Apical akinesis and dilation in the absence of obstructive coronary artery disease is a typical feature of stress-induced (takotsubo) cardiomyopathy, whereas apical hypertrophy isS tress-induced cardiomyopathy involving akinesis of the left ventricular (LV) apex can mimic acute coronary syndrome but typically lacks obstructive coronary artery disease (CAD).1 Regional wall-motion abnormalities are usually transient, and the overall prognosis is favorable. Hypertrophic cardiomyopathy (HCM) is an autosomal dominant genetic disorder that can be localized in the LV apex. 2 We describe the cases of 2 patients whose diagnoses of apical-variant HCM were initially masked by their presentations with apical ballooning.
Case Reports Patient 1In June 2011, a 43-year-old white woman with a history of alcohol abuse emergently presented with confusion, agitation, and shortness of breath of 2 days' duration. She had discontinued alcohol use and metoprolol succinate therapy 3 days before presentation. Her medical history included hypertension, previous tobacco use, and alcoholrelated liver disease. She had no known coronary disease. Her temperature was 36.7 °C; heart rate, 125 beats/min; blood pressure, 100/64 mmHg; respiratory rate, 34 breaths/min; and oxygen saturation, 96% on room air. Physical examination revealed tachycardia, non-tender hepatomegaly, and mild pitting edema in the lower extremities. The patient was confused, disoriented, and irritable without focal neurologic deficits.An electrocardiogram (ECG) showed sinus tachycardia with T-wave inversions and nonspecific ST-T-wave abnormalities in the anterolateral leads. Laboratory results included an elevated troponin T level of 0.27 ng/mL (normal, <0.03 ng/mL) and normal renal function. A transthoracic echocardiogram (TTE) showed an LV ejection fraction (LVEF) of 0.47 with hyperdynamic basal function but with a dilated, akinetic apex that suggested an apical variant of stress-induced cardiomyopathy (Fig. 1).