Aberrant, Elevated Papillary Muscle and LV Wall Forces Associated With Mitral Valve Prolapse Are Normalized by...

Recent studies have linked mitral valve prolapse to increased papillary muscle (PM) traction in mitral valve prolapse and MitraClip patients. We aimed to biomechanically compare edge-to-edge repair via MitraClip implantation and neochordal repair for mitral valve prolapse on PM forces ex vivo.

We developed a force transduction system to measure the forces exerted on the PMs throughout the cardiac cycle in a left heart simulator. Using a randomized, paired procedure with porcine mitral valves (n=8), we measured the hemodynamic parameters and PM forces for control, prolapse, chordal rupture, MitraClip edge-to-edge repair, surgical edge-to-edge repair, and neochordal repair conditions.

Hemodynamic parameters, including maximum ventricular pressure and transmitral pressure gradients, remained consistent across all experimental conditions. The rupture condition induced pathological mitral regurgitation relative to control valves (23.7±18.5% versus 3.1±1.0%; P<0.001). In the chordal rupture model, composite peak PM forces were 7.8±1.3 N, ≈16% higher than baseline control valves (6.7±0.7 N, P=0.005). Both surgical and transcatheter edge-to-edge repair conditions resulted in significantly higher peak PM forces compared with both baseline (P<0.001) and diseased prolapse conditions (P=0.03). MitraClip repair valves recorded peak PM forces ≈23% higher than those of baseline control valves. Neochordal repair of the prolapsed model resulted in significant reductions of peak PM forces to near-baseline levels (6.8±1.3 N; P=0.53). All repair conditions reduced mitral regurgitation levels to moderate (<15%).

We demonstrated that MitraClip, while reducing regurgitation, increases aberrant forces on the PMs. In contrast, neochordal repair both reduces regurgitation and restores PM forces back to physiological levels. Our work suggests that these elevated forces, associated with mitral valve prolapse and MitraClip, predispose the mitral valve to continued traction, altering the mechanical load on the subvalvular apparatus.