Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1996;94:607-609

This Article
Right arrow Full Text
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rosen, M. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rosen, M. R.

(Circulation. 1996;94:607-609.)
© 1996 American Heart Association, Inc.


Articles

Of Oocytes and Runny Noses

Michael R. Rosen, MD

the Departments of Pharmacology and Pediatrics, College of Physicians and Surgeons, New York, NY.

Correspondence to Michael R. Rosen, MD, the Department of Pharmacology, College of Physicians and Surgeons, 630 W 168th St, New York, NY 10032.


Key Words: Editorials • arrhythmia • antiarrhythmia agents


*    Introduction
 
The paper by Roy et al1 detailing the effects of the nonsedating antihistamine terfenadine on two K channels in an oocyte system and published in the current issue of Circulation may seem at first blush to deal with esoterica. Yet, a disturbing number of case reports2 3 and papers4 5 6 7 in the medical literature have documented QT-interval prolongation and torsade de pointes in patients taking terfenadine alone or together with antimycotics such as ketoconazole or antibiotics such as erythromycin. On the basis of such information, any physician considering therapy with nonsedating antihistamines must incorporate awareness of the acquired long-QT syndrome in the decision-making process.

The study by Roy et al1 is also a reminder that our knowledge concerning acquired long-QT syndrome is advancing with impressive rapidity in ways that impact directly on our understanding of pathophysiology and patient care. Families of drugs including but not limited to antiarrhythmics that prolong repolarization by blocking K+ channels or increasing inward Na+ currents,8 macrolide antibiotics, and pyrrole antimycotics3 4 5 6 7 all have the potential to prolong the QT interval and induce arrhythmias and/or death. With respect to the mechanism whereby nonsedating antihistamines prolong the QT interval, the focus of investigation has been the delayed rectifier current, IK. A major breakthrough here came in the report by Woosley et al4 demonstrating terfenadine block of IK in feline ventricle. Subsequently, terfenadine has been reported to block the transient outward current (Ito1) as well as the ultrarapid (IKur), rapid (IKr), and slow (IKs) components of . . . [Full Text of this Article]




This article has been cited by other articles:


Home page
Eur Heart JHome page
W Haverkamp, G Breithardt, A.J Camm, M.J Janse, M.R Rosen, C Antzelevitch, D Escande, M Franz, M Malik, A Moss, et al.
The potential for QT prolongation and proarrhythmia by non-antiarrhythmic drugs: clinical and regulatory implications. Report on a Policy Conference of the European Society of Cardiology
Eur. Heart J., August 1, 2000; 21(15): 1216 - 1231.
[PDF]


Home page
Cardiovasc ResHome page
W. Haverkamp, G. Breithardt, A.J. Camm, M. J Janse, M. R Rosen, C. Antzelevitch, D. Escande, M. Franz, M. Malik, A. Moss, et al.
The potential for QT prolongation and pro-arrhythmia by non-anti-arrhythmic drugs: Clinical and regulatory implications: Report on a Policy Conference of the European Society of Cardiology
Cardiovasc Res, August 1, 2000; 47(2): 219 - 233.
[Full Text] [PDF]