Identifies sarcoplasmic reticulum Ca2+ leak and ryanodine receptor dysregulation as key cellular mechanisms driving arrhythmogenesis in paroxysmal atrial fibrillation.
Increased diastolic sarcoplasmic reticulum Ca2+ leak and related delayed after-depolarizations/triggered activity promote cellular arrhythmogenesis in pAF patients. Biochemical, functional, and modeling studies point to a combination of increased sarcoplasmic reticulum Ca2+ load related to phospholamban hyperphosphorylation and ryanodine receptor dysregulation as underlying mechanisms.
Voigt et al. (Tue,) studied this question.