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. 2022 Apr 12;9:862044. doi: 10.3389/fcvm.2022.862044

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Copyright © 2022 Pype, Bertrand, Paelinck, Heidbuchel, Van Craenenbroeck and Van De Heyning.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Central image: mechanisms of left ventricular remodeling in mitral valve prolapse. Schematic view of LV remodeling mechanisms in MVP, addressing the hypothesis of a cardiomyopathy on the left and total volume load on the right. Different pathophysiological mechanisms exist regarding the development of a cardiomyopathy in MVP, including a genetic substrate, second hit phenomenon and PVC-induced remodeling. On the other hand, the excessive volume load of chronic MR itself can induce LV dilatation, especially when a significant prolapse volume is added to the total volume load. LV, left ventricular; MVP, mitral valve prolapse; MR, mitral regurgitation; CMR, cardiac magnetic resonance imaging; TTN, titin; FLNC, filamin C; PVC, premature ventricular contraction.