title: Cellular and molecular correlates of ectopic activity in patients with atrial fibrillation.
abstract: 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.
authors.affiliation: Division of Experimental Cardiology, Medical Faculty Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, Mannheim, Germany.
authors.forename: Niels
authors.initials: N
authors.lastname: Voigt
authors.forename: Dobromir
authors.initials: D
authors.lastname: Dobrev
mesh_terms: D000200:Action Potentials; D001281:Atrial Fibrillation / Q000150:complications / Q000503:physiopathology*; D018880:Atrial Premature Complexes / Q000150:complications / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling; D003198:Computer Simulation; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008955:Models, Cardiovascular; D032383:Myocytes, Cardiac; D013223:Statistics as Topic
chemical_list: D002118:Calcium