Abstract
Mitral valve prolapse (MVP) refers to an excessive billowing of the mitral valve (MV) leaflets across the mitral annular plane into the left atrium during the systolic portion of the cardiac cycle. The underlying mechanisms for the development of MVP and mitral regurgitation in association with MV tissue remodeling are still unclear. We performed computational MV simulations to investigate the pathophysiologic developmental mechanisms of MVP. A parametric MV geometry model was utilized for this study. Posterior leaflet enlargement and posterior chordal elongation models were created by adjusting the geometry of the posterior leaflet and chordae, respectively. Dynamic finite element simulations of MV function were performed over the complete cardiac cycle. Computational simulations demonstrated that enlarging posterior leaflet area increased large stress concentration in the posterior leaflets and chordae, and posterior chordal elongation decreased leaflet coaptation. When MVP was accompanied by both posterior leaflet enlargement and chordal elongation simultaneously, the posterior leaflet was exposed to extremely large prolapse with a substantial lack of leaflet coaptation. These data indicate that MVP development is closely related to tissue alterations of the leaflets and chordae. This biomechanical evaluation strategy can help us better understand the pathophysiologic developmental mechanisms of MVP.