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(Circulation. 2005;111:388-390.)
© 2005 American Heart Association, Inc.

Editorial

Recognition of the Apical Ballooning Syndrome in the United States

G. William Dec, MD

From the Cardiology Division, Massachusetts General Hospital, Boston, Mass.

Correspondence to G. William Dec, MD, Cardiology Division, Massachusetts General Hospital, Bigelow 800, Mailstop 847, Fruit St, Boston, MA 02114. E-mail gdec@partners.org

Key Words: Editorials • cardiomyopathy • magnetic resonance imaging • angiography • heart failure

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Acute dilated cardiomyopathy is an uncommon but often life-threatening cardiovascular event. Despite varied clinical presentations that may include cardiogenic shock, ventricular tachyarrhythmias, and chest pain mimicking acute myocardial infarction, a growing list of potentially reversible pathogeneses should be considered in the initial differential diagnosis. These may include cardiotoxins, such as excessive alcohol, cocaine, or antiretroviral agents; nutritional deficiencies (eg, thiamine, selenium, carnitine); endocrine disturbances (hyperthyroidism, hypothyroidism, pheochromocytoma); viral myocarditis; Lyme carditis; hypersensitivity reactions; infiltrative processes, such as hemochromatosis; peripartum disease; and tachycardia-induced cardiomyopathy.¹ Recently, a newly described left ventricular apical ballooning syndrome has been added to the growing list of diagnostic possibilities.²

See p 472

The apical ballooning syndrome is characterized by the abrupt onset of angina-like chest pain, ECG changes that typically demonstrate ST-segment elevation, diffuse T-wave inversions and abnormal QS-wave development, discrete wall motion abnormalities involving the lower anterior wall and apex on echocardiography or left ventriculography, and limited myocardial enzyme release relative to the extent of ventricular akinesia. The clinical presentation mimics acute myocardial infarction but always occurs in patients without evidence for hemodynamically significant coronary arterial stenoses by angiography. It was first described in the Japanese literature in 1991 by Dote and colleagues,² who proposed the term "tako-tsubo" (Japanese for octopus trap) cardiomyopathy on the basis of the peculiar appearance of a rounded bottom and narrow neck on the end-systolic left ventriculogram. The clinical features and outcomes of the syndrome have been well characterized in Asian populations in studies by Kurisu et al³ (n=30 patients) and . . . [Full Text of this Article]

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