Icahn School of Medicine at Mount Sinai, New York, New York.
J Am Soc Echocardiogr. 2013 Oct;26(10):1107-1117. doi: 10.1016/j.echo.2013.07.003. Epub 2013 Aug 14.
Ischemic mitral regurgitation (MR) is a common complication of myocardial infarction thought to result from leaflet tethering caused by displacement of the papillary muscles that occurs as the left ventricle remodels. The author explores the possibility that left atrial remodeling may also play a role in the pathogenesis of ischemic MR, through a novel mechanism: atriogenic leaflet tethering. When ischemic MR is hemodynamically significant, the left ventricle compensates by dilating to preserve forward output using the Starling mechanism. Left ventricular dilatation, however, worsens MR by increasing the mitral valve regurgitant orifice, leading to a vicious cycle in which MR begets more MR. The author proposes that several structural adaptations play a role in reducing ischemic MR. In contrast to the compensatory effects of left ventricular enlargement, these may reduce, rather than increase, its severity. The suggested adaptations involve the mitral valve leaflets, the papillary muscles, the mitral annulus, and the left ventricular false tendons. This review describes the potential role each may play in reducing ischemic MR. Therapies that exploit these adaptations are also discussed.
缺血性二尖瓣反流(MR)是心肌梗死的常见并发症,其被认为是由于左心室重构时乳头肌移位导致的瓣叶牵张所致。作者通过一种新的机制——心源性瓣叶牵张,探讨了左心房重构在缺血性 MR 发病机制中的可能作用。当缺血性 MR 具有血流动力学意义时,左心室通过扩张来利用 Starling 机制来维持前向输出进行代偿。然而,左心室扩张通过增加二尖瓣反流口使 MR 恶化,导致 MR 恶性循环,即 MR 导致更多的 MR。作者提出,一些结构适应性在减轻缺血性 MR 中发挥作用。与左心室扩大的代偿作用相反,这些适应性可能会降低而不是增加其严重程度。建议的适应性涉及二尖瓣瓣叶、乳头肌、二尖瓣环和左心室假腱索。本文描述了每个结构可能在减轻缺血性 MR 中的作用。还讨论了利用这些适应性的治疗方法。