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Takotsubo cardiomyopathy triggered by lateral wall ST-segment elevation myocardial infarction
Journal of Cardiology Cases 9 (2014) 117–120
Contents lists available at www.sciencedirect.com
Journal of Cardiology Cases journal homepage: www.elsevier.com/locate/jccase
Case Report
Takotsubo cardiomyopathy triggered by lateral wall ST-segment elevation myocardial infarction Satoshi Maeda (MD) a , Akira Tamura (MD) a,∗ , Yoshiyuki Kawano (MD) a , Shigeru Naono (MD) b , Kazuhiro Shinozaki (MD) b , Hirofumi Zaizen (MD) b a b
Department of Cardiology and Clinical Examination, Oita University, Yufu, Japan Division of Cardiovascular Medicine, Koseiren Tsurumi Hospital, Beppu, Japan
a r t i c l e
i n f o
Article history: Received 18 July 2013 Received in revised form 3 December 2013 Accepted 6 December 2013 Keywords: Takotsubo cardiomyopathy Acute myocardial infarction Mid-ventricular ballooning Recurrence
a b s t r a c t We herein report the case of a 72-year-old female with a lateral wall acute myocardial infarction (MI) complicated by takotsubo cardiomyopathy (TC). The patient presented with “severe” chest pain lasting for one hour. She did not experience any obvious emotional or physical stress preceding the chest pain. An admission electrocardiogram showed ST-segment elevation in leads I, aVL, and V6 and ST-segment depression in leads II, III, aVF, and V1 . Emergent coronary angiography showed total occlusion of the obtuse marginal branch. Subsequently, primary percutaneous old balloon angioplasty followed by everolimus-eluting stenting was performed. Left ventriculography performed immediately after final coronary angiography revealed hypokinesis in the lateral wall and mid-ventricular ballooning. The electrocardiographic findings and left ventricular wall motion later normalized. Cardiac magnetic resonance imaging showed late gadolinium enhancement in the lateral wall. In conclusion, to the best of our knowledge, this is the second case report of TC triggered by an acute MI, which provides further evidence that an acute MI can potentially trigger TC. © 2013 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
Introduction Takotsubo cardiomyopathy (TC) is an acute cardiac syndrome characterized by transient wall motion abnormalities typically involving the apical region and midportion of the left ventricle with hyperkinesis of the basal segment in the absence of significant coronary artery disease [1–9]. Because the symptoms and electrocardiographic findings of TC mimic those of anterior wall acute ST-segment elevation myocardial infarction (STEMI), making an early differential diagnosis between the two diseases is important for determining the appropriate treatment strategy. TC usually develops after exposure to an acute emotional or physical stressor in postmenopausal females. Koeth et al. [10] first reported a patient with TC triggered by an acute myocardial infarction (MI),
∗ Corresponding author at: Department of Cardiology and Clinical Examination, Oita University, Idaigaoka 1-1, Hasama-machi, Yufu, Japan. Tel.: +81 097 586 5804; fax: +81 097 549 4245. E-mail address: [email protected] (A. Tamura).
a condition that is frequently associated with emotional stress. We herein report the second case of TC triggered by an acute MI.
Case report A 72-year-old depressive female with diabetes mellitus, dyslipidemia, and hypertension was admitted to Koseiren Tsurumi Hospital with “severe” chest pain lasting for one hour. Two years earlier, she had suffered from typical TC, which was diagnosed by ST-segment elevation in precordial leads on the electrocardiogram (ECG) (Fig. 1A), no significant stenosis in the coronary arteries on emergent coronary angiography, and apical ballooning on emergent left ventriculography (Fig. 1B), triggered by her husband’s death. On the present admission, she had a pulse rate of 88 beats/min and a blood pressure of 158/100 mmHg. The findings of the physical examination were normal. An admission ECG showed ST-segment elevation in leads I, aVL, and V6 and ST depression in leads II, III, aVF, and V1 (Fig. 2A), which were indicative of lateral wall acute STEMI. Echocardiography showed hypokinesis in the lateral wall and akinesis in the mid-ventricular wall. The patient
1878-5409/$ – see front matter © 2013 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.jccase.2013.12.001
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S. Maeda et al. / Journal of Cardiology Cases 9 (2014) 117–120
Fig. 1. An electrocardiogram (A) and left ventriculograms at the time of the first takotsubo cardiomyopathy two years earlier (B).
received aspirin, clopidogrel, lansoprazole and unfractionated heparin and was immediately transferred to the catheter laboratory. Emergent coronary angiography showed total occlusion of the obtuse marginal branch without significant stenosis in the other coronary arteries (Fig. 3A and B). Subsequently, we successfully performed primary percutaneous old balloon angioplasty (Powerline® 2.0 × 15 mm, Biosensors Japan Co. Ltd., Tokyo, Japan) followed by everolimus-eluting stenting (Xience V® 2.5 × 12 mm, Abbott Vascular, Santa Clara, CA, USA) (Fig. 3C). Following stent implantation, the patient’s chest pain gradually eased. Left ventriculography performed immediately after final coronary angiography showed hypokinesis in the lateral wall and mid-ventricular ballooning
(Fig. 4A), with an ejection fraction of 37%. From the findings of the left ventriculogram, we considered that the patient had lateral wall STEMI complicated by TC. An ECG after emergent coronary intervention showed improvement in both ST-segment elevation in leads I and aVL and ST-segment depression in leads III, aVF, and V1 and worsening of ST-segment elevation in leads V3–6 (Fig. 2B). Thereafter, the patient was additionally treated with atorvastatin, candesartan, and carvedilol. The serum creatine kinase level on day 2 was 760 IU/L. An ECG on day 2 showed terminal T-wave inversion in leads I, aVL, and V3–6 (Fig. 2C), followed by improvement in the terminal T-wave inversion on day 4 (Fig. 2D). Cardiac magnetic resonance imaging performed on day 14 showed late gadolinium enhancement in the lateral wall (Fig. 5). An ECG on day 18 showed inverted T waves in leads I, aVL, and V3–6 again (Fig. 2E). On day 18, coronary angiography and left ventriculography were again performed. The site of coronary stent implantation was patent, and the left ventricular wall motion had almost normalized (Fig. 4B). The patient was discharged from the hospital on day 20 and thereafter experienced no chest pain. Six months after the acute MI, the patient underwent follow-up coronary angiography and left ventriculography, which showed no significant stenosis in the site of stent implantation (Fig. 3D) and almost normal left ventricular wall motion with an ejection fraction of 72% (Fig. 4C), respectively. An ECG showed no abnormal Q waves and T-wave normalization in leads I, aVL, and V3–6 (Fig. 2F). Discussion To the best of our knowledge, this is the second case report of TC triggered by an acute MI. In the present case, mid-ventricular ballooning was observed on emergent left ventriculography. Considering the territory of blood supply in the obtuse marginal branch in the patient, acute occlusion of the branch does not explain the mid-ventricular ballooning observed on emergent left ventriculography. Similarly, transient thrombotic obstruction or spasm in the other coronary arteries does not explain the mid-ventricular ballooning. Rather, considering the time course of the left ventricular wall motion abnormality and late
Fig. 2. Electrocardiograms obtained on admission (A), after emergent coronary intervention (B), on day 2 (C), day 4 (D), day 18 (E), and 6 months after admission (F).
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Fig. 3. Coronary angiograms. (A) An emergent right coronary angiogram showing no significant stenosis in the right coronary artery; (B) an emergent left coronary angiogram showing total occlusion of the obtuse marginal branch (arrow); (C) a left coronary angiogram obtained after everolimus-eluting stenting (arrow); and (D) a 6-month follow-up left coronary angiogram showing no significant stenosis in the site of the coronary stent (arrow).
Fig. 4. Left ventriculograms obtained on admission (A), day 18 (B), and 6 months after admission (C).
gadolinium enhancement in the lateral wall on cardiac magnetic resonance imaging, the lateral wall acute STEMI was most likely complicated by TC. Furthermore, only lateral wall STEMI does not explain the worsening of ST-segment elevation in leads V3–6 with
improvement in ST-segment elevation in leads I and aVL after recanalization of the obtuse marginal branch. The lack of typically electrocardiographic findings of TC in the acute phase is thought to be due to the effect of injury current caused by transmural
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S. Maeda et al. / Journal of Cardiology Cases 9 (2014) 117–120
Conclusions This is the second case report of TC triggered by an acute MI. This case provides further evidence that acute MI itself can potentially trigger TC. Conflicts of interest Authors have no conflict of interest that should be disclosed. References
Fig. 5. A cardiac magnetic resonance image showing delayed enhancement in the lateral wall.
myocardial ischemia in the lateral region. The present patient did not experience any emotional or physical stress preceding the chest pain, but she complained of severe chest pain with a fear of death after the onset of acute MI. Therefore, the emotional stress caused by the lateral wall STEMI was most likely to be the trigger of the TC. Considering the prevalence of acute MI, the following question is raised. Why have only two cases of TC triggered by an acute MI been reported thus far? We do not have any definitive answers to this important question; however, some patients with an acute MI complicated by TC might have been overlooked. Especially, it would be very difficult to diagnose patients with an anterior wall STEMI complicated by apical ballooning in the acute phase [11]. The present patient had previously suffered from typical TC. Elesber et al. [12] reported that the recurrence rate of TC is 11.4% over the 4 years following the initial presentation. The present patient was not treated with a beta-blocker at the time of recurrence of TC. It is unclear as to whether beta-blockers can prevent the recurrence of TC [12]. Interestingly, in the present case, the first TC involved apical ballooning, while the second TC was characterized by mid-ventricular ballooning. Recurrent TC with different patterns of left ventricular involvement has been previously reported [13–15], which raises a question regarding the currently proposed hypothesis of variability in beta-adrenergic receptor density and sensitivity in the pathogenesis of TC [15].
[1] Kawai S, Suzuki H, Yamaguchi H, Tanaka K, Sawada H, Aizawa T, Watanabe M, Tamura T, Umawatari K, Kawata M, Nakamura T, Yamanaka O, Okada R. Ampulla cardiomyopathy (‘Takotsubo’ cardiomyopathy) – reversible left ventricular dysfunction: with ST segment elevation. Jpn Circ J 2000;64:156–9. [2] Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, Yoshiyama M, Miyazaki S, Haze K, Ogawa H, Honda T, Hase M, Kai R, Morii I, Angina Pectoris-Myocardial Infarction Investigations in Japan. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol 2001;38:11–8. [3] Akashi YJ, Musha H, Nakazawa K, Miyake F. Plasma brain natriuretic peptide in takotsubo cardiomyopathy. QJM 2004;97:599–607. [4] Kurisu S, Sato H, Kawagoe T, Ishihara M, Shimatani Y, Nishioka K, Kono Y, Umemura T, Nakamura S. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448–55. [5] Abe Y, Kondo M, Matsuoka R, Miyake F. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol 2003;41:737–42. [6] Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, Rihal CS. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004;141:858–65. [7] Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J 2006;27:1523–9. [8] Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: a new form of acute, reversible heart failure. Circulation 2008;118:2754–62. [9] Pilgrim TM, Wyss TR. Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: a systematic review. Int J Cardiol 2008;124:283–92. [10] Koeth O, Zeymer U, Schiele R, Zahn R. Inferior ST-elevation myocardial infarction associated with takotsubo cardiomyopathy. Case Rep Med 2010, pii:467867. [11] Chao T, Lindsay J, Collins S, Woldeyes L, Joshi SB, Steinberg DH, Satler LF, Kent KM, Suddath WO, Pichard AD, Waksman R. Can acute occlusion of the left anterior descending coronary artery produce a typical “takotsubo” left ventricular contraction pattern. Am J Cardiol 2009;104:202–4. [12] Elesber AA, Prasad A, Lennon RJ, Wright RS, Lerman A, Rihal CS. Four-year recurrence rate and prognosis of the apical ballooning syndrome. J Am Coll Cardiol 2007;50:448–52. [13] Mansencal N, El Mahmoud R, Pillière R, Dubourg O. Relationship between pattern of Tako-Tsubo cardiomyopathy and age: from midventricular to apical ballooning syndrome. Int J Cardiol 2010;138:e18–20. [14] Wever-Pinzon O, Wever-Pinzon J, Tami L. Recurrent Takotsubo cardiomyopathy presenting with different morphologic patterns. Int J Cardiol 2011;148:379–81. [15] Kaushik M, Alla VM, Madan R, Arouni AJ, Mohiuddin SM. Recurrent stress cardiomyopathy with variable regional involvement: insights into etiopathogenetic mechanisms. Circulation 2011;124:e556–7.
Contents lists available at www.sciencedirect.com
Journal of Cardiology Cases journal homepage: www.elsevier.com/locate/jccase
Case Report
Takotsubo cardiomyopathy triggered by lateral wall ST-segment elevation myocardial infarction Satoshi Maeda (MD) a , Akira Tamura (MD) a,∗ , Yoshiyuki Kawano (MD) a , Shigeru Naono (MD) b , Kazuhiro Shinozaki (MD) b , Hirofumi Zaizen (MD) b a b
Department of Cardiology and Clinical Examination, Oita University, Yufu, Japan Division of Cardiovascular Medicine, Koseiren Tsurumi Hospital, Beppu, Japan
a r t i c l e
i n f o
Article history: Received 18 July 2013 Received in revised form 3 December 2013 Accepted 6 December 2013 Keywords: Takotsubo cardiomyopathy Acute myocardial infarction Mid-ventricular ballooning Recurrence
a b s t r a c t We herein report the case of a 72-year-old female with a lateral wall acute myocardial infarction (MI) complicated by takotsubo cardiomyopathy (TC). The patient presented with “severe” chest pain lasting for one hour. She did not experience any obvious emotional or physical stress preceding the chest pain. An admission electrocardiogram showed ST-segment elevation in leads I, aVL, and V6 and ST-segment depression in leads II, III, aVF, and V1 . Emergent coronary angiography showed total occlusion of the obtuse marginal branch. Subsequently, primary percutaneous old balloon angioplasty followed by everolimus-eluting stenting was performed. Left ventriculography performed immediately after final coronary angiography revealed hypokinesis in the lateral wall and mid-ventricular ballooning. The electrocardiographic findings and left ventricular wall motion later normalized. Cardiac magnetic resonance imaging showed late gadolinium enhancement in the lateral wall. In conclusion, to the best of our knowledge, this is the second case report of TC triggered by an acute MI, which provides further evidence that an acute MI can potentially trigger TC.
Introduction Takotsubo cardiomyopathy (TC) is an acute cardiac syndrome characterized by transient wall motion abnormalities typically involving the apical region and midportion of the left ventricle with hyperkinesis of the basal segment in the absence of significant coronary artery disease [1–9]. Because the symptoms and electrocardiographic findings of TC mimic those of anterior wall acute ST-segment elevation myocardial infarction (STEMI), making an early differential diagnosis between the two diseases is important for determining the appropriate treatment strategy. TC usually develops after exposure to an acute emotional or physical stressor in postmenopausal females. Koeth et al. [10] first reported a patient with TC triggered by an acute myocardial infarction (MI),
∗ Corresponding author at: Department of Cardiology and Clinical Examination, Oita University, Idaigaoka 1-1, Hasama-machi, Yufu, Japan. Tel.: +81 097 586 5804; fax: +81 097 549 4245. E-mail address: [email protected] (A. Tamura).
a condition that is frequently associated with emotional stress. We herein report the second case of TC triggered by an acute MI.
Case report A 72-year-old depressive female with diabetes mellitus, dyslipidemia, and hypertension was admitted to Koseiren Tsurumi Hospital with “severe” chest pain lasting for one hour. Two years earlier, she had suffered from typical TC, which was diagnosed by ST-segment elevation in precordial leads on the electrocardiogram (ECG) (Fig. 1A), no significant stenosis in the coronary arteries on emergent coronary angiography, and apical ballooning on emergent left ventriculography (Fig. 1B), triggered by her husband’s death. On the present admission, she had a pulse rate of 88 beats/min and a blood pressure of 158/100 mmHg. The findings of the physical examination were normal. An admission ECG showed ST-segment elevation in leads I, aVL, and V6 and ST depression in leads II, III, aVF, and V1 (Fig. 2A), which were indicative of lateral wall acute STEMI. Echocardiography showed hypokinesis in the lateral wall and akinesis in the mid-ventricular wall. The patient
1878-5409/$ – see front matter © 2013 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.jccase.2013.12.001
118
S. Maeda et al. / Journal of Cardiology Cases 9 (2014) 117–120
Fig. 1. An electrocardiogram (A) and left ventriculograms at the time of the first takotsubo cardiomyopathy two years earlier (B).
received aspirin, clopidogrel, lansoprazole and unfractionated heparin and was immediately transferred to the catheter laboratory. Emergent coronary angiography showed total occlusion of the obtuse marginal branch without significant stenosis in the other coronary arteries (Fig. 3A and B). Subsequently, we successfully performed primary percutaneous old balloon angioplasty (Powerline® 2.0 × 15 mm, Biosensors Japan Co. Ltd., Tokyo, Japan) followed by everolimus-eluting stenting (Xience V® 2.5 × 12 mm, Abbott Vascular, Santa Clara, CA, USA) (Fig. 3C). Following stent implantation, the patient’s chest pain gradually eased. Left ventriculography performed immediately after final coronary angiography showed hypokinesis in the lateral wall and mid-ventricular ballooning
(Fig. 4A), with an ejection fraction of 37%. From the findings of the left ventriculogram, we considered that the patient had lateral wall STEMI complicated by TC. An ECG after emergent coronary intervention showed improvement in both ST-segment elevation in leads I and aVL and ST-segment depression in leads III, aVF, and V1 and worsening of ST-segment elevation in leads V3–6 (Fig. 2B). Thereafter, the patient was additionally treated with atorvastatin, candesartan, and carvedilol. The serum creatine kinase level on day 2 was 760 IU/L. An ECG on day 2 showed terminal T-wave inversion in leads I, aVL, and V3–6 (Fig. 2C), followed by improvement in the terminal T-wave inversion on day 4 (Fig. 2D). Cardiac magnetic resonance imaging performed on day 14 showed late gadolinium enhancement in the lateral wall (Fig. 5). An ECG on day 18 showed inverted T waves in leads I, aVL, and V3–6 again (Fig. 2E). On day 18, coronary angiography and left ventriculography were again performed. The site of coronary stent implantation was patent, and the left ventricular wall motion had almost normalized (Fig. 4B). The patient was discharged from the hospital on day 20 and thereafter experienced no chest pain. Six months after the acute MI, the patient underwent follow-up coronary angiography and left ventriculography, which showed no significant stenosis in the site of stent implantation (Fig. 3D) and almost normal left ventricular wall motion with an ejection fraction of 72% (Fig. 4C), respectively. An ECG showed no abnormal Q waves and T-wave normalization in leads I, aVL, and V3–6 (Fig. 2F). Discussion To the best of our knowledge, this is the second case report of TC triggered by an acute MI. In the present case, mid-ventricular ballooning was observed on emergent left ventriculography. Considering the territory of blood supply in the obtuse marginal branch in the patient, acute occlusion of the branch does not explain the mid-ventricular ballooning observed on emergent left ventriculography. Similarly, transient thrombotic obstruction or spasm in the other coronary arteries does not explain the mid-ventricular ballooning. Rather, considering the time course of the left ventricular wall motion abnormality and late
Fig. 2. Electrocardiograms obtained on admission (A), after emergent coronary intervention (B), on day 2 (C), day 4 (D), day 18 (E), and 6 months after admission (F).
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Fig. 3. Coronary angiograms. (A) An emergent right coronary angiogram showing no significant stenosis in the right coronary artery; (B) an emergent left coronary angiogram showing total occlusion of the obtuse marginal branch (arrow); (C) a left coronary angiogram obtained after everolimus-eluting stenting (arrow); and (D) a 6-month follow-up left coronary angiogram showing no significant stenosis in the site of the coronary stent (arrow).
Fig. 4. Left ventriculograms obtained on admission (A), day 18 (B), and 6 months after admission (C).
gadolinium enhancement in the lateral wall on cardiac magnetic resonance imaging, the lateral wall acute STEMI was most likely complicated by TC. Furthermore, only lateral wall STEMI does not explain the worsening of ST-segment elevation in leads V3–6 with
improvement in ST-segment elevation in leads I and aVL after recanalization of the obtuse marginal branch. The lack of typically electrocardiographic findings of TC in the acute phase is thought to be due to the effect of injury current caused by transmural
120
S. Maeda et al. / Journal of Cardiology Cases 9 (2014) 117–120
Conclusions This is the second case report of TC triggered by an acute MI. This case provides further evidence that acute MI itself can potentially trigger TC. Conflicts of interest Authors have no conflict of interest that should be disclosed. References
Fig. 5. A cardiac magnetic resonance image showing delayed enhancement in the lateral wall.
myocardial ischemia in the lateral region. The present patient did not experience any emotional or physical stress preceding the chest pain, but she complained of severe chest pain with a fear of death after the onset of acute MI. Therefore, the emotional stress caused by the lateral wall STEMI was most likely to be the trigger of the TC. Considering the prevalence of acute MI, the following question is raised. Why have only two cases of TC triggered by an acute MI been reported thus far? We do not have any definitive answers to this important question; however, some patients with an acute MI complicated by TC might have been overlooked. Especially, it would be very difficult to diagnose patients with an anterior wall STEMI complicated by apical ballooning in the acute phase [11]. The present patient had previously suffered from typical TC. Elesber et al. [12] reported that the recurrence rate of TC is 11.4% over the 4 years following the initial presentation. The present patient was not treated with a beta-blocker at the time of recurrence of TC. It is unclear as to whether beta-blockers can prevent the recurrence of TC [12]. Interestingly, in the present case, the first TC involved apical ballooning, while the second TC was characterized by mid-ventricular ballooning. Recurrent TC with different patterns of left ventricular involvement has been previously reported [13–15], which raises a question regarding the currently proposed hypothesis of variability in beta-adrenergic receptor density and sensitivity in the pathogenesis of TC [15].
[1] Kawai S, Suzuki H, Yamaguchi H, Tanaka K, Sawada H, Aizawa T, Watanabe M, Tamura T, Umawatari K, Kawata M, Nakamura T, Yamanaka O, Okada R. Ampulla cardiomyopathy (‘Takotsubo’ cardiomyopathy) – reversible left ventricular dysfunction: with ST segment elevation. Jpn Circ J 2000;64:156–9. [2] Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, Yoshiyama M, Miyazaki S, Haze K, Ogawa H, Honda T, Hase M, Kai R, Morii I, Angina Pectoris-Myocardial Infarction Investigations in Japan. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol 2001;38:11–8. [3] Akashi YJ, Musha H, Nakazawa K, Miyake F. Plasma brain natriuretic peptide in takotsubo cardiomyopathy. QJM 2004;97:599–607. [4] Kurisu S, Sato H, Kawagoe T, Ishihara M, Shimatani Y, Nishioka K, Kono Y, Umemura T, Nakamura S. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448–55. [5] Abe Y, Kondo M, Matsuoka R, Miyake F. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol 2003;41:737–42. [6] Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, Rihal CS. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004;141:858–65. [7] Gianni M, Dentali F, Grandi AM, Sumner G, Hiralal R, Lonn E. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review. Eur Heart J 2006;27:1523–9. [8] Akashi YJ, Goldstein DS, Barbaro G, Ueyama T. Takotsubo cardiomyopathy: a new form of acute, reversible heart failure. Circulation 2008;118:2754–62. [9] Pilgrim TM, Wyss TR. Takotsubo cardiomyopathy or transient left ventricular apical ballooning syndrome: a systematic review. Int J Cardiol 2008;124:283–92. [10] Koeth O, Zeymer U, Schiele R, Zahn R. Inferior ST-elevation myocardial infarction associated with takotsubo cardiomyopathy. Case Rep Med 2010, pii:467867. [11] Chao T, Lindsay J, Collins S, Woldeyes L, Joshi SB, Steinberg DH, Satler LF, Kent KM, Suddath WO, Pichard AD, Waksman R. Can acute occlusion of the left anterior descending coronary artery produce a typical “takotsubo” left ventricular contraction pattern. Am J Cardiol 2009;104:202–4. [12] Elesber AA, Prasad A, Lennon RJ, Wright RS, Lerman A, Rihal CS. Four-year recurrence rate and prognosis of the apical ballooning syndrome. J Am Coll Cardiol 2007;50:448–52. [13] Mansencal N, El Mahmoud R, Pillière R, Dubourg O. Relationship between pattern of Tako-Tsubo cardiomyopathy and age: from midventricular to apical ballooning syndrome. Int J Cardiol 2010;138:e18–20. [14] Wever-Pinzon O, Wever-Pinzon J, Tami L. Recurrent Takotsubo cardiomyopathy presenting with different morphologic patterns. Int J Cardiol 2011;148:379–81. [15] Kaushik M, Alla VM, Madan R, Arouni AJ, Mohiuddin SM. Recurrent stress cardiomyopathy with variable regional involvement: insights into etiopathogenetic mechanisms. Circulation 2011;124:e556–7.