Journal
JOURNAL OF ARRHYTHMIA
Volume 30, Issue 6, Pages 389-394Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.joa.2013.12.008
Keywords
Cardiac fibrosis; Ventricular fibrillation; Repolarization reserve; Oxidative stress; Anti-fibrotic therapy
Categories
Funding
- AHA Western State Affiliate Research Fellowship Award [0725218Y, 0555057Y]
- National Institutes of Health Grants [P01HL-78931]
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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. (C) 2014 Japanese Heart Rhythm Society. Published by Elsevier B.V. All rights reserved.
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