JACC
HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
 QUICK SEARCH:   [advanced]


     


J Am Coll Cardiol, 2008; 51:802-809, doi:10.1016/j.jacc.2007.09.064
© 2008 by the American College of Cardiology Foundation
This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow View Current Clinical Collection-Atrial Fibrillation
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Google Scholar
Right arrow Articles by Burstein, B.
Right arrow Articles by Nattel, S.
PubMed
Right arrow Articles by Burstein, B.
Right arrow Articles by Nattel, S.

FOCUS ISSUE: ATRIAL FIBRILLATION: STATE-OF-THE-ART PAPER

Atrial Fibrosis: Mechanisms and Clinical Relevance in Atrial Fibrillation

Brett Burstein, BSc and Stanley Nattel, MD*

Research Center and Department of Medicine, Montreal Heart Institute and Université de Montréal, and Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada.

Manuscript received June 21, 2007; revised manuscript received August 16, 2007, accepted September 7, 2007.

* Reprint requests and correspondence: Dr. Stanley Nattel, 5000 Belanger Street East, Montreal H1T 1C8, Quebec, Canada. (Email: stanley.nattel{at}icm-mhi.org).

Atrial fibrillation (AF) is the most common arrhythmia in the clinical setting, and traditional pharmacological approaches have proved to have important weaknesses. Structural remodeling has been observed in both clinical and experimental AF paradigms, and is an important feature of the AF substrate, producing fibrosis that alters atrial tissue composition and function. The precise mechanisms underlying atrial fibrosis are not fully elucidated, but recent experimental studies and clinical investigations have provided valuable insights. A variety of signaling systems, particularly involving angiotensin II and related mediators, seem to be centrally involved in the promotion of fibrosis. This paper reviews the current understanding of how atrial fibrosis creates a substrate for AF, summarizes what is known about the mechanisms underlying fibrosis and its progression, and highlights emerging therapeutic approaches aimed at attenuating structural remodeling to prevent AF.

Abbreviations and Acronyms
  ACE = angiotensin-converting enzyme
  AF = atrial fibrillation
  AngII = angiotensin II
  AT1 = angiotensin II type 1
  CHF = congestive heart failure
  ECM = extracellular matrix
  PDGF = platelet-derived growth factor
  TGF = transforming growth factor
  VTP = ventricular tachypacing




This article has been cited by other articles:


Home page
Circ Arrhythmia ElectrophysiolHome page
S. Nattel, B. Burstein, and D. Dobrev
Atrial Remodeling and Atrial Fibrillation: Mechanisms and Implications
Circ Arrhythmia Electrophysiol, April 1, 2008; 1(1): 62 - 73.
[Full Text] [PDF]




HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
Copyright © 2008 by the American College of Cardiology Foundation.