Arrhythmogenic right ventricular dysplasia: a clinical model for the study of chronic ventricular tachycardia.
Arrhythmogenic right ventricular dysplasia: a clinical model for the study of chronic ventricular tachycardia.
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致心律失常性右心室发育不良：研究慢性室性心动过速的临床模型。
DOI：
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发表时间：
1984
期刊：
影响因子：
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通讯作者：
G. Y
中科院分区：
文献类型：
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作者：
F. G;F. R;T. L;G. G;C. C;C. G;G. Y
致心律失常性右心室发育不良（ARVD）是一个最近出现的个体化临床实体，有时会出现室性心动过速（VT）发作。这些攻击可能是抵抗抗疟疾治疗和新的治疗方法已开发用于治疗这种情况。这些新方法主要是外科手术，基于对窦性心律和VT期间心脏电激活的分析。这种方法增加了我们对室性心动过速的病理生理学的理解，不仅在ARVD的背景下，而且在心肌梗死后最常见的室性心动过速的临床背景下。对发育不良区心外膜激活的电生理学研究表明，在QRS波群结束后记录到延迟电位。这可以通过这些组织的组织病理学来解释。ARVD的组织学特征为心肌壁部分变性。大多数肌肉纤维被脂肪组织取代，其中一些健康的纤维存活下来。这些变化主要在心肌内和心外膜下层观察到，内膜下几乎正常。非传导性脂肪变性内的孤立肌纤维束可能导致相对于邻近健康组织的非常延迟的激活。激活的传播被延迟，因为它通过这个丛状结构，并在邻近健康肌肉的区域，折返现象可能会出现。在ARVD中，这些变化主要位于右心室，因此解释了在这种情况下观察到的大多数形式的VT的右心室起源。然而，我们也观察到一个病例，这表明一个孤立的致瘤性左心室发育不良。心外膜标测将VT的起源点定位在位于慢传导组织和正常传导组织之间的区域中。在室性心动过速的心外膜突破点进行简单的心室切开术，即心室壁的全层切片，可防止绝大多数患者复发。相同的病理生理学概念可应用于VT并发心肌梗塞，但在这种情况下，能够缓慢进行激活的心肌纤维在梗塞边缘区的纤维组织内被隔离。室性心动过速的起源点通常位于室间隔内，心外膜突破点可能位于一定距离处。不同的手术技术已经被开发来处理这种情况。环绕式脑室切开术通过示踪将致瘤区与其他健康组织隔离开，
Arrhythmogenic right ventricular dysplasia (ARVD) is a recently individualised clinical entity which sometimes presents with episodes of ventricular tachycardia (VT). These attacks may be resistant to anti-arrhythmic therapy and new therapeutic approaches have been developed for the treatment of this condition. These new methods are mainly surgical, based on the analysis of the electrical activation of the heart in sinus rhythm and during VT. This approach has increased our understanding of the physiopathology of VT, not only in the context of ARVD, but also in the most commonly encountered clinical setting of VT, after myocardial infarction. Electrophysiological study of the epicardial activation of the dysplastic zones has demonstrated the presence of delayed potentials recorded after the end of the QRS complex. This can be explained by the histopathology of these tissues. ARVD is characterised histologically by partial degeneration of the myocardial wall. Most of the muscle fibers are replaced by fatty tissue in the middle of which some healthy fibers survive. These changes are mainly observed in the intramyocardial and subepicardial layers, the subendocardium being almost normal. Strands of isolated muscle fibers within the non-conducting fatty degeneration may lead to very delayed activation with respect to the adjacent healthy tissues. The propagation of activation is delayed as it passes through this plexiform structure and in the zones adjacent to healthy muscle were reentry phenomena may arise. In ARVD, these changes are mainly located over the right ventricle, so explaining the right ventricular origin of most forms of VT observed in this condition. However, we have also observed a case which suggested an isolated arrhythmogenic left ventricular dysplasia. Epicardial mapping localizes the point of origin of VT in zones situated between the slow and normally conducting tissues. Simple ventriculotomy, a full thickness section of the ventricular wall, at the point of epicardial breakthrough of the VT prevents recurrence in the great majority of patients. The same pathophysiological concepts may be applied to VT complicating myocardial infarction but in this situation the myocardial fibers capable of slowly conducting the activation are isolated within the fibrous tissue in the border zone of the infarct. The point of origin of VT is usually within the interventricular septum with a point of epicardial breakthrough which could be located some distance away. Different surgical techniques have been developed to deal with this condition. Encircling endocardial ventriculotomy isolates the arrhythmogenic zone from the rest of healthy tissues by tracin