Miki T, Yokota Y, Miki T, Takarada A, Yoshida H, Fukuzaki H
First Department of Internal Medicine, Kobe University School of Medicine.
J Cardiol Suppl. 1990;23:113-26; discussion 127-9.
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.
两例二尖瓣脱垂(MVP)患者,初始评估时无其他心脏异常,在随访期间出现了类似扩张型心肌病(DCM)的临床特征。病例1. 一名40岁男性于1982年5月来我院评估心脏杂音。标准12导联心电图(ECG)显示Ⅲ导联有异常Q波。超声心动图显示二尖瓣脱垂,但未观察到左心室(LV)扩张或室壁运动异常。铊-201心肌显像显示心尖和下壁铊摄取异常。他没有急性心肌梗死或心肌炎发作,但出现了完全性右束支传导阻滞,因此于1984年10月住院。他没有冠状动脉病变,左心室造影仅显示轻度二尖瓣反流。超声心动图显示室间隔和心尖运动减弱,铊-201心肌显像显示下壁和室间隔持续灌注缺损。1985年12月,他因完全性房室传导阻滞发生阿-斯发作。超声心动图显示左心室扩大,室壁运动异常以及铊-201心肌显像的灌注缺损相对严重。病例2. 一名46岁女性自1977年起偶尔出现短暂心悸和胸部压迫感。1982年因心脏症状入院。听到莱文氏二级心脏杂音,标准12导联心电图显示单发性室上性早搏,Ⅲ导联和aVF导联T波倒置。超声心动图显示二尖瓣脱垂和轻度二尖瓣反流,但未观察到左心室扩张或室壁运动异常。在6年随访期间,发生了永久性心房颤动,左心室出现扩张且室壁运动异常进展。因此,在随访期间,两例最初仅有二尖瓣脱垂这一超声心动图异常、伴有收缩期杂音和非特异性心电图改变的患者出现了类似扩张型心肌病的特征。我们认为这两例可能是重要病例,可能显示心肌病过程与二尖瓣脱垂之间的关系。