Cardiac fibrosis as a determinant of ventricular tachyarrhythmias. Issue 6 (6th March 2014)

• Record Type: Journal Article
• Authors: Morita, Norishige; Mandel, William J.; Kobayashi, Yoshinori; Karagueuzian, Hrayr S.
• Is Part Of: Journal of arrhythmia. Volume 30:Issue 6(2014)
• Page Start: 389
• Page End: 394
• Publication Date: 2014-03-06
• Subjects: Cardiac fibrosis -- Ventricular fibrillation -- Repolarization reserve -- Oxidative stress -- Anti‐fibrotic therapy; Arrhythmia -- Periodicals; Cardiac pacing -- Periodicals; Arrhythmias, Cardiac; Arrhythmia; Cardiac pacing; Periodicals; Electronic journals; Periodicals; 616.128
• DOI: 10.1016/j.joa.2013.12.008
• Languages: English
• ISSNs: 1880-4276

Abstract

Abstract: 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.