S econdary ischemic mitral regurgitation (IMR) is a frequent complication of myocardial infarction (13% to 59% of cases) that doubles the risk of death during follow-up (1). The management of IMR remains debated and suboptimal, and current recommendations have only low levels of evidence as their basis (2,3). Secondary IMR is related to left ventricular (LV) global and regional remodeling, as well as dysfunction and distortion of the components of the mitral valve including the chordae, annulus, and leaflets, thus resulting in imbalance of the closing and tethering forces. Although IMR was initially considered purely functional, without organic or tissue changes, in 2008 and 2009 Chaput et al. (4,5) demonstrated that the mitral valve adapts to the mechanical stress imposed by tethering. Indeed, in addition to an early increase in mitral valve leaflet area (up to 35%) (4,5) or even in chordae length (6), investigators have shown that the histologic composition of mitral leaflets is also modified, with stiffening and fibrosis resulting from endothelial-to-mesenchymal transformation (EMT) and matrix remodeling promoting leaflet growth. Hypothetically, this mechanism is seen as compensatory and could aim to reduce tethering forces and decrease the severity

中文翻译：

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治疗缺血性二尖瓣关闭不全的新药理学靶点

继发性缺血性二尖瓣关闭不全 (IMR) 是一种常见的心肌梗死并发症（占病例的 13% 至 59%），在随访期间会使死亡风险增加一倍 (1)。IMR 的管理仍然存在争议和次优，目前的建议只有低水平的证据作为其基础 (2,3)。继发性 IMR 与左心室 (LV) 全局和区域重构以及二尖瓣组件（包括腱索、瓣环和瓣叶）的功能障碍和变形有关，从而导致关闭和束缚力的不平衡。尽管 IMR 最初被认为是纯功能性的，没有器质性或组织变化，但在 2008 年和 2009 年 Chaput 等人。(4,5) 证明二尖瓣适应系绳施加的机械应力。确实，除了早期增加二尖瓣小叶面积（高达 35%）(4,5) 或什至增加腱索长度 (6) 外，研究人员还表明二尖瓣小叶的组织学组成也发生了改变，导致变硬和纤维化从内皮到间充质转化 (EMT) 和基质重塑促进小叶生长。假设，这种机制被视为补偿性的，旨在减少束缚力并降低严重性