Abstract 13491: Mitral Valve Annular Dilatation & Augmented Valve Closing Force to Tract Papillary Muscle as a Possible Mechanism of Late-systolic Mitral Valve Prolapse: Pre- & Post-operative Echocardiographic Study With Speckle Tracking Analysis

Abstract

Introduction: Stable papillary muscle (PM) position and contraction enable constant PM tip distance from mitral valve (MV) annulus, which can contribute to constant MV coaptation height during systole (Figure A). Hypothesis: In patients with late-systolic MV prolapse (L-MVP), superior shift of MV coaptation toward left atrium (LA) during systole may be linked to abnormal PMs superior shift, which can be related to augmented MV closing force by MV annular dilatation. Methods: In 15 controls and 20 with L-MVP, MV coaptation height from its annulus was measured at early- and late-systole by echocardiography to evaluate systolic superior shift of MV coaptation. Distances of PMs tip and MV annulus from external reference point around the apex were monitored by 2 points speckle tracking, and systolic shift of PMs tip toward MV annulus was measured (Figures B and C). MV closing force was calculated as MV annular area х (systolic blood pressure - 10). Echocardiography was repeated after MV plasty in 5 L-MVP patients. Results: Systolic superior shift of MV coaptation (3.3±0.9 vs 1.4±0.5 mm/m 2 ) and PMs tip (2.9±1.3 vs 1.3±0.4 mm/m 2 ) relative to MV annulus were greater in L-MVP compared to controls (p<0.001) (Figures C and D). Systolic superior shift of MV coaptation was independently determined by systolic superior shift of PMs tip (β=0.66, p<0.001), which was related to augmented MV closing force with MV annular dilatation (β=0.72, p<0.001). Systolic superior shift of PMs tip (4.2±2.0 to -0.5±1.2 mm/m 2 , p=0.007) and MV coaptation (4.2±1.7 to 0.9±0.3 mm/m 2 , p=0.006) disappeared after surgical MV plasty with reduction in MV annulus and MV closing force in 5 patients with L-MVP. Conclusions: Systolic superior shift of MV coaptation in patients with L-MVP was associated with systolic superior shift of PM tip. Disappearance of these abnormalities after surgical MV plasty suggests that primarily augmented MV closing force with MV annular dilatation acting on PM traction may promote L-MVP.