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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.
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Voigt et al. (2013) studied this question.
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