Abstract
Animal and clinical studies have demonstrated that oxidative stress, a common pathophysiological factor in cardiac disease, reduces repolarization reserve by enhancing the L-type calcium current, the late Na, and the Na-Ca exchanger, promoting early afterdepolarizations (EADs) that can initiate ventricular tachycardia and ventricular fibrillation (VT/VF) in structurally remodeled hearts. Increased ventricular fibrosis plays a key facilitatory role in allowing oxidative-stress induced EADs to manifest as triggered activity and VT/VF, since normal non-fibrotic hearts are resistant to arrhythmias when challenged with similar or higher levels of oxidative stress. The findings imply that antifibrotic therapy, in addition to therapies designed to suppress EAD formation at the cellular level, may be synergistic in reducing the risk of sudden cardiac death.
Highlights
Reviewed by: Ruslan Rafikov, Georgia Health Sciences University, USA Xiao-feng Yang, Temple University School of Medicine, USA
Increased ventricular fibrosis plays a key facilitatory role in allowing oxidative-stress induced early afterdepolarizations (EADs) to manifest as triggered activity and ventricular tachycardia and ventricular fibrillation (VT/ventricular fibrillation (VF)), since normal non-fibrotic hearts are resistant to arrhythmias when challenged with similar or higher levels of oxidative stress
We briefly review the early work done on EADs and triggered activity, summarize the state of knowledge on the dynamic and ionic basis of oxidative stress-mediated initiation and termination of EAD-mediated triggered activity, and discuss how myocardial structural remodeling in the form of increased cardiac tissue fibrosis critically promotes EAD-mediated VT/VF both in experimental and simulation studies
Summary
Reviewed by: Ruslan Rafikov, Georgia Health Sciences University, USA Xiao-feng Yang, Temple University School of Medicine, USA. Animal and clinical studies have demonstrated that oxidative stress, a common pathophysiological factor in cardiac disease, reduces repolarization reserve by enhancing the L-type calcium current, the late Na, and the Na-Ca exchanger, promoting early afterdepolarizations (EADs) that can initiate ventricular tachycardia and ventricular fibrillation (VT/VF) in structurally remodeled hearts.
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