Skip Navigation

Cardiovascular Research 2002 54(2):347-360; doi:10.1016/S0008-6363(01)00562-4
© 2002 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Nattel, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nattel, S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2002, European Society of Cardiology

Therapeutic implications of atrial fibrillation mechanisms: can mechanistic insights be used to improve AF management?

Stanley Nattela,b,c,*

aDepartment of Medicine and Research Center, Montreal Heart Institute, 5000 Belanger Street E., Montreal, Quebec, Canada H1T 1C8
bDepartment of Medicine, University of Montreal, Montreal, Quebec, Canada
cDepartment of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada

* Present address: Montreal Heart Institute, Research Center, University of Montreal, 5000 Belanger Street E., Montreal, Quebec, Canada H1T 1C8. Tel.: +1-514-376-3330x3990; fax: +1-514-376-1355 nattel{at}icm.umontreal.ca

Atrial fibrillation (AF) is a very common clinical problem, and presently available treatment options are suboptimal. A tremendous amount has been learned over the past 10 years about the atrial substrates that support sustained AF at the tissue, ionic and molecular levels. This understanding of the fundamental mechanisms underlying AF has opened up a variety of new, rationally-based therapeutic approaches. The present paper reviews what is known about the mechanistic substrates that lead to AF and discusses the potential therapeutic consequences.

KEYWORDS Antiarrhythmic agents; Arrhythmia (mechanisms); Gene expression; Ion channels; Remodeling


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Eur Heart J SupplHome page
P. Dorian and B. N. Singh
Upstream therapies to prevent atrial fibrillation
Eur. Heart J. Suppl., September 1, 2008; 10(suppl_H): H11 - H31.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
M. Sakabe, A. Shiroshita-Takeshita, A. Maguy, B. J.J.M. Brundel, A. Fujiki, H. Inoue, and S. Nattel
Effects of a heat shock protein inducer on the atrial fibrillation substrate caused by acute atrial ischaemia
Cardiovasc Res, April 1, 2008; 78(1): 63 - 70.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.