Abstract 11335: Mitral Valve Prolapse Increases the Force Exerted on the Papillary Muscles

Introduction: Recent studies have linked mitral valve prolapse (MVP) to localized myocardial fibrosis, ventricular arrhythmia, and even sudden cardiac death independent of mitral regurgitation (MR). The primary mechanistic theory is rooted in increased papillary muscle (PM) traction force, yet there is no biomechanical evidence to support it. Thus we aimed to evaluate the biomechanical relationship between prolapse and PM forces, leveraging advances in ex vivo simulation technology. Methods: We developed an ex vivo PM force transduction system (Fig. A, B) and a novel neochord length adjustment system (Fig. C) capable of modeling targeted prolapse without creating severe MR. Using unique models of bileaflet and posterior leaflet prolapse, we directly measured hemodynamics and forces, comparing optimally coapting (i.e., physiologic) and prolapsing valves. Results: Throughout the experiments, hemodynamics and MR severity remained comparable between the physiologic and prolapse conditions. We found that bileaflet prolapse in this experimental setting increases PM forces by 5-15% (p<0.001) compared to a physiologic valve. We furthermore observed fundamental differences in the force profiles for prolapsing valves with higher primary peaks (Fig. D) . In the isolated posterior leaflet prolapse condition, prolapsing valves had significantly higher primary peak forces ( p=0.044 ), with a strong trend towards higher overall PM force magnitudes (p=0.051 ), when compared to physiologic valves. Conclusions: Through advances in ex vivo heart simulation technology, we discovered that bileaflet prolapse, with MR similar to the physiologic valve, results in significantly elevated forces and altered dynamics on the PMs. Our work carries deeper implications, suggesting that interventions might reduce abnormal PM forces (and subsequent ventricular effects of MVP) in addition to MR correction, with possible benefit even in less-than-severe MR.