Tako-Tsubo Stress Cardiomyopathy-A Quantum Event of the Heart?

Tako-tsubo cardiomyopathy, named for a Japanese fisherman’s octopus trap, is an extraordinary event wherein a so-called stress event induces a large area of myocardial stunning. Tako-tsubo cardiomyopathy was first described in Japan by Dr. Sato at the Hiroshima City Hospital in 1990. In its classic form, there is aneurysmal dysfunction of the apical myocardium with dyskinesis and bulging of the ventricular wall, but with preserved function of the base of the heart. As might be predicted, there are also other atypical variants, including one, which is reported to affect selectively the midportion of the left ventricle. Tako-tsubo’s cardiomyopathy is now considered to represent a group of acute onset cardiomyopathies, which are also named stress-induced cardiomyopathies.

We would like to open a discussion around the prevailing opinions and the available evidence that this cardiomyopathy is the result of an adrenaline surge, with stress causing microvascular dysfunction on a wide scale. Atherosclerotic plaque rupture or erosion with in situ thrombosis resulting in ST elevation myocardial infarction (STEMI or acute heart attack) has been considered a distinct event, unrelated to Tako-tsubo cardiomyopathy. 

However, many of the measurements demonstrating a catecholamine excess and abnormal  vasoreactivity, signs of microvascular dysfunction, have been recorded after the inciting event is complete. Thus, only a snapshot of the devastation is seen. Just as when a photographer captures the after effects of a tidal wave, the initial seismic event that results in a tsunami is not recorded.

We would like to suggest that plaque erosion and thrombosis with distal emboli causing downstream or distal microvascular occlusions may be, like a tidal wave that wreaks havoc on the shoreline, the initiating events for a cardiomyopathy such as Tako-tsubo. It is certainly well understood that the coagulation serine protease system, the inflammatory and also the hemodynamic vascular systems that regulate arterial pressure and tone have very close interactions. This editorial is intended to open up a discussion on the potential inciting events for this cardiomyopathy.