Key result
Bileaflet MVP increases papillary muscle forces up to ~15% ex vivo versus normal valves.
Why the study?
Mitral valve prolapse has been linked to localized myocardial fibrosis and arrhythmia, but biomechanical evidence of increased papillary muscle forces is lacking.
Does mitral valve prolapse increase papillary muscle forces compared to optimally coapting valves in an ex vivo ovine model?
Does mitral valve prolapse increase papillary muscle forces compared to optimally coapting valves in an ex vivo ovine model?
Ex vivo ovine models demonstrate that mitral valve prolapse significantly increases papillary muscle forces, providing a potential biomechanical mechanism for localized fibrosis and arrhythmias.
Potential mechanism for fibrosis/arrhythmias in prolapse; leaves open human validation before clinical inference.
BACKGROUND: Recent studies have linked mitral valve prolapse to localized myocardial fibrosis, ventricular arrhythmia, and even sudden cardiac death independent of mitral regurgitation or hemodynamic dysfunction. The primary mechanistic theory is rooted in increased papillary muscle traction and forces due to prolapse, yet no biomechanical evidence exists showing increased forces. Our objective was to evaluate the biomechanical relationship between prolapse and papillary muscle forces, leveraging advances in ex vivo modeling and technologies. We hypothesized that mitral valve prolapse with limited hemodynamic dysfunction leads to significantly higher papillary muscle forces, which could be a possible trigger for cellular and electrophysiological changes in the papillary muscles and adjacent myocardium. METHODS: We developed an ex vivo papillary muscle force transduction and novel neochord length adjustment system capable of modeling targeted prolapse. Using 3 unique ovine models of mitral valve prolapse (bileaflet or posterior leaflet prolapse), we directly measured hemodynamics and forces, comparing physiologic and prolapsing valves. RESULTS: We found that bileaflet prolapse significantly increases papillary muscle forces by 5% to 15% compared with an optimally coapting valve, which are correlated with statistically significant decreases in coaptation length. Moreover, we observed significant changes in the force profiles for prolapsing valves when compared with normal controls. CONCLUSIONS: We discovered that bileaflet prolapse with the absence of hemodynamic dysfunction results in significantly elevated forces and altered dynamics on the papillary muscles. Our work suggests that the sole reduction of mitral regurgitation without addressing reduced coaptation lengths and thus increased leaflet surface area exposed to ventricular pressure gradients (ie, billowing leaflets) is insufficient for an optimal repair.
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Park et al. (2022) studied Mitral valve prolapse (n=3). Bileaflet prolapse vs. Optimally coapting valve was evaluated on Papillary muscle forces (5% to 15% increase). Bileaflet mitral valve prolapse significantly increased papillary muscle forces by 5% to 15% compared with an optimally coapting valve in an ex vivo ovine model.
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