This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Woosley, R. L. Articles by Oates, J. A. Search for Related Content PubMed PubMed Citation Articles by Woosley, R. L. Articles by Oates, J. A.

Circulation, Vol 60, 819-827, Copyright © 1979 by American Heart Association

ARTICLES

Suppression of chronic ventricular arrhythmias with propranolol

RL Woosley, D Kornhauser, R Smith, S Reele, SB Higgins, AS Nies, DG Shand and JA Oates

The antiarrhythmic efficacy of propranolol was evaluated in 32 patients with chronic high frequency ventricular arrhythmias in a placebo- controlled protocol. After a placebo control period, propranolol was begun and the dosage increased sequentially until arrhythmia suppression was achieved, side effects appeared, or a maximum dosage of 960 mg/day was reached. Computerized analysis of ambulatory recordings was used to quantify the arrhythmias. Twenty-four patients had 70--100% arrhythmia suppression at plasma levels ranging from 12--1100 ng/ml (end of dosing interval). Eight patients in this group had frequent episodes of ventricular tachycardia that were totally suppressed at or below the dosage that produced greater than or equal to 70% suppression of ventricular ectopic depolarizations (VEDs). A biphasic dose-response curve was seen in five patients who responded with a decrease in arrhythmia frequency in the lower ranges of dosages but had increased frequency of ectopic rhythms as the dosage was increased above the optimal level. Only one-third of patients responded at doses less than or equal to 160 mg/day. However, with dosages of 200--640 mg/day, an additional 40% responded. Propranolol appears to control ventricular arrhythmias safely and effectively in many patients. The finding that the antiarrhythmic effect in many patients required plasma concentrations greater than those that produce substantial beta- adrenergic blockage raises a question whether blockade of cardiac beta receptors can directly account for all of the antiarrhythmic actions of propranolol.

This article has been cited by other articles:

				L. Brynne, M. O. Karlsson, and L. K. Paalzow Concentration-Effect Relationship of l-Propranolol and Metoprolol in Spontaneous Hypertensive Rats after Exercise-Induced Tachycardia J. Pharmacol. Exp. Ther., September 1, 1998; 286(3): 1152 - 1158. [Abstract] [Full Text]

				P. C. Deedwania Sotalol Is More Powerful Than Propranolol in Suppressing Complex Ventricular Arrhythmias Journal of Cardiovascular Pharmacology and Therapeutics, January 1, 1997; 2(4): 259 - 272. [Abstract] [PDF]

				E. L. Carey JR., D. Robertson, J. N. Wells, and R. M. Robertson Contraction of Isolated Porcine Coronary Arteries is Inhibited by High Concentrations of Propranolol Angiology, June 1, 1995; 46(6): 453 - 460. [Abstract] [PDF]

				D. M. Roden Risks and Benefits of Antiarrhythmic Therapy N. Engl. J. Med., September 22, 1994; 331(12): 785 - 791. [Full Text]