Skip Navigation


European Heart Journal Advance Access originally published online on February 15, 2005
European Heart Journal 2005 26(6):536-537; doi:10.1093/eurheartj/ehi155
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
26/6/536    most recent
ehi155v1
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 Related articles in EHJ
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
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 arrow Search for citing articles in:
ISI Web of Science (1)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Viskin, S.
Right arrow Articles by Rosovski, U.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Viskin, S.
Right arrow Articles by Rosovski, U.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

The degree of potassium channel blockade and the risk of torsade de pointes: the truth, nothing but the truth, but not the whole truth

Sami Viskin* and Uri Rosovski

Department of Cardiology, Tel-Aviv Sourasky Medical Center and Sackler School of Medicine, Tel Aviv University, Weizman 6, Tel Aviv 64239, Israel

* Corresponding author. Tel: +972 524266859; fax: +972 36974416. E-mail address: saviskin@tasmc.health.gov.il

This editorial refers to ‘Anti-HERG activity and the risk of drug-induced arrhythmias and sudden death’{dagger} by M.L. De Bruin et al., on page 590

The first 10% of the full text of this article appears below.

Several anti-arrhythmic drugs, as well as medications not intended for cardiac indications, block a specific potassium channel named IKr (the rapid delayed rectifying potassium current). In the case of the anti-arrhythmic drugs, IKr channels are purposely targeted. By blocking potassium outflow currents, the anti-arrhythmic drugs prolong the action potential. This action (depicted in the electrocardiogram as prolongation of the QT interval) can be advantageous given that prolongation of the action potential also lengthens the refractory period, thereby suppressing common arrhythmias. Unfortunately, by a mechanism explained elsewhere,1 IKr blockade may lead to excessive QT prolongation and trigger a polymorphic ventricular tachyarrhythmia (torsade de pointes) that may degenerate into ventricular fibrillation. Furthermore, because of its unique three-dimensional characteristics,2 IKr channels are very easily blocked by the small molecules of numerous non-cardiac drugs. The . . . [Full Text of this Article]


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

Related articles in EHJ:

Anti-HERG activity and the risk of drug-induced arrhythmias and sudden death
M.L. De Bruin, M. Pettersson, R.H.B. Meyboom, A.W. Hoes, and H.G.M. Leufkens
EHJ 2005 26: 590-597. [Abstract] [FREE Full Text]  



This article has been cited by other articles:


Home page
CirculationHome page
B. R. Chaitman
Ranolazine for the Treatment of Chronic Angina and Potential Use in Other Cardiovascular Conditions
Circulation, May 23, 2006; 113(20): 2462 - 2472.
[Full Text] [PDF]