Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1983;68:865-871

This Article
Right arrow Full Text (PDF)
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 Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cobbe, S. M.
Right arrow Articles by Senges, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cobbe, S. M.
Right arrow Articles by Senges, J.

Circulation, Vol 68, 865-871, Copyright © 1983 by American Heart Association


ARTICLES

Action of sotalol on potential reentrant pathways and ventricular tachyarrhythmias in conscious dogs in the late postmyocardial infarction phase

SM Cobbe, E Hoffman, A Ritzenhoff, J Brachmann, W Kubler and J Senges

Sotalol is a beta-adrenergic blocker that also prolongs action potential duration and myocardial refractoriness over the short term (class III effect). Its short-term antiarrhythmic effects were compared with those of metoprolol, which has neither short-term class III nor membrane-stabilizing action, on reentrant ventricular arrhythmias produced by programmed stimulation in 17 conscious dogs 3 to 8 days after myocardial infarction. Ventricular arrhythmias were prevented or significantly slowed by sotalol in 11 of 19 studies (58%) compared with in one of 14 (7%) studies with metoprolol. Sotalol prolonged refractoriness in the infarct zone, measured from an implanted "composite" electrode, by 41 +/- 45% (mean +/- SD, p less than .01), which was significantly greater than the increases it produced in effective refractory period of the normal ventricle (14.0 +/- 5.5%) or QT interval (12.5 +/- 7.8%). Metoprolol had no effect on infarct-zone refractoriness. Sotalol differentially increases refractoriness in potential reentry circuits in ischemic myocardium. Its antiarrhythmic effect in this model is not due to beta-blockade, and is presumably related to prolongation of action potential duration.


This article has been cited by other articles:


Home page
Cardiovasc ResHome page
K. D Freigang, A. Bauer, R. Becker, J. C Senges, P. Kraft, J. Brachmann, W. Kubler, and W. Schoels
Differential effects of d-sotalol on normal and infarcted myocardium: an experimental study using epicardial mapping
Cardiovasc Res, July 1, 1997; 35(1): 52 - 59.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
E. Patterson, B. J. Scherlag, S. Sangiah, G. L. Garrison, K. M. Couch, K. D. Berlin, and R. Lazzara
Class III Electrophysiologic Actions of Imidazole-Substituted Diheterabicyclononanes in Canine Myocardium
J. Pharmacol. Exp. Ther., April 1, 1997; 281(1): 155 - 162.
[Abstract] [Full Text]


Home page
NEJMHome page
S. H. Hohnloser and R. L. Woosley
Sotalol
N. Engl. J. Med., July 7, 1994; 331(1): 31 - 38.
[Full Text]