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二尖瓣脱垂病理生理发育机制的生物力学评估:瓣膜形态改变的影响。

Biomechanical evaluation of the pathophysiologic developmental mechanisms of mitral valve prolapse: effect of valvular morphologic alteration.

作者信息

Choi Ahnryul, McPherson David D, Kim Hyunggun

机构信息

Division of Cardiovascular Medicine, Department of Internal Medicine, The University of Texas Health Science Center at Houston, 6431 Fannin St, MSB 1.246, Houston, TX, 77030, USA.

出版信息

Med Biol Eng Comput. 2016 May;54(5):799-809. doi: 10.1007/s11517-015-1371-y. Epub 2015 Aug 26.

DOI:10.1007/s11517-015-1371-y
PMID:26307201
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4769117/
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.

摘要

二尖瓣脱垂(MVP)是指在心动周期的收缩期,二尖瓣(MV)瓣叶过度膨入二尖瓣环平面进入左心房。与MV组织重塑相关的MVP和二尖瓣反流发生的潜在机制仍不清楚。我们进行了MV计算模拟,以研究MVP的病理生理发展机制。本研究采用了参数化MV几何模型。分别通过调整后叶和腱索的几何形状,建立了后叶增大和后腱索延长模型。在整个心动周期内对MV功能进行了动态有限元模拟。计算模拟表明,后叶面积增大增加了后叶和腱索中的大应力集中,而后腱索延长降低了瓣叶贴合度。当MVP同时伴有后叶增大和腱索延长时,后叶暴露于极大的脱垂状态,且瓣叶贴合度严重不足。这些数据表明,MVP的发展与瓣叶和腱索的组织改变密切相关。这种生物力学评估策略可以帮助我们更好地理解MVP的病理生理发展机制。

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