Abstract 15014: Aberrant, Elevated Papillary Muscle and Left Ventricular Wall Forces Associated With Mitral Valve Prolapse Are Normalized by Surgical Neochordal Repair but Not by Transcatheter Edge-to-Edge Repair

Abstract

Introduction: Recent studies have linked mitral valve prolapse (MVP) to localized myocardial fibrosis and ventricular arrhythmia, and early imaging work has shown altered ventricular motion with papillary muscle (PM) traction in MVP and MitraClip patients. We aimed to biomechanically compare MitraClip and neochordal repair for MVP on PM forces ex vivo . Methods: We developed a force transduction system to measure the forces exerted on the PMs throughout the cardiac cycle in a left heart simulator ( Fig A ) with consistent pressures. Using a randomized, paired procedure with porcine MVs (n=4), we measured the hemodynamics and forces for control, diseased (P2 prolapse via chordal rupture), MitraClip repair ( Fig B, C, D ) (single P2 clip), and neochordal repair (P2 primary neochord on each PM) conditions. Results: We found that MitraClip PM forces (7.19 ± 0.31 N) are higher by 9.34% compared with those of controls (6.58 ± 0.21 N, p<0.001 ). This result is similar to MVP valves modeled by superior PM displacement, which showed 9.23% higher forces than those of controls (n=10, p<0.001 ). Moreover, MitraClip repaired valves showed PM force increases of 6.4% compared with forces of neochordal repair (6.76 ± 0.22 N, p<0.001 ), despite having similarly reduced regurgitation fractions (5.05% ± 1.98% vs. 4.25% ± 1.51%, respectively, p>0.05 ) compared with those of the diseased state (16.96% ± 3.04%, p<0.001 ) and controls (2.66% ± 0.87%). Additionally, neochordal repair valves had 2.79% higher forces compared to those of control valves ( p<0.001 ). Conclusions: We discovered that MitraClip, while reducing regurgitation, does not restore aberrant forces on the PM induced in MVP to baseline or reduced levels, while neochordal repair does. Our work suggests that these elevated forces, associated with MVP and MitraClip, predisposes the MV to continued traction, which may present a long-term harm to patients by catalyzing localized fibrosis and ventricular arrhythmia.