Pathogenesis of the Takotsubo syndrome: a unifying hypothesis

Abstract

The takotsubo syndrome (TS) is defined by a constellation of clinical observations in a subgroup of patients with acute coronary syndromes. Separating patients with TS from the general population with acute ischemic events are 2 important findings: obstructive coronary artery disease is missing, but the sine qua non is a distinctive pattern of abnormal left ventricular contraction. As with many newly recognized clinical syndromes, TS seems not to conform to accepted pathogenetic mechanisms. Thus, physicians are challenged to identify previously unrecognized mechanisms of disease. Two schools of thought have emerged in this regard. Most consider its pathogenesis to be a stress-induced neurohormonal phenomenon, while a smaller but substantial group believe that the transient occlusion of an epicardial coronary artery is responsible and that the syndrome is simply an unusual manifestation of coronary atherosclerosis. This editorial outlines briefly the evidence for each of these positions and presents a novel construct that may encompass the 2 views. Central to this unifying hypothesis is the belief that a neurohormonal surge triggers the hallmark left ventricular contraction abnormality, the sine qua non of the TS. In conclusion, the authors postulate that this pattern will result regardless of the state of the epicardial coronary arteries and can be observed in patients with angiographically normal coronary arteries, as well as those with obstructed or occluded arteries.