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.
|
Authors | Norishige Morita, William J Mandel, Yoshinori Kobayashi, Hrayr S Karagueuzian |
Journal | Journal of arrhythmia
(J Arrhythm)
Vol. 30
Issue 6
Pg. 389-394
(Dec 01 2014)
ISSN: 1880-4276 [Print] Japan |
PMID | 25642299
(Publication Type: Journal Article)
|