Stress cardiomyopathy, also known as broken heart syndrome or Takotsubo cardiomyopathy, is an entity characterized by, usually transient, left ventricular dysfunction. It was first described in 1990 in Japan. It derives its name from the characteristic shape of the heart in imaging tests (invasive ventriculography, ultrasound or magnetic resonance imaging of the heart). This shape looks like a typical Japanese jar, called Takotsubo, used to catch octopuses. It is also referred to as broken heart syndrome because it is more frequent in women after intense emotional stress.

The clinical presentation is similar to that of an acute coronary event (electrocardiogram findings, positive myocardial necrosis markers, symptoms), but coronary angiography reveals the absence of any significant narrowing of the arteries that supply the myocardium. In the context of the left cardiac catheterization, which is required for coronary angiography, a left ventriculography may also be performed (ie, a contrast agent is injected into the left ventricle to visualize it).

Stress cardiomyopathy overwhelmingly affects postmenopausal women (90% of cases are women 60-70 years old). It occurs after intense physical or mental stress (eg exacerbation of another disease, surgery, severely unpleasant or pleasant event). The etiology, although not fully elucidated, appears to be related to the increased circulation of stress hormones (catecholamines) which directly affect the myocardium and the arterial network (increasing the afterload, thus increasing the effort the heart must put to achieve sufficient blood flow).

Formerely, it used to be considered a benign condition that resolves completely after 4-6 weeks. More recent data indicate that in-hospital mortality corresponds to that of a true ischemic heart attack (~ 2-7%), while there are cases in which the clinical presentation can be adverse (acute heart failure – shock). In hemodynamically stable patients, the treatment during the acute phase beyond drug treatment consists of close monitoring so that timely intervention is possible in case of complications. In the chronic phase, angiotensin converting enzyme inhibitors are administered for a time-frame of one year (beta-blockers have been used but probably offer no additional benefit). Relapses are not considered to be frequent.