Brutsaert’s hypothesis on preferential LV apical involvement in Takotsubo cardiomyopathy

Brutsaert’s hypothesis on preferential LV apical involvement in Takotsubo cardiomyopathy

Takotsubo cardiomyopathy is also known as apical ballooning syndrome because of preferential involvement of the left ventricular apex. Other names of the syndrome are stress cardiomyopathy and broken heart syndrome. Brutsaert’s hypothesis [1] on preferential involvement of the left ventricular apex in Takotsubo cardiomyopathy has to do with the trabeculation pattern in the left ventricle. According to Brutsaert, left ventricular apex is the most trabeculated and thinnest portion of the left ventricle. The resulting higher surface to volume ratio would mean more of exposed endothelial surface lining the apex. This would make the apex more vulnerable to the effect of excessive catecholamines in the circulation, which is known to damage the endothelial cells. Brutsaert presumes that the endothelial damage would lead on to transient contractile dysfunction in regions with high surface to volume ratio, namely the apex of the left ventricle and some regions of the right ventricle, leading to apical ballooning cardiomyopathy. But this would not explain the mid ventricular variant of Takotsubo cardiomyopathy [2].

References

1. Dirk L Brutsaert. Tako-Tsubo cardiomyopathy. Eur J Heart Fail 2007; 9: 854.
2. Paolo Angelini. Midventricular variant of transient apical ballooning: a likely demonstration of its pathophysiologic mechanism. Mayo Clin Proc. 2009; 84: 92-3.