Fibrosis-Induced Abnormalities of the Cardiac Conduction System andMalignant Arrhythmias in Patients with Chagas Disease

Centurión Oa, García Lb
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Abstract

Histopathological evidence of extensive fibrosis may produce myocardial areas where fibrous tissue separates the muscle fibers from each other. The dismally connected fibers in infected myocardial tissue with continuous fibro-degenerative modification may induce anomalous electrophysiological characteristics. Electrical coupling between adjacent fibers is difficult to occur when fibrosis surrounds groups of myocytes [1-4]. The microarchitecture and anisotropic characteristics may play an important role in re-entry by causing inhomogeneous and discontinuous propagation of the impulse. This non-uniform anisotropic property causes an irregular and fractionated propagation of the depolarization wave in the transverse direction [5-8]. Structural inhomogeneity or the common distinction in electrophysiological or ultra-structural properties plays a major role in the induction of re-entrant circuits and malignant arrhythmias due to the elevated probability of unidirectional block of the premature impulse and conduction delay [7-10].
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恰加斯病患者纤维化诱导的心脏传导系统异常和恶性心律失常
广泛纤维化的组织病理学证据可能产生心肌区,其中纤维组织将肌纤维彼此分离。在感染的心肌组织中,连续的纤维退行性改变会引起异常的电生理特征。当纤维化围绕着肌细胞群时,相邻纤维之间很难发生电偶联[1-4]。微结构和各向异性特性可能通过引起脉冲的非均匀和不连续传播而在再入中起重要作用。这种非均匀的各向异性特性导致去极化波在横向上的不规则和分次传播[5-8]。结构不均匀性或电生理或超结构特性的共同差异,由于过早冲动单向阻滞和传导延迟的可能性增加,在诱导重入回路和恶性心律失常中起主要作用[7-10]。
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