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A rare case of tako-tsubo cardiomyopathy documented during Holter monitoring
International Journal of Cardiology 132 (2009) e105 – e108 www.elsevier.com/locate/ijcard
Letter to the Editor
A rare case of tako-tsubo cardiomyopathy documented during Holter monitoring Tetsuro Yoshida a,⁎, Takeshi Hibino a , Tetsuo Fujimaki a , Mitsutoshi Oguri a , Kimihiko Kato a , Kazuhiro Yajima a , Nobuyuki Ohte b , Kiyoshi Yokoi a , Genjiro Kimura b b
a Department of Cardiovascular Medicine, Gifu Prefectual Government Tajimi Hospital, 5-161 Maehata, Tajimi, Gifu 5078522, Japan Department of Cardio-Renal Medicine and Hypertension, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan
Received 11 July 2007; accepted 4 August 2007 Available online 26 November 2007
Abstract We report a rare case of Holter monitoring documenting the onset of tako-tsubo cardiomyopathy in a 70-year-old woman. The patient experienced sudden chest discomfort after a quarrel in her hospital stay. Follow-up echocardiography on day 22 revealed a marked improvement of left ventricular apical akinesis. Angiographic examination at discharge showed neither coronary artery disease nor left ventricular asynergy. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Tako-tsubo cardiomyopathy; Emotional or physical stress; Catecholamines
1. Introduction Transient left ventricular dysfunction characterized by apical ballooning akinesis and hypercontraction of the basal segments is referred to as tako-tsubo cardiomyopathy [1]. Patients with tako-tsubo cardiomyopathy have clinical features resembling an acute coronary syndrome such as chest pain, dyspnea, electrographical changes (particularly ST-segment elevation or T-wave inversion), and mild elevation of serum cardiac enzymes [2]. However, angiographic evaluation of these patients reveals no sign of significant coronary artery disease and a large area of left ventricular apical akinesis or dyskinesis that extends beyond the area supplied by a single coronary artery [2]. Tako-tsubo cardiomyopathy predominantly affects females and is often triggered by a preceding emotional or physical stress [3]. We describe the herein case of a 70-year-old woman whose onset ⁎ Corresponding author. Tel.: +81 572 22 5311; fax: +81 572 25 1246. E-mail address: [email protected] (T. Yoshida). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.08.035
of tako-tsubo cardiomyopathy was documented during Holter monitoring after a quarrel. Our findings suggest that a sudden emotional stress may cause this syndrome. 2. Case report A 70-year-old woman visited our hospital with the chief complaint of palpitations and was admitted due to tachycardia. She had been prescribed medication to treat hypertension for 8 years. She was also a non-smoker and did not drink alcohol to excess. Physical examination on admission revealed high blood pressure (156/88 mmHg) and atrial fibrillation with a heart rate of approximately 150 bpm. The oxygen saturation was normal. The remainder of the physical examination was normal. Routine laboratory examination of the blood was within normal limits. Electrocardiography revealed atrial fibrillation and no ST-segment elevation, while echocardiography indicated no abnormalities in left ventricular wall motion. After admission, we began treatment with metildigoxin and an angiotensin receptor antagonist.
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On the second day of admission, the tachycardia had improved with a heart rate of approximately 90 bpm and the patient's symptoms had resolved. We performed Holter monitoring for this patient because the atrial fibrillation was persistent. On the 3rd day of admission, the patient had a violent quarrel with another patient because the television was too loud in the hospital room. After that, the patient experienced sudden heavy chest pressure that was her first-ever episode. She informed the medical staff about this event 10 h after its onset. Therefore, we immediately performed electrocardiography and echocardiography with suspicion of an acute coronary syndrome. Electrocardiography revealed a normal sinus rhythm and inverted T waves in the inferior and anterior leads with prolongation of the QT interval (Fig. 1). In addition, a contractile pattern with preserved basal function, moderateto-severe dysfunction in the midventricle, and apical akinesis was demonstrated by echocardiography. The ejection fraction was estimated to be 44%. Laboratory examination after the onset revealed a slight rise in serum creatine kinase (CK) to 469 IU/l (normal range 24–170 IU/l) and CK-MB sub-fraction (CK-MB) of 59 IU/l (normal range 0–25 IU/l), while the white blood cell count and C reactive protein (CRP) level were not elevated. Although we tried to perform emergent coronary angiography to evaluate coronary artery disease, we were not able to obtain her consent for this examination. We made a
diagnosis of acute coronary syndrome, and initiated oral aspirin (100 mg/day) and a continuous intravenous drip infusion of heparin (10,000 U/day). Holter monitoring analysis showed ST-segment elevations simultaneous with the sudden chest discomfort (Fig. 2). On the 4th day of admission, the patient's symptoms had improved significantly, and her diet was restarted. The plasma CPK and CK-MB levels gradually decreased, while the lactate dehydrogenase (LDH 447 IU/l) level was elevated. On the 6th hospital day, the laboratory data normalized. On the 22nd hospital day, echocardiography revealed near-complete resolution of the left ventricular apical akinesis and the ejection fraction improved to be 66%. On the 34th day, we performed coronary angiography and left ventriculography with the patient's consent for cardiac catheterization. Coronary angiography showed no evidence of occlusion or significant stenosis of the coronary vessels and left ventriculography showed neither ventricular dyskinesis nor an intraventricular pressure gradient. These serial contractile findings were consistent with a diagnosis of takotsubo cardiomyopathy. During her stay in our hospital, the serum concentrations of catecholamines were also elevated more than two times the upper limit of normal. The concentrations of catecholamines showed peak values at the onset and gradually decreased during the hospital stay. There were no clinical features of
Fig. 1. Electrocardiography after the onset of tako-tsubo cardiomyopathy showed inverted T waves in the inferior and anterior leads with prolongation of the QT interval.
T. Yoshida et al. / International Journal of Cardiology 132 (2009) e105–e108
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Fig. 2. Holter monitoring analysis showed ST-segment elevations at the same time as the onset of tako-tsubo cardiomyopathy. Panel A: Prior to onset of takotsubo cardiomyopathy. Panel B: Subsequent to onset of tako-tsubo cardiomyopathy.
arrhythmia or heart failure. The patient was discharged the day after the coronary angiography in stable condition. 3. Discussion Tako-tsubo cardiomyopathy is characterized by reversible left ventricular apical wall motion abnormalities with chest symptoms, electrocardiographic changes and minimal myocardial enzymatic release, which mimics an acute coronary syndrome in patients without angiographic stenosis in the epicardial coronary artery [1]. The patient reported in this paper met the diagnostic criteria for tako-tsubo cardiomyop-
athy, as proposed by the Mayo Clinic: 1) transient akinesis or dyskinesis of the left ventricular apical and mid-ventricular segments with regional wall motion abnormalities, 2) absence of obstructive coronary disease or angiographic evidence of acute plaque rupture, 3) ST-segment elevation or T-wave inversion, 4) absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis, or hypertrophic cardiomyopathy [4]. Wittstein et al. [5] reported that sudden elevations in plasma epinephrine levels after emotional or physical stress are possibly involved in the pathogenesis of tako-tsubo
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cardiomyopathy. Similarly, the previous observations suggest that supraphysiologic levels of plasma catecholamines induced by emotional or physical stress may play a central role in the development of this condition [6]. Indeed, in the case presented herein, the serum concentrations of catecholamines were elevated after an emotional stress. A possible explanation for this epiphenomenon is that direct catecholamine injury to myocytes may predominantly account for the pathophysiologic mechanism underlying tako-tsubo cardiomyopathy; however, the pathophysiologic mechanism underlying the deteriorating effect of catecholamines on the myocardium remains unclear. To the best of our knowledge, this is the first time that the onset of tako-tsubo cardiomyopathy has been recorded on Holter monitoring, while electrocardiographic findings have been reported in many other reports during and after the development of tako-tsubo cardiomyopathy. Our findings suggest that a sudden emotional stress such as a violent quarrel might be a causative trigger of tako-tsubo cardiomyopathy. In conclusion, a unique pattern of transient myocardial dysfunction can occur after severe emotional or physical stress which may induce abnormal activation of adrenoceptors and
catecholamine-induced myocardial damage. Although our case suggests that sudden stress may be a causative mechanism of tako-tsubo cardiomyopathy, a more complete understanding of the pathogenesis of this syndrome awaits further research. References [1] Desmet WJ, Adriaenssens BF, Dens JA. Apical ballooning of the left ventricle: first series in white patients. Heart 2003;89:1027–31. [2] Kurisu S, Sato H, Kawagoe T, et al. 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. [3] 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. [4] Bybee KA, Kara T, Prasad A, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004;141:858–65. [5] Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539–48. [6] Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol 2003;41:737–42.
Letter to the Editor
A rare case of tako-tsubo cardiomyopathy documented during Holter monitoring Tetsuro Yoshida a,⁎, Takeshi Hibino a , Tetsuo Fujimaki a , Mitsutoshi Oguri a , Kimihiko Kato a , Kazuhiro Yajima a , Nobuyuki Ohte b , Kiyoshi Yokoi a , Genjiro Kimura b b
a Department of Cardiovascular Medicine, Gifu Prefectual Government Tajimi Hospital, 5-161 Maehata, Tajimi, Gifu 5078522, Japan Department of Cardio-Renal Medicine and Hypertension, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan
Received 11 July 2007; accepted 4 August 2007 Available online 26 November 2007
Abstract We report a rare case of Holter monitoring documenting the onset of tako-tsubo cardiomyopathy in a 70-year-old woman. The patient experienced sudden chest discomfort after a quarrel in her hospital stay. Follow-up echocardiography on day 22 revealed a marked improvement of left ventricular apical akinesis. Angiographic examination at discharge showed neither coronary artery disease nor left ventricular asynergy. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Tako-tsubo cardiomyopathy; Emotional or physical stress; Catecholamines
1. Introduction Transient left ventricular dysfunction characterized by apical ballooning akinesis and hypercontraction of the basal segments is referred to as tako-tsubo cardiomyopathy [1]. Patients with tako-tsubo cardiomyopathy have clinical features resembling an acute coronary syndrome such as chest pain, dyspnea, electrographical changes (particularly ST-segment elevation or T-wave inversion), and mild elevation of serum cardiac enzymes [2]. However, angiographic evaluation of these patients reveals no sign of significant coronary artery disease and a large area of left ventricular apical akinesis or dyskinesis that extends beyond the area supplied by a single coronary artery [2]. Tako-tsubo cardiomyopathy predominantly affects females and is often triggered by a preceding emotional or physical stress [3]. We describe the herein case of a 70-year-old woman whose onset ⁎ Corresponding author. Tel.: +81 572 22 5311; fax: +81 572 25 1246. E-mail address: [email protected] (T. Yoshida). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.08.035
of tako-tsubo cardiomyopathy was documented during Holter monitoring after a quarrel. Our findings suggest that a sudden emotional stress may cause this syndrome. 2. Case report A 70-year-old woman visited our hospital with the chief complaint of palpitations and was admitted due to tachycardia. She had been prescribed medication to treat hypertension for 8 years. She was also a non-smoker and did not drink alcohol to excess. Physical examination on admission revealed high blood pressure (156/88 mmHg) and atrial fibrillation with a heart rate of approximately 150 bpm. The oxygen saturation was normal. The remainder of the physical examination was normal. Routine laboratory examination of the blood was within normal limits. Electrocardiography revealed atrial fibrillation and no ST-segment elevation, while echocardiography indicated no abnormalities in left ventricular wall motion. After admission, we began treatment with metildigoxin and an angiotensin receptor antagonist.
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On the second day of admission, the tachycardia had improved with a heart rate of approximately 90 bpm and the patient's symptoms had resolved. We performed Holter monitoring for this patient because the atrial fibrillation was persistent. On the 3rd day of admission, the patient had a violent quarrel with another patient because the television was too loud in the hospital room. After that, the patient experienced sudden heavy chest pressure that was her first-ever episode. She informed the medical staff about this event 10 h after its onset. Therefore, we immediately performed electrocardiography and echocardiography with suspicion of an acute coronary syndrome. Electrocardiography revealed a normal sinus rhythm and inverted T waves in the inferior and anterior leads with prolongation of the QT interval (Fig. 1). In addition, a contractile pattern with preserved basal function, moderateto-severe dysfunction in the midventricle, and apical akinesis was demonstrated by echocardiography. The ejection fraction was estimated to be 44%. Laboratory examination after the onset revealed a slight rise in serum creatine kinase (CK) to 469 IU/l (normal range 24–170 IU/l) and CK-MB sub-fraction (CK-MB) of 59 IU/l (normal range 0–25 IU/l), while the white blood cell count and C reactive protein (CRP) level were not elevated. Although we tried to perform emergent coronary angiography to evaluate coronary artery disease, we were not able to obtain her consent for this examination. We made a
diagnosis of acute coronary syndrome, and initiated oral aspirin (100 mg/day) and a continuous intravenous drip infusion of heparin (10,000 U/day). Holter monitoring analysis showed ST-segment elevations simultaneous with the sudden chest discomfort (Fig. 2). On the 4th day of admission, the patient's symptoms had improved significantly, and her diet was restarted. The plasma CPK and CK-MB levels gradually decreased, while the lactate dehydrogenase (LDH 447 IU/l) level was elevated. On the 6th hospital day, the laboratory data normalized. On the 22nd hospital day, echocardiography revealed near-complete resolution of the left ventricular apical akinesis and the ejection fraction improved to be 66%. On the 34th day, we performed coronary angiography and left ventriculography with the patient's consent for cardiac catheterization. Coronary angiography showed no evidence of occlusion or significant stenosis of the coronary vessels and left ventriculography showed neither ventricular dyskinesis nor an intraventricular pressure gradient. These serial contractile findings were consistent with a diagnosis of takotsubo cardiomyopathy. During her stay in our hospital, the serum concentrations of catecholamines were also elevated more than two times the upper limit of normal. The concentrations of catecholamines showed peak values at the onset and gradually decreased during the hospital stay. There were no clinical features of
Fig. 1. Electrocardiography after the onset of tako-tsubo cardiomyopathy showed inverted T waves in the inferior and anterior leads with prolongation of the QT interval.
T. Yoshida et al. / International Journal of Cardiology 132 (2009) e105–e108
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Fig. 2. Holter monitoring analysis showed ST-segment elevations at the same time as the onset of tako-tsubo cardiomyopathy. Panel A: Prior to onset of takotsubo cardiomyopathy. Panel B: Subsequent to onset of tako-tsubo cardiomyopathy.
arrhythmia or heart failure. The patient was discharged the day after the coronary angiography in stable condition. 3. Discussion Tako-tsubo cardiomyopathy is characterized by reversible left ventricular apical wall motion abnormalities with chest symptoms, electrocardiographic changes and minimal myocardial enzymatic release, which mimics an acute coronary syndrome in patients without angiographic stenosis in the epicardial coronary artery [1]. The patient reported in this paper met the diagnostic criteria for tako-tsubo cardiomyop-
athy, as proposed by the Mayo Clinic: 1) transient akinesis or dyskinesis of the left ventricular apical and mid-ventricular segments with regional wall motion abnormalities, 2) absence of obstructive coronary disease or angiographic evidence of acute plaque rupture, 3) ST-segment elevation or T-wave inversion, 4) absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis, or hypertrophic cardiomyopathy [4]. Wittstein et al. [5] reported that sudden elevations in plasma epinephrine levels after emotional or physical stress are possibly involved in the pathogenesis of tako-tsubo
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T. Yoshida et al. / International Journal of Cardiology 132 (2009) e105–e108
cardiomyopathy. Similarly, the previous observations suggest that supraphysiologic levels of plasma catecholamines induced by emotional or physical stress may play a central role in the development of this condition [6]. Indeed, in the case presented herein, the serum concentrations of catecholamines were elevated after an emotional stress. A possible explanation for this epiphenomenon is that direct catecholamine injury to myocytes may predominantly account for the pathophysiologic mechanism underlying tako-tsubo cardiomyopathy; however, the pathophysiologic mechanism underlying the deteriorating effect of catecholamines on the myocardium remains unclear. To the best of our knowledge, this is the first time that the onset of tako-tsubo cardiomyopathy has been recorded on Holter monitoring, while electrocardiographic findings have been reported in many other reports during and after the development of tako-tsubo cardiomyopathy. Our findings suggest that a sudden emotional stress such as a violent quarrel might be a causative trigger of tako-tsubo cardiomyopathy. In conclusion, a unique pattern of transient myocardial dysfunction can occur after severe emotional or physical stress which may induce abnormal activation of adrenoceptors and
catecholamine-induced myocardial damage. Although our case suggests that sudden stress may be a causative mechanism of tako-tsubo cardiomyopathy, a more complete understanding of the pathogenesis of this syndrome awaits further research. References [1] Desmet WJ, Adriaenssens BF, Dens JA. Apical ballooning of the left ventricle: first series in white patients. Heart 2003;89:1027–31. [2] Kurisu S, Sato H, Kawagoe T, et al. 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. [3] 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. [4] Bybee KA, Kara T, Prasad A, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004;141:858–65. [5] Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539–48. [6] Abe Y, Kondo M, Matsuoka R, Araki M, Dohyama K, Tanio H. Assessment of clinical features in transient left ventricular apical ballooning. J Am Coll Cardiol 2003;41:737–42.