title: Cellular bases for human atrial fibrillation.
abstract: Atrial fibrillation (AF) causes substantial morbidity and mortality. It may be triggered and sustained by either reentrant or nonreentrant electrical activity. Human atrial cellular refractory period is shortened in chronic AF, likely aiding reentry. The ionic and molecular mechanisms are not fully understood and may include increased inward rectifier K(+) current and altered Ca(2+) handling. Heart failure, a major cause of AF, may involve arrhythmogenic atrial electrical remodeling, but the pattern is unclear in humans. Beta-blocker therapy prolongs atrial cell refractory period; a potentially antiarrhythmic influence, but the ionic and molecular mechanisms are unclear. The search for drugs to suppress AF without causing ventricular arrhythmias has been aided by basic studies of cellular mechanisms of AF. It remains to be seen whether such drugs will improve patient treatment.
authors.affiliation: British Heart Foundation Glasgow Cardiovascular Research Centre, Faculty of Medicine, University of Glasgow, Glasgow, United Kingdom. A.J.Workman@clinmed.gla.ac.uk
authors.forename: Antony J
authors.initials: AJ
authors.lastname: Workman
authors.forename: Kathleen A
authors.initials: KA
authors.lastname: Kane
authors.forename: Andrew C
authors.initials: AC
authors.lastname: Rankin
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000378:metabolism*; D016275:Atrial Function; D002118:Calcium / Q000378:metabolism*; D055724:Electrophysiological Phenomena; D006325:Heart Atria / Q000166:cytology; D006333:Heart Failure / Q000378:metabolism*; D006801:Humans; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism
chemical_list: D000319:Adrenergic beta-Antagonists; D024661:Potassium Channels, Inwardly Rectifying; D002118:Calcium