This Article Full Text Full Text (PDF) 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 Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Spach, M. S. Search for Related Content PubMed PubMed Citation Articles by Spach, M. S. Related Collections Related Article

(Circulation Research. 2007;101:743.)
© 2007 American Heart Association, Inc.

Editorials

Mounting Evidence That Fibrosis Generates a Major Mechanism for Atrial Fibrillation

Madison S. Spach

From the Department of Pediatrics, Duke University Medical Center, Durham, NC.

Correspondence to Madison S. Spach, MD, Department of Pediatrics, P.O. Box 3475, Duke University Medical Center, Durham, NC 27710. E-mail cspach@duke.edu

See related article, pages 839–847

Key Words: atrial fibrillation • fibrosis • reentry triggered activity

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
It is widely known that atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, with the problem magnified by the clinical sequelae; eg, thromboembolic events. It is pertinent that the incidence of AF is expected to increase in the future,¹ especially in aging patients. Thus, finding preventive measures for this arrhythmia has become an increasingly important goal. In addition to considering clinical risk factors, focusing on prevention necessitates knowledge of the associated pathophysiology of AF,² which involves the initiation of AF and the wavefront dynamics that sustain it.

In recent years considerable new information has appeared concerning AF mechanisms that occur in different regions of the atria in different cardiac states.³ This point is highlighted by the report of Tanaka et al⁴ in this issue of Circulation Research. These authors used high-resolution electrophysiological and microstructural techniques, along with computer model simulations, to study wavefront dynamics during acetylcholine (ACh)-induced AF in heart failure sheep hearts. The heart failure hearts had developed prominent fibrotic patches in the posterior left atrium near the pulmonary veins, whereas in the control (normal) hearts patches of fibrosis were smaller, diffusely distributed, and more centrally located with respect to the 4 pulmonary vein ostia. In the heart failure hearts, during AF variable wavefront breakthroughs to the endocardium occurred in the area of fibrotic patches adjacent to the pulmonary veins. The authors concluded that scroll waves within the posterior left atrial wall produced a microreentry source for the endocardial breakthroughs in the region of the larger . . . [Full Text of this Article]

Related Article:

Spatial Distribution of Fibrosis Governs Fibrillation Wave Dynamics in the Posterior Left Atrium During Heart Failure

Kazuhiko Tanaka, Sharon Zlochiver, Karen. L. Vikstrom, Masatoshi Yamazaki, Javier Moreno, Matthew Klos, Alexey. V. Zaitsev, Ravi Vaidyanathan, David S. Auerbach, Steve Landas, Gérard Guiraudon, José Jalife, Omer Berenfeld, and Jérôme Kalifa
Circ. Res. 2007 101: 839-847. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				N W F Linton and S W Dubrey Narrow complex (supraventricular) tachycardias Postgrad. Med. J., October 1, 2009; 85(1008): 546 - 551. [Abstract] [Full Text] [PDF]

				J. W. Magnani, M. A. Williamson, P. T. Ellinor, K. M. Monahan, and E. J. Benjamin P Wave Indices: Current Status and Future Directions in Epidemiology, Clinical, and Research Applications Circ Arrhythm Electrophysiol, February 1, 2009; 2(1): 72 - 79. [Full Text] [PDF]

				B. Yang, Y. Lu, and Z. Wang Control of cardiac excitability by microRNAs Cardiovasc Res, September 1, 2008; 79(4): 571 - 580. [Abstract] [Full Text] [PDF]

				V. Jacquemet and C. S. Henriquez Loading effect of fibroblast-myocyte coupling on resting potential, impulse propagation, and repolarization: insights from a microstructure model Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H2040 - H2052. [Abstract] [Full Text] [PDF]