Mitral Plasticity: The Way to Prevent the Burden of Ischemic Mitral Regurgitation?

心脏病学 医学 心室 内科学 二尖瓣反流 收缩性 心室重构 乳头肌 二尖瓣 功能性二尖瓣反流 心力衰竭 射血分数
作者
Mattia Vinciguerra,Silvia Romiti,Eleonora Wretschko,Mizar D’Abramo,David Rose,Fabio Miraldi,Ernesto Greco
出处
期刊:Frontiers in Cardiovascular Medicine [Frontiers Media SA]
卷期号:8 被引量:6
标识
DOI:10.3389/fcvm.2021.794574
摘要

The ischemic impairment of the left ventricular contractility, followed by an adverse remodeling leading to the displacement of the papillary muscles (PMs), increased tethering forces and loss of valve competence has been the long-term accepted definition of ischemic mitral regurgitation (IMR). Over the years, different approaches of management have attempted to address valve regurgitation, nevertheless failing to achieve satisfactory outcomes. Recent studies have observed some structural and molecular changes of the mitral valve (MV), challenging the concept of a bystander passive to the subvalvular involvement. Indeed, the solely mechanical stretch of the PMs, as in the dilated left ventricle because of the aortic valve regurgitation, is not enough in causing relevant MV regurgitation. This setting triggers a series of structural changes called “mitral plasticity,” leaflets increase in their size among others, ensuring an adequate systolic area closure. In contrast, the ischemic injury not only triggers the mechanical stretch on the subvalvular apparatus but is also a powerful promotor of profibrotic processes, with an upregulation of the transforming growth factor (TGF)-β signaling pathway, leading to a MV with exuberant leaflet thickness and impaired mobility. In this article, we revise the concept of IMR, particularly focusing on the new evidence that supports dynamic changes in the MV apparatus, discussing the consequent clinical insights of “mitral plasticity” and the potential therapeutic implications.

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