Volume 9, Issue 3 p. 144-153

Proarrhythmia: A Paradoxic Response to Antiarrhythmic Agents

Dr. Patrick L. McCollam Pharm.D.

Dr. Patrick L. McCollam Pharm.D.

Department of Pharmacy Practice

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Dr. Robert B. Parker Pharm.D.

Dr. Robert B. Parker Pharm.D.

Department of Pharmacy Practice

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Dr. Karen J. Beckman M.D.

Dr. Karen J. Beckman M.D.

Department of Medicine, Section of Cardiology, University of Illinois at Chicago, Chicago, Illinois.

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Dr. Robert J. Hariman M.D.

Dr. Robert J. Hariman M.D.

Department of Medicine, Section of Cardiology, University of Illinois at Chicago, Chicago, Illinois.

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Dr. Jerry L. Bauman Pharm.D.

Corresponding Author

Dr. Jerry L. Bauman Pharm.D.

Department of Pharmacy Practice

Department of Medicine, Section of Cardiology, University of Illinois at Chicago, Chicago, Illinois.

Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago, 833 South Wood Street, Room 244 (M/C 886), Chicago, IL 60612.Search for more papers by this author
First published: May‐June 1989
Citations: 11

Abstract

Antiarrhythmic drugs may effectively terminate and prevent symptomatic tachycardias, but they may also provoke life-threatening rhythm disturbances. The electrophysiologic mechanisms responsible for proarrhythmia can be extrapolated from the existing models of reentry and abnormal automaticity. Although all antiarrhythmic drugs may cause proarrhythmia with seemingly similar frequency, the profile of the disturbance with each class of agents appears somewhat distinct. All agents may cause an increased frequency of premature beats or new or worsened ventricular tachycardia, but the classic form of proarrhythmia due to type Ia agents is torsades de pointes. Recent information has provided clues to the underlying mechanism of drug-induced torsades de pointes and has provided a clinical picture of patients with this adverse effect. Types Ib and Ic agents only rarely precipitate torsades de pointes. The latter, however, may cause a rapid, sustained, monomorphic ventricular tachycardia in certain high-risk patients that can be resistant to resuscitation efforts. Amiodarone may cause a broad variety of arrhythmias that are complicated by their extended duration and difficulty in distinguishing proarrhythmia from simple inefficacy. Proarrhythmia is a relatively common, paradoxic side effect that necessitates the clinician to make careful risk-benefit decisions in choosing antiarrhythmic drug therapy.