Proarrhythmic actions of antiarrhythmic drugs: a review

Abstract

The ability of antiarrhythmic drugs to aggravate and even cause arrhythmias is now well-established. The incidence of such effects for a wide range of agents is of the order of 3-15%. The two major mechanisms are facilitation of reentry circuits and the production of triggered activity due to early after depolarisations. This latter effect probably underlies the drug-induced long QT syndromes and associated arrhythmias including 'torsade de pointes' and is more likely to occur in association with bradycardia, hypokalaemia, or concomitant digitalis therapy. While some or all of these mechanisms are capable of producing or aggravating both supraventricular and ventricular arrhythmias, this review deals only with 'proarrhythmic' effects in the ventricles. These are known to be more likely in the presence of poor ventricular function (left ventricular rejection fraction less than 35%). Optimal management may include withdrawal of antiarrhythmic agents, replacement of potassium, infusion of magnesium and overdrive pacing.