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心室重构的病理生理过程:从梗死到衰竭。

The pathophysiologic process of ventricular remodeling: from infarct to failure.

作者信息

Paul S

出版信息

Crit Care Nurs Q. 1995 May;18(1):7-21. doi: 10.1097/00002727-199505000-00003.

DOI:10.1097/00002727-199505000-00003
PMID:7719950
Abstract

In the past, hypertensive heart disease was the principal cause of congestive heart failure, but currently ischemic heart disease is the major etiologic factor. In the last 20 years, the role of myocardial infarction (MI) and the subsequent alteration in ventricular architecture of the infarcted and noninfarcted myocardium have become increasingly associated with a phenomenon known as ventricular remodelling. This process consists of left ventricular wall thinning in the infarction area, ventricular chamber dilatation, and compensatory hypertrophy of the noninfarcted portion of the myocardium. This article describes the pathophysiologic transformation that begins with MI and ventricular remodeling and ends in congestive heart failure.

摘要

过去,高血压性心脏病是充血性心力衰竭的主要病因,但目前缺血性心脏病是主要的病因因素。在过去20年里,心肌梗死(MI)以及梗死心肌和未梗死心肌随后的心室结构改变,与一种称为心室重构的现象越来越相关。这个过程包括梗死区域左心室壁变薄、心室腔扩张以及心肌未梗死部分的代偿性肥大。本文描述了始于心肌梗死和心室重构并以充血性心力衰竭告终的病理生理转变。

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