Cardiac fibrosis as a determinant of ventricular tachyarrhythmias.
Cardiac fibrosis as a determinant of ventricular tachyarrhythmias.
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DOI：
10.1016/j.joa.2013.12.008
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发表时间：
2014-12-01
影响因子：
2
通讯作者：
Karagueuzian HS
中科院分区：
文献类型：
--
作者：
Morita N;Mandel WJ;Kobayashi Y;Karagueuzian HS
动物和新兴的临床研究表明，在复极储备减少的情况下，心室纤维化增加会促进早期后除极（埃兹）和触发活动，从而引发室性心动过速和心室颤动（VT/VF）。心室纤维化增加在允许氧化和代谢应激诱导的埃兹表现为触发活动导致VT/VF中起关键促进作用。在正常非纤维化心脏中，相同的应激源缺乏这种致瘤效应，这突出了纤维化在VT/VF起始中的重要性。这些结果表明，抗纤维化治疗与旨在增加心室复极储备的治疗相结合，可能会协同作用，以降低心脏性猝死的风险。
Animal and emerging clinical studies have demonstrated that increased ventricular fibrosis in a setting of reduced repolarization reserve promotes early afterdepolarizations (EADs) and triggered activity that can initiate ventricular tachycardia and ventricular fibrillation (VT/VF). Increased ventricular fibrosis plays a key facilitatory role in allowing oxidative and metabolic stress-induced EADs to manifest as triggered activity causing VT/VF. The lack of such an arrhythmogenic effect by the same stressors in normal non-fibrotic hearts highlights the importance of fibrosis in the initiation of VT/VF. These findings suggest that antifibrotic therapy combined with therapy designed to increase ventricular repolarization reserve may act synergistically to reduce the risk of sudden cardiac death.