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Management and prognosis of stress (takotsubo) cardiomyopathy

Guy S Reeder, MD
Abhiram Prasad, MD
Section Editor
William J McKenna, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC


Stress cardiomyopathy (also called apical ballooning syndrome, takotsubo cardiomyopathy, broken heart syndrome, and stress-induced cardiomyopathy) is a syndrome characterized by transient regional systolic dysfunction of the left ventricle (LV), mimicking myocardial infarction, but in the absence of angiographic evidence of obstructive coronary artery disease or acute plaque rupture [1-16]. In most cases of stress cardiomyopathy, the regional wall motion abnormality extends beyond the territory perfused by a single epicardial coronary artery.

Stress cardiomyopathy was first described in 1990 in Japan and has since been increasingly recognized around the world [1,2,6,7,9,10,16,17]. The term "takotsubo" is taken from the Japanese name for an octopus trap, which has a shape that is similar to the systolic apical ballooning appearance of the LV in the most common and typical form of this disorder (movie 1 and movie 2); mid and apical segments of the LV are depressed, and there is hyperkinesis of the basal walls. A midventricular type (movie 3) and other variants have also been described. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy", section on 'Approach to diagnosis'.)

This topic will review the management and prognosis of stress cardiomyopathy. The epidemiology, pathogenesis, clinical manifestations, and diagnosis of stress cardiomyopathy are discussed separately. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy".)


Approach to management — Stress cardiomyopathy is generally a transient disorder that is managed with supportive therapy. Conservative treatment and resolution of the physical or emotional stress usually result in rapid resolution of symptoms, although some patients develop acute complications such as shock and acute heart failure (HF) that require intensive therapy. Appropriate management of shock varies depending upon whether significant left ventricular outflow tract (LVOT) obstruction is present. HF management during acute presentation and following stabilization is generally performed according to standard guidelines except that particular care is taken to avoid volume depletion and vasodilator therapy in patients with LVOT obstruction. Recommendations for anticoagulation to prevent thromboembolism in patients with stress cardiomyopathy with LV thrombus or severe LV systolic dysfunction are similar to those for patients post-myocardial infarction.

Hypotension and shock — Approximately 10 percent of patients with stress cardiomyopathy develop cardiogenic shock [16]. The development of shock may not correlate with the extent of left or right ventricular systolic dysfunction [18]. One explanation for discordance between ventricular dysfunction and risk of shock is that some shock is caused by LVOT obstruction, which has been described in 10 to 25 percent of patients with stress cardiomyopathy [3,19-21].

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Literature review current through: Nov 2017. | This topic last updated: Jul 27, 2017.
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