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[心动过速性心肌病:一例报告]

[Tachycardia-induced cardiomyopathy: a case report].

作者信息

Matsuura Y, Chin W, Kurihara T, Yasui K, Asao M, Hayashi T, Fukushima M, Abe H, Kurata A

机构信息

Cardiovascular Department of National Osaka Hospital.

出版信息

J Cardiol. 1990;20(2):509-18.

PMID:2104425
Abstract

A 30-year-old man with chronic sustained ventricular tachycardia (VT) lasting more than seven years was treated with propranolol, 30 mg/day. This resulted in controlled cardiac rates of 90 to 130/min during sleep, and 100 to 195/min while awake. However, he experienced Adams-Stokes attacks twice, in September and December, 1986. During the second attack, ambulatory heart monitoring showed his VT rate of 212/min. An electrophysiological study revealed that the VT focal point was in the lower-mid region of the interventricular septum in the right ventricle. The VT was characterized by abnormal enhanced automaticity. This VT could not be interrupted either by single or multiple combinations of antiarrhythmic drugs. Cardiac catheterization revealed a diffusely enlarged hypokinetic left ventricle, even at the rate of 120/min VT (EF 27%, C.I. 2.3 l/min/m2). Because of his severe hemodynamic state, we performed electrical catheter ablation successfully. After the ablation, his left ventricular wall motion gradually improved. Nine months after the ablation, his left ventricular diastolic dimension decreased from 64 to 48 mm and the left ventricular systolic dimension decreased from 57 to 28 mm on M-mode echocardiography, while ejection fraction increased from 27 to 73% on the left ventriculography. Bi-ventricular myocardial biopsy specimens obtained prior to the ablation revealed only cellular hypertrophy of varying degrees, and vacuole degeneration consistent with non-specific cardiomyopathy. However, nine months after the ablation, these findings were no longer present. Thus, this case was considered tachycardia-induced cardiomyopathy initiated by VT, lasting many years.

摘要

一名患有慢性持续性室性心动过速(VT)达七年以上的30岁男性,接受了每天30毫克普萘洛尔的治疗。这使得他睡眠期间的心率控制在90至130次/分钟,清醒时为100至195次/分钟。然而,他在1986年9月和12月经历了两次阿-斯发作。在第二次发作期间,动态心脏监测显示他的室性心动过速心率为212次/分钟。电生理研究表明,室性心动过速的病灶位于右心室室间隔的中下区域。该室性心动过速的特征是异常的自动性增强。这种室性心动过速无论是单一抗心律失常药物还是多种药物联合使用都无法打断。心脏导管检查显示左心室弥漫性扩大且运动减弱,即使在室性心动过速心率为120次/分钟时也是如此(射血分数27%,心排血量2.3升/分钟/平方米)。由于他严重的血流动力学状态,我们成功进行了电导管消融术。消融术后,他的左心室壁运动逐渐改善。消融术后九个月,M型超声心动图显示他的左心室舒张内径从64毫米降至48毫米,左心室收缩内径从57毫米降至28毫米,而左心室造影显示射血分数从27%增至73%。消融术前获取的双心室心肌活检标本仅显示不同程度的细胞肥大以及与非特异性心肌病相符的空泡变性。然而,消融术后九个月,这些表现不再存在。因此,该病例被认为是由室性心动过速引发的、持续多年的心动过速性心肌病。

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