Virtually all antiarrhythmic agents can, under certain circumstances, be arrhythmogenic. The expected therapeutic and potentially arrhythmogenic effects of these agents may be altered if there is (1) an increase or decrease in the serum concentration of the antiarrhythmic agent due to interaction with other drugs, renal or hepatic disease or altered pharmacokinetics; (2) an idiosyncratic reaction to the antiarrhythmic agent; (3) an alteration in serum potassium or magnesium concentration; (4) interaction between the antiarrhythmic agent and the autonomic nervous system or between the autonomic nervous system and the heart, or (5) alteration of myocardial performance and the peripheral vascular system by the antiarrhythmic agent. Because of the lack of uniform reporting of data, guidelines have been suggested to evaluate proarrhythmic events. Of 412 patients receiving 1,080 drug trials for treatment of ventricular tachycardia or ventricular fibrillation, proarrhythmic events occurred in 33 patients (8%) and 43 drug trials (4%). The proarrhythmic event occurred more often during treatment for sustained ventricular tachycardia than for ventricular fibrillation or nonsustained ventricular tachycardia. The initial step in treating a proarrhythmic event is to discontinue the offending drug. Further recommendations are based on the nature of the particular arrhythmia.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine