Circulation, Vol 53, 101-106, Copyright © 1976 by American Heart Association
W Markiewicz, R Winkle, G Binetti, R Kernoff and DC Harrison
Since quinidine is one of the few agents available to treat and prevent
ventricular arrhythmias in ambulatory patients, its hemodynamic effects
have been reevaluated. When given in therapeutic doses to anesthetized
mongrel dogs, quinidine significantly reduced heart rate, aortic pressure
and flow, but it did not significantly change the first derivative of the
left ventricular pressure curve (left ventricular dp/dt) in nine dogs. A
subsequent group of dogs was studied after vagotomy and practolol
administration to block cardiac reflexes. This group showed significant
reductions in heart rate, aortic pressure and left ventricular dp/dt, with
the latter returning to predrug control values when preload, afterload and
heart rate were maintained constant. These studies suggest that quinidine
does not directly affect myocardial contractility when given in therapeutic
doses. Furthermore, the reduction in heart rate in these animals provides
support for a direct depressant effect of quinidine on the sinus node. The
adverse effects of quinidine on cardiac function previously reported may be
due to the use of toxic doses or are secondary to quinidine peripheral
circulatory effects, rather than due to a direct reduction in cardiac
contractile state.
ARTICLES
Normal myocardial contractile state in the presence of quinidine
This article has been cited by other articles:
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J. S. Gottdiener, R. DiBianco, and R. D. Fletcher Effects of Antiarrhythmic Agents on Cardiac Function Angiology, April 1, 1982; 33(4): 228 - 238. [PDF] |
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