Background: Recent studies have suggested acute mitral regurgitation (MR) as a potentially serious complication of takotsubo cardiomyopathy (TTC); however, the mechanism of acute MR in TTC remains unclear. The aim of this study was to elucidate the mechanisms of acute MR in patients with TTC.
Methods and results: Echocardiography was used to assess the mitral valve and left ventricular outflow tract (LVOT) pressure gradient in 47 patients with TTC confirmed by coronary angiography and left ventriculography. Mitral valve assessment included coaptation distance, tenting area at mid systole in the long-axis view, and systolic anterior motion of the mitral valve (SAM). Of the study patients, 12 (25.5%) had significant (moderate or severe) acute MR. In patients with acute MR versus those without acute MR, we found lower ejection fraction (31.3 ± 6.2% versus 41.5 ± 10.6%, P = 0.001) and higher systolic pulmonary artery pressure (49.3 ± 7.4 versus 35.5 ± 8.9 mm Hg, P < 0.001). Moreover, 6 of the 12 patients with acute MR had SAM, with peak LVOT pressure gradient > 20 mm Hg (average peak LVOT pressure gradient, 81.3 ± 35.8 mm Hg). The remaining 6 patients with acute MR revealed significantly greater mitral valve coaptation distance (10.9 ± 1.6 versus 7.8 ± 1.4 mm, P < 0.001) and tenting area (2.1 ± 0.4 versus 0.95 ± 0.25 cm2, P < 0.001) than those without acute MR. A multivariate analysis revealed that SAM and tenting area were independent predictors of acute MR in patients with TTC (all P < 0.001).
Conclusions: SAM and tethering of the mitral valve are independent mechanisms with differing pathophysiology that can lead to acute MR in patients with TTC.