Microvascular Dysfunction in Takotsubo Cardiomyopathy

Takotsubo cardiomyopathy (TC), also called stress cardiomyopathy, apical ballooning syndrome or broken heart syndrome, is a syndrome characterized by transient regional systolic dysfunction of the left ventricle (LV), mimicking myocardial infarction (MI), but in the absence of evidence of angiographic significant obstructive coronary artery disease (CAD) or acute plaque rupture. In most cases of TC, the regional wall motion abnormality extends beyond the territory perfused by a single epicardial coronary artery. The systolic apical ballooning appearance of the LV is the most typical form of this syndrome associated with mid and apical segmental hypokinesis and hyperkinesis of the basal walls. The first case of TC was described in 1990 in Japan and since then, this syndrome been increasingly recognized around the globe.1 Despite abundant research, the exact pathogenic mechanism of this disease remains elusive to date.2 Several postulated mechanisms for its pathogenesis have been described which include sympathetic or catecholaminergic hyperactivity, mutivessel coronary vasospasm, microcirculatory disorder, and estrogen deficiency. Microvascular dysfunction (MVD) in particular has been recognized as an important pathogenic contributor to the causation of TC in the more recent years and remains the focus of discussion in this review.