Stanley Nattel

TL;DR: RyR2-mediated SR Ca2+ leak directly underlies the development of a substrate for sAF in CREM mice, the first demonstration of a molecular mechanism underlying AF progression and sAF substrate development in an experimental model.

TL;DR: In this article, the authors investigated the hypothesis that rapid atrial cardiomyocyte activation produces factors that influence atrial fibroblast proliferation and secretory functions, and found that atrial fibrillation causes tachycardia-induced atrial electrical remodeling, contributing to the progressive nature of arrhythmia.

TL;DR: The present paper reviews the state of knowledge regarding the mechanisms and clinical consequences for AF of atrial remodeling caused by rapid atrial activation, and likely contributes importantly to a wide variety of clinical phenomena of previously unrecognized mechanism.

TL;DR: Chronically repeated OSA episodes cause AF-promoting cardiac remodeling, with conduction abnormalities related to connexin dysregulation and fibrosis playing a prominent role and this novel animal model provides mechanistic insights into an important clinical problem and may be useful for further exploration of underlying mechanisms and therapeutic approaches.

TL;DR: Findings are the first direct evidence for the frequently-postulated role of Ca(2+)-overload in tachycardia-induced abnormalities of atrial function.