Skip Navigation

Cardiovascular Research 1998 37(3):567-577; doi:10.1016/S0008-6363(97)00293-9
© 1998 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
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
Right arrow Disclaimer
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 © 1998, European Society of Cardiology

Experimental evidence for proarrhythmic mechanisms of antiarrhythmic drugs

Stanley Nattela,b,*

aDepartment of Medicine, Montreal Heart Institute, 5000 Belanger Str. East, Montreal, Quebec H1T 1C8, Canada
bUniversity of Montreal, Montreal, Quebec, Canada

* Tel.: +1 (514) 376-3330; Fax: +1 (514) 376-1355.

The major limitation to antiarrhythmic drug therapy is the risk of arrhythmia promotion, or ‘proarrhythmia.’ This complication may be lethal, and greatly restricts the value of antiarrhythmic agents, particularly for arrhythmias without an intrinsic mortality risk, such as atrial fibrillation. In order for improved antiarrhythmic drug therapy to be developed, it is essential to understand the fundamental mechanisms that cause proarrhythmic reactions to antiarrhythmic drugs. The present article reviews the experimental evidence that has been obtained regarding the mechanisms of proarrhythmia. The evidence available provides important insights, and points to potential strategies for developing newer and safer antiarrhythmic compounds.

KEYWORDS Pharmacology; Ion channel blocker; Cardiac arrhythmia; Sodium channel blocker; Potassium channel blocker; Action potential duration; Early afterdepolarization; Ischemic heart disease


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




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.