Atrial arrhythmia, triggering events and conduction abnormalities in isolated murine <i><scp>R</scp>y<scp>R</scp>2‐<scp>P</scp>2328<scp>S</scp></i> hearts

Abstract

These results suggest that abnormal intracellular Ca(2+) homoeostasis produces both arrhythmic triggers and a slow-conducting arrhythmic substrate in RyR2(S/S) atria. A similar mechanism might also contribute to arrhythmogenesis in other conditions, associated with diastolic Ca(2+) release, such as atrial fibrillation.