- Email: [email protected]
Recurrent stress-induced cardiomyopathy presented with acute decompensated heart failure
International Journal of Cardiology 212 (2016) 307–309
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Recurrent stress-induced cardiomyopathy presented with acute decompensated heart failure Pyung Chun Oh, Kwang Kon Koh ⁎ Department of Cardiology, Gachon University Gil Medical Center, Incheon, Republic of Korea
a r t i c l e
i n f o
Article history: Received 17 February 2016 Accepted 19 March 2016 Available online 24 March 2016 Keyword: Recurrent stress-induced cardiomyopathy
A 73 year-old female patient presented to an emergency room with dyspnea suddenly developed 1 day ago, which was preceded with cough, sputum and sore throat for 1 week. She had a diabetes mellitus and hypertension for about 30 years and had undergone aortobifemoral bypass graft for peripheral arterial disease 13 years ago. One year ago, she had been admitted with sudden onset of dyspnea and had been diagnosed with stress-induced cardiomyopathy presenting acute decompensated heart failure requiring mechanical ventilation, which had been completely recovered with intensive medical treatment [1]. She has been lost for 3 months before developing dyspnea. She was tachypneic (32 breaths per minute) and initial arterial blood gas analysis revealed hypoxemia (PaO2, 50 mmHg), hypercapnia (PaCO2, 55 mmHg), and respiratory acidosis (pH 7.09). Chest radiography showed mild cardiomegaly and acute pulmonary edema (Fig. 1). Transthoracic echocardiography showed severely enlarged left atrium and left ventricle (LV) and LV systolic function was significantly decreased to LV ejection fraction 34% with severe global hypokinesia of LV (Fig. 2A), compared with the last echocardiography (LV ejection fraction 73%) performed 1 year ago. Serum cardiac enzyme levels were within normal limit. Medical therapy was promptly commenced for acute decompensated heart failure including intravenous nitroglycerin, furosemide, and angiotensin II type 1 receptor blocker, and acute respiratory failure was improved without mechanical ventilation. Follow-up echocardiography on the sixth hospital day revealed improved LV systolic function (ejection fraction, 57%) with no wall motion abnormalities (Fig. 2B). Myocardial perfusion scintigraphy using 99mTc-
⁎ Corresponding author at: Cardiology, Gachon University Gil Medical Center, 774 Beongil 21, Namdongdaero, Namdong-Gu, Incheon 405-760, Republic of Korea. E-mail address: [email protected] (K.K. Koh).
http://dx.doi.org/10.1016/j.ijcard.2016.03.126 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
tetrofosmin performed on the sixth hospital day demonstrated no definite perfusion defect at rest and stress (Fig. 3). She was discharged without clinical symptoms on the eighth hospital day. Stress-induced cardiomyopathy also called Takotsubo cardiomyopathy, apical ballooning syndrome, or broken heart syndrome, was characterized by transient systolic dysfunction of apical and/or mid segments of LV with absence of obstructive coronary artery disease, which was preceded with severe emotional or physical stress [2]. Postmenopausal women are most commonly affected by stress-induced cardiomyopathy and the presentation is usually similar to that of an acute coronary syndrome [3]. Catecholamine-induced vascular or myocardial dysfunction is likely to be an important component of the pathogenesis of stress-induced cardiomyopathy [2,4]. Reported in-hospital mortality rate is low (1% to 3%) and long-term prognosis is favorable. Normalization of LV function typically occurs within 1 to 4 weeks [2]. One year ago, we reported a case of stress-induced cardiomyopathy presenting acute decompensated heart failure in postmenopausal women with several risk factors of coronary artery disease [1]. After a
Fig. 1. Chest radiography showed mild cardiomegaly and acute pulmonary edema.
308
Correspondence
Fig. 2. A, Transthoracic echocardiography of apical view showed severely enlarged left ventricle (LV) and depressed LV systolic function (ejection fraction 34%). B, Follow-up echocardiography on the sixth hospital day revealed improved LV systolic function (ejection fraction, 57%) without any regional wall motion abnormalities.
span of 1 year, stress-induced cardiomyopathy was recurred and completely recovered again. Postulated recurrence rates range from 2.7% to 11.4% [5,6]. Genetic predisposition towards developing such a
recurrent syndrome might be speculated. Of note, CD36 deficiency was detected in a patient who developed stress-induced cardiomyopathy [7].
Fig. 3. Myocardial perfusion scintigraphy using 99mTc-tetrofosmin performed on the sixth hospital day demonstrated no definite perfusion defect at rest and stress.
Correspondence
In the current report, we present a typical patient with recurrent stress-induced cardiomyopathy in postmenopausal women and completely recovered by swift and intensive medical treatment. Conflict of interest The authors report no relationships that could be construed as a conflict of interest. References [1] P.C. Oh, K.K. Koh, J. Shin, J. Yu, S.G. Kim, Stress-induced cardiomyopathy presented with acute decompensated heart failure, Int. J. Cardiol. 191 (2015) 114–116.
309
[2] K.A. Bybee, A. Prasad, Stress-related cardiomyopathy syndromes, Circulation 118 (2008) 397–409. [3] S.W. Sharkey, J.R. Lesser, A.G. Zenovich, et al., Acute and reversible cardiomyopathy provoked by stress in women from the United States, Circulation 111 (2005) 472–479. [4] V. Kurowski, A. Kaiser, K. von Hof, et al., Apical and midventricular transient left ventricular dysfunction syndrome (tako-tsubo cardiomyopathy): frequency, mechanisms, and prognosis, Chest 132 (2007) 809–816. [5] A.A. Elesber, A. Prasad, R.J. Lennon, R.S. Wright, A. Lerman, C.S. Rihal, Four-year recurrence rate and prognosis of the apical ballooning syndrome, J. Am. Coll. Cardiol. 50 (2007) 448–452. [6] K.A. Bybee, T. Kara, A. Prasad, et al., Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction, Ann. Intern. Med. 141 (2004) 858–865. [7] T. Kushiro, F. Saito, J. Kusama, et al., Takotsubo-shaped cardiomyopathy with type I CD36 deficiency, Heart Vessel. 20 (2005) 123–125.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Recurrent stress-induced cardiomyopathy presented with acute decompensated heart failure Pyung Chun Oh, Kwang Kon Koh ⁎ Department of Cardiology, Gachon University Gil Medical Center, Incheon, Republic of Korea
a r t i c l e
i n f o
Article history: Received 17 February 2016 Accepted 19 March 2016 Available online 24 March 2016 Keyword: Recurrent stress-induced cardiomyopathy
A 73 year-old female patient presented to an emergency room with dyspnea suddenly developed 1 day ago, which was preceded with cough, sputum and sore throat for 1 week. She had a diabetes mellitus and hypertension for about 30 years and had undergone aortobifemoral bypass graft for peripheral arterial disease 13 years ago. One year ago, she had been admitted with sudden onset of dyspnea and had been diagnosed with stress-induced cardiomyopathy presenting acute decompensated heart failure requiring mechanical ventilation, which had been completely recovered with intensive medical treatment [1]. She has been lost for 3 months before developing dyspnea. She was tachypneic (32 breaths per minute) and initial arterial blood gas analysis revealed hypoxemia (PaO2, 50 mmHg), hypercapnia (PaCO2, 55 mmHg), and respiratory acidosis (pH 7.09). Chest radiography showed mild cardiomegaly and acute pulmonary edema (Fig. 1). Transthoracic echocardiography showed severely enlarged left atrium and left ventricle (LV) and LV systolic function was significantly decreased to LV ejection fraction 34% with severe global hypokinesia of LV (Fig. 2A), compared with the last echocardiography (LV ejection fraction 73%) performed 1 year ago. Serum cardiac enzyme levels were within normal limit. Medical therapy was promptly commenced for acute decompensated heart failure including intravenous nitroglycerin, furosemide, and angiotensin II type 1 receptor blocker, and acute respiratory failure was improved without mechanical ventilation. Follow-up echocardiography on the sixth hospital day revealed improved LV systolic function (ejection fraction, 57%) with no wall motion abnormalities (Fig. 2B). Myocardial perfusion scintigraphy using 99mTc-
⁎ Corresponding author at: Cardiology, Gachon University Gil Medical Center, 774 Beongil 21, Namdongdaero, Namdong-Gu, Incheon 405-760, Republic of Korea. E-mail address: [email protected] (K.K. Koh).
http://dx.doi.org/10.1016/j.ijcard.2016.03.126 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
tetrofosmin performed on the sixth hospital day demonstrated no definite perfusion defect at rest and stress (Fig. 3). She was discharged without clinical symptoms on the eighth hospital day. Stress-induced cardiomyopathy also called Takotsubo cardiomyopathy, apical ballooning syndrome, or broken heart syndrome, was characterized by transient systolic dysfunction of apical and/or mid segments of LV with absence of obstructive coronary artery disease, which was preceded with severe emotional or physical stress [2]. Postmenopausal women are most commonly affected by stress-induced cardiomyopathy and the presentation is usually similar to that of an acute coronary syndrome [3]. Catecholamine-induced vascular or myocardial dysfunction is likely to be an important component of the pathogenesis of stress-induced cardiomyopathy [2,4]. Reported in-hospital mortality rate is low (1% to 3%) and long-term prognosis is favorable. Normalization of LV function typically occurs within 1 to 4 weeks [2]. One year ago, we reported a case of stress-induced cardiomyopathy presenting acute decompensated heart failure in postmenopausal women with several risk factors of coronary artery disease [1]. After a
Fig. 1. Chest radiography showed mild cardiomegaly and acute pulmonary edema.
308
Correspondence
Fig. 2. A, Transthoracic echocardiography of apical view showed severely enlarged left ventricle (LV) and depressed LV systolic function (ejection fraction 34%). B, Follow-up echocardiography on the sixth hospital day revealed improved LV systolic function (ejection fraction, 57%) without any regional wall motion abnormalities.
span of 1 year, stress-induced cardiomyopathy was recurred and completely recovered again. Postulated recurrence rates range from 2.7% to 11.4% [5,6]. Genetic predisposition towards developing such a
recurrent syndrome might be speculated. Of note, CD36 deficiency was detected in a patient who developed stress-induced cardiomyopathy [7].
Fig. 3. Myocardial perfusion scintigraphy using 99mTc-tetrofosmin performed on the sixth hospital day demonstrated no definite perfusion defect at rest and stress.
Correspondence
In the current report, we present a typical patient with recurrent stress-induced cardiomyopathy in postmenopausal women and completely recovered by swift and intensive medical treatment. Conflict of interest The authors report no relationships that could be construed as a conflict of interest. References [1] P.C. Oh, K.K. Koh, J. Shin, J. Yu, S.G. Kim, Stress-induced cardiomyopathy presented with acute decompensated heart failure, Int. J. Cardiol. 191 (2015) 114–116.
309
[2] K.A. Bybee, A. Prasad, Stress-related cardiomyopathy syndromes, Circulation 118 (2008) 397–409. [3] S.W. Sharkey, J.R. Lesser, A.G. Zenovich, et al., Acute and reversible cardiomyopathy provoked by stress in women from the United States, Circulation 111 (2005) 472–479. [4] V. Kurowski, A. Kaiser, K. von Hof, et al., Apical and midventricular transient left ventricular dysfunction syndrome (tako-tsubo cardiomyopathy): frequency, mechanisms, and prognosis, Chest 132 (2007) 809–816. [5] A.A. Elesber, A. Prasad, R.J. Lennon, R.S. Wright, A. Lerman, C.S. Rihal, Four-year recurrence rate and prognosis of the apical ballooning syndrome, J. Am. Coll. Cardiol. 50 (2007) 448–452. [6] K.A. Bybee, T. Kara, A. Prasad, et al., Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction, Ann. Intern. Med. 141 (2004) 858–865. [7] T. Kushiro, F. Saito, J. Kusama, et al., Takotsubo-shaped cardiomyopathy with type I CD36 deficiency, Heart Vessel. 20 (2005) 123–125.