This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Nattel, S. Search for Related Content PubMed PubMed Citation Articles by Nattel, S. Social Bookmarking                         What's this?

Atrial Electrophysiology and Mechanisms of Atrial Fibrillation

Research Center Montreal Heart Institute, Montreal, Canada; nattel{at}icm.umontreal.ca

Atrial fibrillation is the most common cardiac arrhythmia in clinical practice, and its management remains challenging. A solid understanding of the scientific basis for atrial fibrillation therapy requires insight into the mechanisms underlying the arrhythmia, about which an enormous amount has been learned over the past 10 years. The basic information presently available about atrial fibrillation mechanisms is reviewed. The particular properties of normal atrial electrophysiology are discussed, including salient ionic determinants of the atrial action potential and key anatomic features. Reviewed are three crucial arrhythmia mechanisms long held to be involved in atrial fibrillation: 1) rapid ectopic activity, 2) single-circuit reentry with fibrillatory conduction, and 3) multiple-circuit reentry. The determinants of each and the evidence for their involvement in clinical and/or experimental atrial fibrillation are noted. The physiological consequences, various contributing mechanisms, and clinical implications of the role of atrial-tachycardia remodeling are analyzed. Atrial-tachycardia remodeling links the potential mechanisms of atrial fibrillation, since atrial fibrillation beginning by any mechanism is likely to cause tachycardia-remodeling and thus promote the maintenance of atrial fibrillation by multiple-circuit reentry. Atrial structural remodeling is discussed as a paradigm of atrial fibrillation in which the classic features required for reentry (reduced refractory period and reentrant wavelength) may be lacking. Finally, the importance of recent insights into potential genetic determinants of atrial fibrillation is reviewed. The classic understanding of atrial fibrillation pathophysiology saw the different possible mechanisms as being alternative and opposing hypotheses. We now consider the multiple potential mechanisms as contributing to the pathophysiology of the arrhythmia to a different extent in different clinical settings and interacting with each other in a dynamic way at various stages of the natural history in many patients. It is hoped that this improved mechanistic understanding will lead to the development of improved therapeutic options.

Key Words: atrial electrophysiology • atrial fibrillation

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 8, No. 1 suppl, S5-S11 (2003)
DOI: 10.1177/107424840300800102


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				Y. Song, J. C. Shryock, and L. Belardinelli A slowly inactivating sodium current contributes to spontaneous diastolic depolarization of atrial myocytes Am J Physiol Heart Circ Physiol, October 1, 2009; 297(4): H1254 - H1262. [Abstract] [Full Text] [PDF]

				J. Sanchez-Quinones, F. Marin, V. Roldan, and G.Y.H. Lip The impact of statin use on atrial fibrillation QJM, November 1, 2008; 101(11): 845 - 861. [Abstract] [Full Text] [PDF]

				Y. Song, J. C. Shryock, and L. Belardinelli An increase of late sodium current induces delayed afterdepolarizations and sustained triggered activity in atrial myocytes Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H2031 - H2039. [Abstract] [Full Text] [PDF]

				T. Szili-Torok, L. Jordaens, and R. Sutton Alternative pacing sites at the atrial level Eur. Heart J. Suppl., December 1, 2007; 9(suppl_I): I33 - I36. [Abstract] [Full Text] [PDF]

				M. J. Tafreshi and J. Rowles A Review of the Investigational Antiarrhythmic Agent Dronedarone Journal of Cardiovascular Pharmacology and Therapeutics, March 1, 2007; 12(1): 15 - 26. [Abstract] [PDF]

				C. P. Regan, A. A. Wallace, H. K. Cresswell, C. L. Atkins, and J. J. Lynch Jr. In Vivo Cardiac Electrophysiologic Effects of a Novel Diphenylphosphine Oxide IKur Blocker, (2-Isopropyl-5-methylcyclohexyl) Diphenylphosphine Oxide, in Rat and Nonhuman Primate J. Pharmacol. Exp. Ther., February 1, 2006; 316(2): 727 - 732. [Abstract] [Full Text] [PDF]

				B. P. Knight, B. J. Gersh, M. D. Carlson, P. A. Friedman, R. L. McNamara, S. A. Strickberger, H. F. Tse, A. L. Waldo, and for the AHA Writing Group Role of Permanent Pacing to Prevent Atrial Fibrillation: Science Advisory From the American Heart Association Council on Clinical Cardiology (Subcommittee on Electrocardiography and Arrhythmias) and the Quality of Care and Outcomes Research Interdisciplinary Working Group, in Collaboration With the Heart Rhythm Society Circulation, January 18, 2005; 111(2): 240 - 243. [Abstract] [Full Text] [PDF]

				C. Oberti, L. Wang, L. Li, J. Dong, S. Rao, W. Du, and Q. Wang Genome-Wide Linkage Scan Identifies a Novel Genetic Locus on Chromosome 5p13 for Neonatal Atrial Fibrillation Associated With Sudden Death and Variable Cardiomyopathy Circulation, December 21, 2004; 110(25): 3753 - 3759. [Abstract] [Full Text] [PDF]

				J.S. Gill How to perform pulmonary vein isolation Europace, January 1, 2004; 6(2): 83 - 91. [Full Text] [PDF]