© 1999 American Heart Association, Inc.
Editorial |
Ionic Determinants of Atrial Fibrillation and Ca2+ Channel Abnormalities
Cause, Consequence, or Innocent Bystander?
From the Research Center and Department of Medicine, Montreal Heart Institute, Department of Medicine, University of Montreal and the Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada.
Correspondence to Stanley Nattel, MD, Research Center, Montreal Heart Institute, 5000 Belanger St, East, Montreal, Quebec, Canada H1T 1C8. E-mail nattel@icm.umontreal.ca
Key Words: ion channel • Ca2+ current • postoperative atrial fibrillation • cardiac arrhythmia • electrophysiological remodeling
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Introduction |
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Over the past several years, there has been increasing interest in understanding the basic mechanisms underlying atrial fibrillation (AF). The rise in interest is partly related to the prevalence of AF, which is presently the most common arrhythmia in clinical practice, and partly to the fact that the treatment of AF remains inadequate, making new insights into basic mechanisms essential for improving therapy.1 Of great importance, as well, has been the development of new, clinically relevant animal models of the arrhythmia2 3 and advances in scientific methodology, including high-density mapping, patch-clamp recording, and molecular cloning of ion channels, that have permitted much more sophisticated approaches to defining AF mechanisms at very basic levels. The studies by Van Wagoner et al4 reported in this issue of Circulation Research provide important information about the potential role of Ca2+ channel abnormalities in clinical AF and at the same time, raise some intriguing questions. To appreciate the results of these findings presented by Van Wagoner et al, it is important to place them in the context of preceding work on the ionic determinants of AF.
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Ion Channel Abnormalities in Experimental Models of AF |
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The discovery by Wijffels et al2 that AF alters atrial electrophysiology in ways that promote AF maintenance was a substantial advance in understanding the arrhythmia. Not only did it reveal previously unrecognized fundamental and clinically relevant aspects of the physiology of the arrhythmia, but it also permitted investigators to prepare animals with great susceptibility to AF in a clinically relevant model. It was subsequently shown that the remodeling caused by
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