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肥厚型心肌病中二尖瓣收缩期前向运动:一项体外搏动血流研究

Systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: an in vitro pulsatile flow study.

作者信息

Lefebvre X P, He S, Levine R A, Yoganathan A P

机构信息

Cardiovascular Fluid Mechanics Laboratory School of Chemical Engineering Georgia Institute of Technology, Atlanta 30332-0100, USA.

出版信息

J Heart Valve Dis. 1995 Jul;4(4):422-38.

PMID:7582155
Abstract

Hypertrophic cardiomyopathy, or HCM, is a relatively common disease which results in the hospitalization of more than 13,000 patients every year. It is characterized by a thickening of the interventricular septum and by systolic anterior motion, or SAM, of the mitral valve, which occurs when the distal tip of the mitral leaflets contacts the hypertrophied septum during systole and obstructs the left ventricular outflow tract. Using an in vitro pulsatile flow model of the left ventricle, the objective of the study was to investigate the relationship between the ventricular flow field and the mechanism of SAM and to specifically address the hypothesis that papillary muscle displacement can alter left ventricular flow patterns and create drag forces that can initiate SAM. Flow visualization revealed the presence in the ventricle of a large organized recirculation region throughout diastole. Besides maintaining the mitral leaflets close to the posterior wall, normally positioned papillary muscles also caused the diastolic vortex to help the mitral valve close near the posterior wall while simultaneously prepositioning the upcoming systolic outflow stream close to the septum, thereby minimizing the flow forces acting on the mitral valve. In contrast, the anterior displacement of the papillary muscles moves the entire mitral apparatus into the outflow tract. It also reverses the direction of the recirculating diastolic flows: The diastolic vortex now promotes the initiation of SAM by displacing the closing mitral leaflets anteriorly and by positioning the systolic outflow stream close to the posterior wall. These events lead to the creation of form drag forces as the systolic flow impacts the posterior side of the mitral leaflets, initiating SAM.

摘要

肥厚型心肌病(HCM)是一种相对常见的疾病,每年导致超过13000名患者住院。其特征是室间隔增厚以及二尖瓣收缩期前向运动(SAM),即二尖瓣叶的远端在收缩期接触肥厚的室间隔并阻塞左心室流出道时发生的现象。本研究利用左心室体外搏动血流模型,旨在研究心室流场与SAM机制之间的关系,并具体探讨乳头肌移位可改变左心室血流模式并产生可引发SAM的阻力这一假说。血流可视化显示,在整个舒张期心室内存在一个大的有组织的再循环区域。正常定位的乳头肌除了使二尖瓣叶靠近后壁外,还会导致舒张期涡流,帮助二尖瓣在靠近后壁处关闭,同时将即将到来的收缩期流出血流预先定位在靠近室间隔处,从而使作用于二尖瓣的流体力最小化。相比之下,乳头肌向前移位会将整个二尖瓣装置移入流出道。它还会使舒张期再循环血流的方向反转:舒张期涡流现在通过向前移动正在关闭的二尖瓣叶并将收缩期流出血流定位在靠近后壁处来促进SAM的起始。这些事件导致在收缩期血流冲击二尖瓣叶后侧时产生形状阻力,从而引发SAM。

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