation from days 1 to 3; phase 3, transient improvement in T-wave inversion in the subacute period; and phase 4, a second deeper T-wave inversion persisting for several months. Given the time-dependency of ECG findings in TC, the reported heterogeneity of ECG findings may have in part resulted from the wide variability in time from symptom onset to ECG recording. Moreover, the perception of symptoms is subjective, and the timing of symptom onset is unclear in some patients or difficult to decide in others whose symptoms wax and wane. In patients with TC, time from symptom onset to presentation might be able to be estimated from ECG findings: ST-segment elevation indicates the acute phase (phase 1 as mentioned above), and negative T waves after resolution of ST-segment indicate the subacute phase (phase 2 as mentioned above) of TC. ECG changes in TC may reflect the pathologic nature of the myocardium and suggest the clinical phase [9].

ECG features of TC as compared with those of anterior AMI The differential diagnosis of TC and anterior AMI in the acute phase is essential for deciding whether reperfusion therapy is required. Although previous studies have suggested that ECG does not allow reliable differentiation between TC and anterior AMI [1,3,8], several ECG criteria for distinguishing TC from anterior AMI have been proposed [11–15]. The criteria proposed by 4 articles, including our study, are shown in Table 1 [11–14]. The number of subjects was small in the studies by Ogura et al. [11] and Bybee et al. [12] and was considerably larger in our study [13] and the study by Tamura et al. [14] ECG criteria shown in Table 1 allowed TC to be distinguished from anterior AMI with high sensitivities (67%–100%) and specificities (69%–96%), probably because the subjects of most studies [12–14] were limited to patients who were admitted within 6 h from symptom onset. On the basis of these 4 articles [11–14] and previous reports, we summarize ECG findings in the acute phase of TC as compared with those of anterior AMI. Less ST-segment elevation and the absence of abnormal Q waves In both TC and anterior AMI, ST-segment elevation is observed mainly in the precordial leads, but the magnitude of such elevation is usually less in TC than in anterior AMI [1,3,8,11–13,15]. ECG criteria proposed by Bybee et al. [12] appear to have incorporated this finding. Some [3,11,13] but not all [8,12] studies have shown that the absence of abnormal Q waves, an ECG marker of irreversible myocardial necrosis, is more common in TC than in anterior AMI. The magnitude of

the increase in myocardial biomarkers is smaller in patients with TC than in those with anterior AMI [1–3,8,10,11,13]. Scintigraphic imaging and cardiac magnetic resonance imaging have failed to document myocardial necrosis in patients with TC [1,2]. These findings suggest that TC is associated with less myocardial damage/necrosis as compared with anterior AMI. The frequencies of no abnormal Q waves in TC (6%–85%) have widely varied in previous studies [1,3,8,11,13]. Nevertheless, in TC, Q-wave regression and R-wave reappearance are often observed, suggesting electrical stunning, even if abnormal Q waves occur in the acute phase. After the resolution of initial ST-segment elevation, negative T waves progressively develop in association with QT prolongation in both TC and anterior AMI [10,16], and such ECG changes are especially prominent in TC [16]. In patients with reperfused anterior AMI, the development of negative T waves in the acute phase has been attributed to viable but sympathetically denervated myocardium [17], because sympathetic denervation delays repolarization. These ECG findings in association with minor elevations of myocardial biomarkers relative to the degree of severe left ventricular dysfunction in the acute phase suggest that TC might be associated with a greater mass of viable, but sympathetically denervated myocardium (i.e., underlying electrophysiologic mechanisms might differ between TC and anterior AMI). ST-segment deviation in inferior leads ST-segment depression of ≥ 1.0 mm (0.1 mV) in inferior leads has been shown to be suggestive of the LAD coronary artery occlusion proximal to the first septal branch [18]. When the LAD coronary artery is proximally occluded, ST-segment depression in inferior leads can be caused by reciprocal changes associated with transmural ischemia in the high anterobasal region. In contrast, when mid or distal portion of the LAD coronary artery is occluded, ST-segment deviation in inferior leads is not influenced. Furthermore, when mid or distal portion of the LAD coronary artery that wraps around the apex and supplies a large portion of inferior wall is occluded, ST-segment elevation in inferior leads is thought to be often observed [19]. I) No ST-segment depression in inferior leads Several small studies reported that the absence of reciprocal ST-segment depression in inferior leads can facilitate the distinction of TC from anterior AMI [11–13,15], because basal anterior myocardial dysfunction is absent in TC, and reciprocal ST-segment depression consequently does not occur in inferior leads. However, reciprocal ST-segment depression in inferior leads also does not occur in anterior AMI caused by mid or distal LAD coronary artery occlusion, as mentioned above. Specificity for the prediction of TC therefore decreases when this ECG finding is used [13,15]. Inoue et al. [15] demonstrated that no reciprocal change in inferior leads could differentiate TC from anterior AMI associated with a proximal occlusion of the LAD coronary artery, but

TC, takotsubo cardiomyopathy; AMI, acute myocardial infarction; STE, ST-segment elevation; STD, ST-segment depression; NR, not reported.

81% 81% 80% 73% 74% 69% STE ≥1.0 mm in lead V3 and/or V4 without STE ≥ 1.0 mm in lead V1 STE ≥1.0 mm in ≥ 1 of lead V3–5 without STE ≥1.0 mm in lead V1 STE ≥1.0 mm in ≥2 contiguous precordial leads without STE ≥1.0 mm in lead V1

TC: n = 62 AMI: n = 280 b 6 hTC: 2.8 ± 1.8 h AMI: 2.4 ± 1.3 h Tamura et al. [14]

NR

J point

71% 96% 81% 94% 91% 68% No STE in lead V1 N 1.0 mm STD in lead aVR N0.5 mm and no STE in lead V1 N 1.0 mm STE ≥1.0 mm in lead V3 without STE ≥ 1.0 mm in lead V1

72% 75% 94% 97% (3 × STE in lead V2) + (STE in lead V3)+ (2 × STE in lead V5) b 11.5 mm STE in lead − aVR (= STD in lead aVR) N0.5 mm 80 ms after J point TC: 42% AMI: 26% TC: n = 33 AMI: n = 342 b6 h TC: 3.4 ± 2.0 h AMI: 2.7 ± 1.8 h Kosuge et al. [13]

80 ms after J point TC: n = 18 AM I: n = 36 b6 h Bybee et al. [12]

TC: 44% AMI: 53%

83% 80% 67% No abnormal Q waves Sum of STE in leads V4–6/sum of STE in leads V1–3 ≥ 1 STE in lead V2 b 1.75 mm and STE in lead V3 b 2.5 mm

Specificity

69% 77% 94%

100%

Sensitivity

No reciprocal changes in inferior leads 80 ms after J point TC: n = 13 AMI: n = 13 NR Ogura et al. [11]

TC: 85% AMI: 31%

Criteria for distinguishing TC from anterior AMI The point used to measure ST-segment deviation Frequencies of no abnormal Q waves Number of patients Entry criteria (Time from onset to admission) Reference

Table 1 Proposed ECG criteria for distinguishing TC from anterior AMI.

69%

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not from anterior AMI associated with a distal occlusion. Thus, no reciprocal change in inferior leads might be highly sensitive, but is nonspecific for the prediction of TC. II) ST-segment elevation in inferior leads Wall-motion abnormality of TC often extends to the inferior wall. ST-segment elevation in inferior leads is observed in 20% to 50% of patients with TC [8,13–15]. One can speculate that ECG findings as well as the morphologic characteristics of left ventricular wall-motion abnormality in TC closely resemble those associated with mid or distal occlusion of a wrapped LAD coronary artery [3,20]. Therefore, it may be very difficult to discriminate between ECG findings of TC and those of anterior AMI caused by mid or distal occlusion of a wrapped LAD coronary artery, resulting in lower positive predictive values of ECG criteria to differentiate TC from anterior AMI. However, in our [13] and other previous studies [11,12,14], the positive value and negative predictive value of each ECG criterion were not shown. Along with the sensitivity and specificity of ECG criteria, the positive predictive value and negative predictive value in routine clinical practice are equally important. One of the diagnostic criteria for TC is the absence of obstructive coronary artery disease or angiographic evidence of acute plaque rupture [1–5]. Therefore, it is necessary to evaluate coronary angiographic findings by such as coronary angiography or coronary computed tomographic angiography for a diagnosis of TC. High positive predictive value and negative predictive value for the prediction of TC might be useful to select the method to diagnose coronary artery disease. Further studies are needed to assess not only the sensitivity and specificity of ECG criteria for TC but also the positive predictive value and negative predictive value. Distribution and magnitude of ST-segment elevation ST-segment elevation is more extensive in TC than in anterior AMI and involves not only the anterior region [8,13,14]. We studied differences in ST-segment elevation between TC and anterior AMI in patients who were admitted within 6 h after symptom onset, the period associated with acute ST-segment elevation (not negative T waves) [13]. In our study, the anatomically contiguous Cabrera sequence (III, aVF, II, − aVR, I, and aVL) was used to display the limb leads in accordance with current international recommendations for the clinical interpretation of ECG [21]. Use of the Cabrera sequence facilitates understanding of the positional relation between the limb leads and the heart. In the Cabrera sequence, lead − aVR, the inverse lead of aVR, is used. Lead − aVR (+ 30°) bridges the gap between lead I (0°) and lead II (60°); [21] in other words, lead − aVR faces the apical and inferolateral regions. The distribution of ST-segment elevation clearly differed between TC and

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frequently extend to the region faced by lead V1; [1,2] moreover, less ST-segment elevation may result from the electrical force induced by ST-segment elevation in the posterolateral region. One can speculate that TC, but not anterior AMI, is usually associated with ST-segment elevation in the posterolateral region [1,23]. Another reason for less ST-segment elevation in lead V1 in TC might be gender difference (see later section). The underlying reasons remain speculative, but our ECG criteria [13] most accurately predicted TC. In previous studies assessing ECG findings in TC, the frequency of ST-segment elevation in lead V1 was low [12,14], consistent with our findings [13]. ECG criterion for the diagnosis of TC proposed by Ogura et al. [11] (i.e., sum of ST-segment elevation in leads V4–6/sum of ST-segment elevation in leads V1–3 ≥ 1) might also reflect less ST-segment elevation in lead V1. II) The point used to measure ST-segment elevation In our [13] and other previous studies [11,12] investigating ECG criteria able to distinguish TC from anterior AMI, the magnitude of ST-segment elevation was measured 80 ms after the J point. The universal definition of myocardial infarction recommends that ST-segment elevation should be measured at the J point [24]. Tamura et al. [14] examined whether the magnitude of ST-segment elevation measured at the J point can be used differentiate TC from anterior AMI on ECG. In their study [14], less ST-segment elevation in lead V1 was consistent with the results of our study [13], whereas ST-segment elevation in lead − aVR was less

anterior AMI (Fig. 1), and this difference was useful for differential diagnosis. The combination of the presence of ST-segment elevation in lead − aVR, which is reflected in ST-segment depression in the opposing lead aVR, and the absence of ST-segment elevation in lead V1 identified TC with a sensitivity of 91% and a specificity of 96%, which were superior to those of any other ECG findings, including no abnormal Q waves and no reciprocal changes in inferior leads (Fig. 2). I) Differences in the distribution of ST-segment elevation Most patients with anterior AMI have ST-segment elevation in leads V2 to V4 (particularly leads V2 and V3) (Fig. 1), indicating ischemia of the anterior region. The extent of ST-segment elevation in anterior AMI is influenced by the site of the culprit lesion of the LAD coronary artery and reflects the extent of the area at risk. In patients with TC, ST-segment elevation most frequently occurred in lead −aVR facing the apical and inferolateral regions. In anterior AMI, the perfusion territory of the LAD coronary artery usually does not extend to this region; therefore, the prevalence of ST-segment elevation in lead − aVR is low. Interestingly, diffuse ST-segment elevation (most prominent in lead −aVR) in TC is thought to reflect the extensive distribution of wall-motion abnormalities centered around the apex, extending beyond the perfusion territory of any single coronary artery. In contrast, ST-segment elevation was rare in lead V1, which may face the right ventricular anterior region, as well as the right paraseptal region [22]. The most likely reason for less ST-segment elevation in lead V1 in TC is that wall-motion abnormalities in TC less

ST-segment elevation (%)

TC

**

100 80

*

** **

**

20

**

0 III

ST-segment elevation (%)

**

*

60 40

**

**

aVF

II

-aVR

I

aVL

V1

V2

V3

V4

V5

V6

V2

V3

V4

V5

V6

Anterior AMI

100 80 60 40 20 0 III

aVF

II

-aVR

I

aVL

V1

Fig. 1. Prevalence of ST-segment elevation in patients with TC and those with anterior AMI on admission (Reproduced from reference [13]). In limb leads, STsegment elevation was distributed primarily around lead − aVR in TC. In anterior AMI, the prevalence of ST-segment elevation gradually decreased from leads aVL to III. In precordial leads, high rates of ST-segment elevation were found in leads V2 to V4 (particularly leads V2 and V3) in TC as well as in anterior AMI. The prevalence of ST-segment elevation then gradually decreased in leads V5 and V6 in both diseases. Although the patterns of ST-segment elevation in precordial leads were similar in TC and anterior AMI, the prevalences of ST-segment elevation were lower in TC. In particular, the prevalence of ST-segment elevation in lead V1 was markedly lower in TC than in anterior AMI. * p b 0.05, ** p b 0.01 vs anterior AMI.

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Fig. 2. Representative ECGs of TC and anterior AMI on admission (Reproduced from reference [13]). TC (left): ST-segment elevation was observed in leads I, II, aVL, and V2 to V6. ST-segment depression was observed in lead aVR. Anterior AMI (right): ST-segment elevation was observed in leads I, aVL, and V1 to V6. ST-segment depression was observed in leads II, III, and aVF. Abnormal Q waves were seen in lead V1.

frequently observed in TC (only 16%) than in our study (97%) [13]. This difference in the frequencies of ST-segment elevation in lead − aVR is in part attributed to the difference in the point used to measure ST-segment deviation. In the presence of increased T-wave amplitude in the acute phase, a considerable number of patients most likely show ST-segment elevation when the magnitude is measured 80 ms after the J point despite the absence of ST-segment elevation when the magnitude is measured at the J point. The presence or absence of ST-segment elevation could thus be considerably affected by the point used to measure ST-segment deviation (the J point, or 60 or 80 ms after the J point), as well as by the cut-off values of ST-segment elevation. Additional studies are therefore needed to define the optimal point for measurement and the optimal cut-off value of ST-segment elevation for the differential diagnosis of TC and anterior AMI. III) Gender differences in ST-segment elevation Most cases of TC occur in elderly women, whereas the majority of patients with AMI are men. The threshold values of ST-segment elevation are dependent on gender, age, and ECG leads. In healthy individuals, the magnitude of ST-segment elevation in leads V1–3 is generally greater in young and middle-aged males than in females [25]. These findings may be important to consider ECG criteria to differentiate TC from anterior AMI. ECG criteria for the diagnosis of TC proposed by us [13] (i.e., no ST-segment elevation in lead V1) and Ogura et al. [11] (i.e., sum of ST-segment elevation in leads

V4–6/sum of ST-segment elevation in leads V1–3 ≥ 1) might reflect less ST-segment elevation in leads V1–3 in TC because most cases occur in women. ECG criterion proposed by Tamura et al. [14] had sensitivity of 75% and specificity of 79% for identifying TC, when only women patients were analyzed. Thus, their criterion was not affected by the gender difference. Difficulty in establishing ECG criteria for the diagnosis of TC Several precautions should be taken in the determination of ECG findings for the diagnosis of TC. Apart from the aforementioned wide variability in time from symptom onset to presentation, patients with TC have also wide variability in left ventricular morphology. Previously reported studies have documented patients with a small area of akinesis limited to the left ventricular apex to those with a larger area of (nearly global) left ventricular akinesis [1,2,20]. Furthermore, apical-sparing variants of TC have been reported [2] and occur in a clinically significant minority of patients with a clinical presentation similar to that of typical TC. ECG findings of such atypical types of TC of course differ from those of classic TC with apical ballooning, but the incidence is very low and the characteristics of such cases remain to be fully defined. Conclusions ECG findings of TC depend on time from symptom onset to presentation and on left ventricular morphology, resulting

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in wide variability. TC is thus difficult to differentiate from anterior AMI on the basis of ECG findings. Furthermore, it may be very difficult to discriminate between ECG findings of TC and those of anterior AMI caused by mid or distal occlusion of a wrapped LAD coronary artery. However, several ECG criteria have been proposed to facilitate the diagnosis of TC in the acute phase. Further studies are needed to assess the ability of various ECG criteria to accurately differentiate TC from anterior AMI. References [1] Bybee KA, Prasad A. Stress-related cardiomyopathy syndromes. Circulation 2008;118:397. [2] Eitel I, von Knobelsdorff-Brenkenhoff F, Bernhardt P, Carbone I, Muellerleile K, Aldrovandi A, et al. Clinical characteristics and cardiovascular magnetic resonance findings in stress (takotsubo) cardiomyopathy. JAMA 2011;306:277. [3] Pilgrim TM, Wyss TR. Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: a systematic review. Int J Cardiol 2008;124:283. [4] Madhavan M, Prasad A. Proposed Mayo Clinic criteria for the diagnosis of tako-tsubo cardiomyopathy and long-term prognosis. Herz 2010;35:240. [5] Kurisu S, Kihara Y. Tako-tsubo cardiomyopathy: clinical presentation and underlying mechanism. J Cardiol 2012;60:429. [6] Simoons ML, Maggioni AP, Knatterud G, et al. Individual risk assessment for intracranial haemorrhage during thrombolytic therapy. Lancet 1993;342:1523. [7] Brass LM, Lichtman JH, Wang Y, Gurwitz JH, Radford MJ, Krumholz HM, et al. Intracranial hemorrhage associated with thrombolytic therapy for elderly patients with acute myocardial infarction: results from the Cooperative Cardiovascular Project. Stroke 2000;31:1802. [8] Sharkey SW, Lesser JR, Menon M, Parpart M, Maron MS, Maron BJ. Spectrum and significance of electrocardiographic patterns, troponin levels, and thrombolysis in myocardial infarction frame count in patients with stress (tako-tsubo) cardiomyopathy and comparison to those in patients with ST-elevation anterior wall myocardial infarction. Am J Cardiol 2008;101:1723. [9] Mitsuma W, Kodama M, Ito M, Tanaka K, Yanagawa T, Ikarashi N, et al. Serial electrocardiographic findings in women with Takotsubo cardiomyopathy. Am J Cardiol 2007;100:106. [10] Kurisu S, Inoue I, Kawagoe T, Ishihara M, Shimatani Y, Nakamura S, 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. [11] Ogura R, Hiasa Y, Takahashi T, Yamaguchi K, Fujiwara K, Ohara Y, et al. Specific findings of the standard 12-lead ECG in patients with 'Takotsubo' cardiomyopathy: comparison with the findings of acute anterior myocardial infarction. Circ J 2003;67:687. [12] Bybee KA, Motiei A, Syed IS, Kara T, Prasad A, Lennon RJ, et al. Electrocardiography cannot reliably differentiate transient left ventricular apical ballooning syndrome from anterior ST-segment elevation myocardial infarction. J Electrocardiol 2007;40:38.e1. [13] Kosuge M, Ebina T, Hibi K, Morita S, Okuda J, Iwahashi N, et al. Simple and accurate electrocardiographic criteria to differentiate takotsubo cardiomyopathy from anterior acute myocardial infarction. J Am Coll Cardiol 2010;55:2514.

[14] Tamura A, Watanabe T, Ishihara M, Ando S, Naono S, Zaizen H, et al. A new electrocardiographic criterion to differentiate between Takotsubo cardiomyopathy and anterior wall ST-segment elevation acute myocardial infarction. Am J Cardiol 2011;108:630. [15] Inoue M, Shimizu M, Ino H, Yamaguchi M, Terai H, Fujino N, et al. Differentiation between patients with takotsubo cardiomyopathy and those with anterior acute myocardial infarction. Circ J 2005;69:89. [16] Kosuge M, Ebina T, Hibi K, Iwahashi N, Tsukahara K, Endo M, et al. Differences in negative T waves between takotsubo cardiomyopathy and reperfused anterior acute myocardial infarction. Circ J 2012;76:462. [17] Matetzky S, Barabash GI, Shahar A, Rabinowitz B, Rath S, Zahav YH, et al. Early T wave inversion after thrombolytic therapy predicts better coronary perfusion: clinical and angiographic study. J Am Coll Cardiol 1994;24:378. [18] Engelen DJ, Gorgels AP, Cheriex EC, De Muinck ED, Ophuis AJ, Dassen WR, et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol 1999;34:389. [19] Sasaki K, Yotsukura M, Sakata K, Yoshino H, Ishikawa K. Relation of ST-segment changes in inferior leads during anterior wall acute myocardial infarction to length and occlusion site of the left anterior descending coronary artery. Am J Cardiol 2001;87:1340. [20] Ibanez B, Benezet-Mazuecos J, Navarro F, Farre J. Takotsubo syndrome: a Bayesian approach to interpreting its pathogenesis. Mayo Clin Proc 2006;81:732. [21] Wagner GS, Macfarlane P, Wellens H, Josephson M, Gorgels A, Mirvis DM, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: 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. J Am Coll Cardiol 2009;53:1003. [22] Ben-Gal T, Sclarovsky S, Herz I, Strasberg B, Zlotikamien B, Sulkes J, et al. Importance of the conal branch of the right coronary artery in patients with acute anterior wall myocardial infarction: electrocardiographic and angiographic correlation. J Am Coll Cardiol 1997;29:506. [23] Patel SM, Lennon RJ, Prasad A. Regional wall motion abnormality in apical ballooning syndrome (Takotsubo/stress cardiomyopathy): importance of biplane left ventriculography for differentiating from spontaneously aborted anterior myocardial infarction. Int J Cardiovasc Imaging 2012;28:687. [24] Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD, et al, the Writing Group on behalf of the Joint ESC/ACCF/AHA/ WHF Task Force for the Universal Definition of Myocardial Infarction. Third universal definition of myocardial infarction. Circulation 2012;126:2020. [25] Rautaharju PM, Surawicz B, Gettes LS, Bailey JJ, Childers R, Deal BJ, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part IV: the ST segment, T and U waves, and the QT interval: 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. J Am Coll Cardiol 2009;53:982.

Electrocardiographic findings of takotsubo cardiomyopathy as compared with those of anterior acute myocardial infarction.

Takotsubo cardiomyopathy (TC) is a recently recognized novel cardiac syndrome characterized by transient left ventricular dysfunction without obstruct...
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