Key result
Abnormal intracellular calcium signaling contributes to ectopic electrical activity in human atrial fibrillation, highlighting calcium-handling abnormalities as potential therapeutic targets.
Targeting atrial calcium-handling abnormalities underlying ectopic activity may offer novel mechanism-based therapeutic approaches for treating atrial fibrillation.
May guide calcium-targeted AF therapies; leaves open clinical translation pending prospective trials.
Atrial fibrillation (AF) is the most frequent arrhythmia and is associated with increased morbidity and mortality. Current drugs for AF treatment have limited efficacy and a substantial risk of proarrhythmic side effects, making novel drug development critical. Emerging evidence suggests that abnormal intracellular calcium (Ca(2+)) signalling is a key contributor to ectopic (triggered) electrical activity in human AF. Accordingly, atrial Ca(2+)-handling abnormalities underlying ectopic activity may constitute novel mechanism-based therapeutic approaches to treat AF. This article reviews the recent evidence for a role of cellular ectopic activity in human AF pathophysiology, discusses the molecular mechanisms underlying triggered activity in human atrial myocytes, and considers their relevance to the design of novel therapeutic options.
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Voigt et al. (2012) conducted a review in Atrial fibrillation. Abnormal intracellular calcium signaling contributes to ectopic electrical activity in human atrial fibrillation, highlighting calcium-handling abnormalities as potential therapeutic targets.
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