A 73-year-old female with a past medical history significant for hypertension, hyperlipidemia, and diabetes mellitus presented with new onset chest pain. The chest discomfort was characterized as a dull, non-radiating, pressure-like pain that was precipitated by an intense emotional stressor. She denied experiencing rest or exertional angina prior to this episode. The history was otherwise unremarkable. Cardiovascular examination was notable for normal carotid upstrokes, a quiet precordium with normal first and second heart sounds and absence of distended neck veins and any murmurs, rubs, or gallops. An electrocardiogram revealed normal sinus rhythm with bigeminy, coved ST segment elevation, and T wave inversions in the anterior precordial leads. A chest radiograph, initial cardiac enzymes and pertinent laboratory evaluations were normal. The patient was taken to the cardiac catheterization laboratory, where coronary angiography revealed no evidence of obstructive epicardial coronary artery disease. Left ventriculography and subsequent echocardiogram demonstrated a hypercontractile base and ballooning of the mid and apical left ventricle. The remainder of the hospital course was unremarkable. Several weeks later, a repeat transthoracic echocardiogram showed resolution of the mid and apical wall motion abnormalities with normal left ventricular systolic function. Based on the clinical presentation and findings at the time of cardiac catheterization, the diagnosis of transient left ventricular apical ballooning or Tako-Tsubo cardiomyopathy was made. Typically seen in elderly females, symptoms are manifested by the acute onset of chest discomfort triggered by intense emotional or physical stress. Electrocardiograms commonly reveal ST segment elevation or pronounced T wave inversions. Cardiac biomarkers are often abnormal, indicating myocardial damage. Findings at cardiac catheterization include normal epicardial coronary arteries and a characteristic pattern of a hypercontractile base and ballooning of the mid and apical segments. The distribution of the wall motion abnormalities does not correlate with an individual epicardial coronary artery. The characteristic wall motion abnormalities and left ventricular systolic dysfunction rarely persist for more than 4 weeks. The etiology of this cardiomyopathy is uncertain; however, suggested causes include multivessel coronary artery spasm, an intense catecholamine discharge, and an impairment of the coronary microcirculation. Case reports reveal incidences of thrombus formation, but otherwise the course is benign with resolution of symptoms and echocardiogram abnormalities.
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