American Journal of Emergency Medicine 33 (2015) 476.e1–476.e3

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Case report

Stimulant-related Takotsubo cardiomyopathy Abstract Takotsubo cardiomyopathy (TC) is a rare but increasingly recognized mimic of acute coronary syndrome. Patients present with angina, ST-segment changes on electrocardiogram (both elevations and depressions), and rapid rises in cardiac biomarkers. Many kinds of stressful events have been associated with TC, but only a handful of drug-related cases have previously been reported. We describe the case of a 58-year-old woman who developed TC 2 days after crack cocaine use, a diagnosis first suggested as bedside echocardiography in the emergency department. Recognition of the classic echocardiographic appearance of TC—apical hypokinesis causing “ballooning” of the left ventricle during systole—may greatly assist providers in the early identification of this condition. Takotsubo cardiomyopathy (TC), also known as transient left ventricular apical ballooning syndrome, refers to acute dysfunction of the left ventricular apex after a stressful event [1]. A diverse array of physiologic insults have been associated with this rare condition, including severe emotional distress (leading to its nickname, “Broken heart syndrome”), surgery or physical trauma, pheochromocytoma, dobutamine stress testing, and others [2,3]. Here, we describe a case of cocaine-related TC whose diagnosis was first suggested during bedside echocardiography in the emergency department. A 58-year-old woman with a history of hypertension and cocaine abuse was brought by ambulance to the emergency department for chest discomfort. She described severe left-sided chest pain that had begun suddenly 3 hours earlier, while she was cleaning her kitchen. She smoked crack cocaine regularly and had last done so the day before. On presentation, the patient's vital signs and cardiopulmonary examination were normal. Pertinent findings from her workup in the emergency department included a toxicology screen that was positive for cocaine and negative serum troponin. Her initial electrocardiogram (EKG) showed normal sinus rhythm with right axis deviation, poor R-wave progression, and diffuse J-point elevation in the inferolateral leads. Bedside echocardiography revealed circumferential hypokinesis of the cardiac apex, suggestive of a left anterior descending coronary artery lesion vs TC (Figs. 1 and 2; Videos 1 and 2). The patient's chest pain was relieved with nitroglycerin paste, and she was consulted to the medical service. Notably, troponin level 6 hours later returned at 1.29 ng/mL and at 12 hours increased to 4.06 ng/mL. Her follow-up EKG revealed that T-wave inversions had replaced the diffuse J-point elevations in the inferolateral leads (Fig. 3). While the patient remained free of chest pain over the next 24 hours, her troponin rose to a peak of 8.39 ng/mL and then slowly trended downward. She underwent left heart catheterization on hospital day 2, which failed to show significant atherosclerotic disease in any coronary distribution. Ventriculography estimated an ejection fraction of 23% and confirmed apical dilation consistent with TC (Fig. 4). The

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patient was medically managed and discharged without event. A follow-up transthoracic echocardiogram 4 months later showed normalization of her left ventricular systolic function. In TC, the apex of the left ventricle dilates during systole, giving it the appearance of a Japanese octopus trap (Takotsubo) [4]. Although the precise pathophysiologic mechanisms behind this phenomenon are unknown, it is thought to be triggered by the catecholamine surge produced during the body's “fight or flight” response to stress. Takotsubo cardiomyopathy has a similar presentation to acute coronary syndrome (ACS), as it is frequently accompanied by chest pain, acute EKG changes (including ST elevation and depression), and elevated serum troponin levels. However, cardiac catheterization fails to reveal significant coronary stenosis, and systolic function usually returns to baseline within weeks. Although TC has increasingly been reported in English-language journals over the past decade, only a handful of cases have linked this condition with stimulant drug abuse. The 2 previously described cases of cocaine-related TC involved a 54-year-old woman whose symptoms began 2 hours after smoking crack; the other was a 53-year-old man who admitted to “heavy cocaine use” during the previous day [5,6]. While the woman's EKG demonstrated lateral ST elevations, the man's EKG was unchanged. An additional case report from 1989 described a patient who presented with “global” dilated cardiomyopathy after freebasing crack, which resolved during hospital admission [7]. The 1 reported case of methamphetamine-related TC involved a 25-year-old

Fig. 1. Parasternal short axis view demonstrating apical ballooning during peak systole (arrow).

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Fig. 4. Ventriculogram demonstrating apical ballooning.

settings may greatly assist providers in the early determination of the cause of cardiac symptoms and dysfunction in these patients. Supplementary data to this article can be found online at http://dx. doi.org/10.1016/j.ajem.2014.08.058. Fig. 2. Parasternal short axis view demonstrating dilation of the left ventricular apex during diastole (top) and systole (bottom).

woman who had reverse apical (ie, basal) ballooning (a known variant of the syndrome) but no ST changes [8]. All 3 of the true Takotsubo cases had elevated troponins and initially decreased ejection fractions but otherwise uncomplicated hospital courses. Stimulant drug abuse predisposes to atherosclerosis and may be complicated by true ACS [9]. However, TC mimics ACS and should remain on the clinician's differential for chest pain syndromes in this population. Although it cannot rule out a coronary lesion, the use of point-of-care ultrasound echocardiography in emergency and inpatient

Mike Butterfield, MD, MS, MPH Tulane University Medical Center, New Orleans, LA Corresponding author. Tel.: +1 510 318 1063 E-mail address: mcbutterfi[email protected] Christine Riguzzi, MD Oron Frenkel, MD, MS Arun Nagdev, MD Highland General Hospital, Oakland, CA http://dx.doi.org/10.1016/j.ajem.2014.08.058

Fig. 3. Normal sinus rhythm with new T-wave inversions in lateral leads.

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References [1] Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, et al. 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(1):11–8. [2] Vergez M, Pirracchio R, Mateo J, Payen D, Cholley B. Takotsubo cardiomyopathy in a patient with multiple trauma. Resuscitation 2009;80(9):1074–7. [3] Morita S, Inokuchi S, Yamagiwa T, Aoki H, Nakagawa Y, Yamamoto I. Takotsubo-like left ventricular dysfunction with ST-segment elevation after central spinal cord injury: a case report. J Emerg Med 2010;39(3):301–4. [4] Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics STsegment elevation myocardial infarction. Ann Intern Med 2004;141(11):858–65.

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[5] Arora S, Alfayoumi F, Srinivasan V. Transient left ventricular apical ballooning after cocaine use: is catecholamine cardiotoxicity the pathologic link? Mayo Clin Proc 2006; 81(6):829–32. [6] Sarkar S, Arguelles E, de Elia C. Takosubo cardiomyopathy presenting as a non-ST segment elevation myocardial infarction in the setting of cocaine use and asthma exacerbation. Int J Cardiol 2013;168(1):e1–2. [7] Chokshi SK, Moore R, Pandian NG, Isner JM. Reversible cardiomyopathy associated with cocaine intoxication. Ann Intern Med 1989;111(12): 1039–40. [8] Movahed M-R, Mostafizi K. Reverse or inverted left ventricular apical ballooning syndrome (reverse Takotsubo cardiomyopathy) in a young woman in the setting of amphetamine use. Echocardiography 2008;25(4):429–32. [9] Jones JH, Weir WB. Cocaine-associated chest pain. Med Clin North Am 2005;89(6): 1323–42.

Stimulant-related Takotsubo cardiomyopathy.

Takotsubo cardiomyopathy (TC) is a rare but increasingly recognized mimic of acute coronary syndrome. Patients present with angina,ST-segment changes ...
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