title: Recent advances in the molecular pathophysiology of atrial fibrillation.
abstract: Atrial fibrillation (AF) is an extremely common cardiac rhythm disorder that causes substantial morbidity and contributes to mortality. The mechanisms underlying AF are complex, involving both increased spontaneous ectopic firing of atrial cells and impulse reentry through atrial tissue. Over the past ten years, there has been enormous progress in understanding the underlying molecular pathobiology. This article reviews the basic mechanisms and molecular processes causing AF. We discuss the ways in which cardiac disease states, extracardiac factors, and abnormal genetic control lead to the arrhythmia. We conclude with a discussion of the potential therapeutic implications that might arise from an improved mechanistic understanding.
authors.affiliation: Research Center, Department of Medicine, Montreal Heart Institute and Université de Montréal, Montreal, Quebec, Canada.
authors.forename: Reza
authors.initials: R
authors.lastname: Wakili
authors.forename: Niels
authors.initials: N
authors.lastname: Voigt
authors.forename: Stefan
authors.initials: S
authors.lastname: Kääb
authors.forename: Dobromir
authors.initials: D
authors.lastname: Dobrev
authors.forename: Stanley
authors.initials: S
authors.lastname: Nattel
mesh_terms: D001281:Atrial Fibrillation / Q000235:genetics* / Q000503:physiopathology*; D002309:Cardiology / Q000379:methods / Q000639:trends; D049109:Cell Proliferation; D004562:Electrocardiography / Q000379:methods; D020022:Genetic Predisposition to Disease; D014644:Genetic Variation; D006325:Heart Atria / Q000503:physiopathology; D006352:Heart Ventricles; D006801:Humans; D008954:Models, Biological; D008957:Models, Genetic; D009200:Myocardial Contraction; D010766:Phosphorylation; D015398:Signal Transduction