[二尖瓣脱垂作为扩张型心肌病的初始临床特征:附2例报告]。

Journal of cardiology. Supplement Pub Date : 1990-01-01
T Miki, Y Yokota, T Miki, A Takarada, H Yoshida, H Fukuzaki
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引用次数: 0

摘要

2例二尖瓣脱垂(MVP)患者,初诊时无其他心脏异常,随访期间出现类似扩张型心肌病(DCM)的临床特征。案例1。1982年5月,一名40岁男子来我院检查心脏杂音。标准12导联心电图显示III导联Q波异常。超声心动图显示MVP,但未见左心室扩张和壁运动异常。铊-201显像显示顶端和下壁的铊摄取异常。他没有急性心肌梗死或心肌炎发作,但出现完全性右束支阻滞,因此于1984年10月住院。他没有冠状动脉病变,左心室造影显示只有轻微的二尖瓣反流。超声心动图显示室间隔及心尖运动减弱,Tl-201闪烁图显示下壁及室间隔持续灌注缺损。1985年12月,由于完全性房室传导阻滞,他经历了亚当斯-斯托克斯发作。超声心动图示左心室增大,Tl-201闪烁图壁运动异常及灌注缺损较严重。例2。一位46岁的女性,自1977年以来,偶尔出现短暂的心悸和胸部压迫。她于1982年因心脏症状入院。列文II型心脏杂音,标准12导联心电图显示单室上性心动过速,III型导联和aVF T波反转。超声心动图显示MVP和轻度二尖瓣反流,但未见左室扩张和壁运动异常。随访6年,发生永久性房颤,左室扩张,室壁运动异常。因此,在随访期间,两例超声心动图异常仅为MVP伴收缩期杂音和非特异性心电图改变的患者出现了dcm样特征。我们认为这两例可能是心肌病过程与MVP之间关系的重要病例。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Mitral valve prolapse as an initial clinical feature of dilated cardiomyopathy: report of two cases].

Two cases with mitral valve prolapse (MVP), without any other cardiac abnormalities at the initial evaluation, developed the clinical features mimic to dilated cardiomyopathy (DCM) during follow-up period. Case 1. A 40-year-old man visited our hospital in May 1982 to evaluate a heart murmur. A standard 12-lead electrocardiogram (ECG) showed an abnormal Q wave in lead III. Echocardiography revealed MVP, but neither dilatation nor wall motion abnormality of the left ventricle (LV) were observed. Thallium-201 scintigraphy revealed an abnormal thallium uptake at the apex and inferior wall. He had no episode of acute myocardial infarction or myocarditis, but complete right bundle branch block developed, thus, he was hospitalized in October 1984. He had no coronary artery lesions, and had only mild mitral regurgitation on left ventriculography. The motion of the interventricular septum and apex was reduced on echocardiogram and a persistent perfusion defect was observed at the inferior wall and the interventricular septum on Tl-201 scintigrams. In December 1985, he experienced an Adams-Stokes attack due to complete atrioventricular block. Echocardiographically, the left ventricle enlarged, and the wall motion abnormalities and a perfusion defect on Tl-201 scintigrams were relatively severe. Case 2. A 46-year-old woman occasionally experienced palpitation of short duration and chest oppression since 1977. She was admitted to our hospital because of cardiac symptoms in 1982. A heart murmur of Levine II was heard and a standard 12-lead ECG showed single supraventricular extrasystole and T wave inversion in lead III and aVF. Echocardiography revealed MVP and mild mitral regurgitation, but neither dilatation nor wall motion abnormality of the LV was observed. During 6-year follow-up period, permanent atrial fibrillation developed and LV developed dilatation and wall motion abnormalities progressed. Thus, during follow-up periods, DCM-like features developed in two cases who had had MVP as a sole echocardiographic abnormality with systolic murmur and non-specific ECG changes. We consider that these two may be important cases who may show a relation between cardiomyopathic process and MVP.

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