The arrhythmogenicity of antiarrhythmic agents (original) (raw)

In the last decade the awareness of ventricular arrhythmias and the associated potential for sudden cardiac death has increased. Along with this changing perception, the technology by which these arrhythmias can be detected has also developed. This has led to the testing of new antiarrhythmic agents and to an increased use of the currently available drugs. Along with the increase in the use of antiarrhythmic agents, an increase in associated side effects has been noted. In addition to side effects one also notes the worsening or facilitation of cardiac arrhythmias. There are many case reports of quinidine causing ventricular tachycardia (VT) or fibrillation.1-4 However, this action is not unique to quinidine. There are reports implicating other available conventional agents as well as the newly developed investigational agents.5-10 However, there are few studies that have tried to look at the incidence of this problem and try to provide evidence for a causative relation between antiarrhythmic agents and their possible exacerbation of arrhythmias. Velebit et al." reported aggravation of ventricular arrhythmias in 11% of 722 drug tests. This group employs Holter monitoring techniques and bicycle exercise to evaluate the potential proarrhythmic action of antiarrhythmic drugs. Recently, Ruskin et all* reported on six survivors of out-of-hospital cardiac arrest. Using programmed electrical stimulation (PES), they showed that these patients had their life-threatening arrhythmia induced while they were receiving antiarrhythmic drugs, but the same arrhythmia was not provoked when they were not taking the drug. Poser et all3 have also used PES techniques to analyze the incidence of antiarrhythmic drug aggravation of arrhythmias. This group employs electrophysiologic studies in a minority of From the Cardi ac Arrhythmia Service, Cardiology Division,