Open AccessCardiac fibrosis as a determinant of ventricular tachyarrhythmias
Author(s) -
Morita Norishige,
Mandel William J.,
Kobayashi Yoshinori,
Karagueuzian Hrayr S.
Publication year - 2014
Publication title -
journal of arrhythmia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.463
H-Index - 21
eISSN - 1883-2148
pISSN - 1880-4276
DOI - 10.1016/j.joa.2013.12.008
Subject(s) - medicine , cardiology , ventricular fibrillation , afterdepolarization , ventricular tachycardia , fibrosis , myocardial fibrosis , sudden cardiac death , repolarization , electrophysiology
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.