Simulation of Mitral Valve Plasticity in Response to Myocardial Infarction

Left ventricular myocardial infarction (MI) has broad and debilitating effects on cardiac function. In many cases, MI leads to ischemic mitral regurgitation (IMR), a condition characterized by incompetency of the mitral valve (MV). IMR has many deleterious effects as well as a high mortality rate. While various clinical treatments for IMR exist, success of these procedures remains limited, in large part because IMR dramatically alters the geometry and function of the MV in ways that are currently not well understood. Previous investigations of post-MI MV remodeling have elucidated that MV tissues have a significant ability to undergo a form of permanent inelastic deformations in the first phase of the post-MI period. These changes appear to be attributable to the altered loading and boundary conditions on the MV itself, as opposed to an independent pathophysiological process. Mechanistically, these results suggest that the MV mostly responds passively to MI during the first 8 weeks post-MI by undergoing a permanent deformation. In the present study, we developed the first computational model of this post-MI MV remodeling process, which we term mitral valve plasticity. Integrating methodologies and insights from previous studies of in vivo ovine MV function, image-based patient-specific model development, and post-MI MV adaptation, we constructed a representative geometric model of a pre-MI MV. We then performed finite element simulations of the entire MV apparatus under time-dependent boundary conditions and accounting for changes to material properties equivalent to those observed 0-8 weeks post-MI. Our results suggest that during this initial period of adaptation, the MV response to MI can be accurately modeled using a soft tissue plasticity approach, similar to permanent set frameworks that have been applied previously in the context of exogenously crosslinked tissues.

Automated summary

Left ventricular myocardial infarction has significant effects on cardiac function and often leads to ischemic mitral regurgitation, which has deleterious effects and a high mortality rate. Clinical treatments for this condition have limited success due to a lack of understanding of the mitral valve remodeling process. This study developed a computational model to accurately depict the post-MI mitral valve remodeling, suggesting that the valve responds to the infarction through permanent deformations during the initial 8 weeks.