Native and Post-Repair Residual Mitral Valve Prolapse Increases Forces Exerted on the Papillary Muscles: A Possible Mechanism for Localized Fibrosis?

Author:

Park Matthew H.12,van Kampen Antonia345ORCID,Melnitchouk Serguei3,Wilkerson Robert J.1,Nagata Yasufumi4ORCID,Zhu Yuanjia16,Wang Hanjay1,Pandya Pearly K.12,Morningstar Jordan E.7,Borger Michael A.5ORCID,Levine Robert A.4,Woo Y. Joseph16ORCID

Affiliation:

1. Department of Cardiothoracic Surgery, Stanford University, CA (M.H.P., R.J.W., Y.Z., H.W., P.K.P., Y.J.W.).

2. Department of Mechanical Engineering, Stanford University, CA (M.H.P., P.K.P.).

3. Division of Cardiac Surgery, Massachusetts General Hospital, Harvard Medical School, Boston (A.v.K., S.M.).

4. Cardiac Ultrasound Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston (A.v.K., Y.N., R.A.L.).

5. University Department of Cardiac Surgery, Leipzig Heart Center, Germany (A.v.K., M.A.B.).

6. Department of Bioengineering, Stanford University, CA (Y.Z., Y.J.W.).

7. Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston (J.E.M.).

Abstract

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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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