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肥厚型心肌病演变为左心室运动减弱和扩张:冠状动脉栓塞可能是一种发病机制。

Hypertrophic cardiomyopathy evolving into a hypokinetic and dilated left ventricle: coronary embolization as a probable pathogenetic mechanism.

作者信息

Gravanis M B, Robinson P H, Hertzler G L

机构信息

Department of Pathology, Emory University School of Medicine, Atlanta, GA 30322.

出版信息

Clin Cardiol. 1990 Jul;13(7):500-5. doi: 10.1002/clc.4960130714.

Abstract

A long-term follow-up (9 years) in a patient with hypertrophic cardiomyopathy revealed an evolution to a hypokinetic and dilated left ventricle. The patient underwent heart transplantation, and therefore the native heart was available for morphologic studies. Gross and microscopic stigmata of hypertrophic cardiomyopathy were present, as well as evidence of left ventricular dilatation. Multiple myocardial scars in both ventricles indicated past ischemic episodes, most probably due to coronary embolization from left ventricular mural thrombi. Other possible pathogenetic mechanisms for the progression of hypertrophic cardiomyopathy to a dilated one are discussed.

摘要

对一名肥厚型心肌病患者进行的长期随访(9年)显示,其左心室演变为运动减弱和扩张。该患者接受了心脏移植,因此其原生心脏可用于形态学研究。存在肥厚型心肌病的大体和微观特征,以及左心室扩张的证据。两个心室中的多处心肌瘢痕表明过去曾发生过缺血性发作,很可能是由于左心室壁血栓导致的冠状动脉栓塞。文中还讨论了肥厚型心肌病进展为扩张型心肌病的其他可能致病机制。

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