Early and late proarrhythmia from antiarrhythmic drug therapy.

Abstract

Antiarrhythmic drug therapy is used with the hope of suppressing arrhythmias and therefore decreasing their associated symptoms or prolonging life. Unfortunately, many antiarrhythmic drugs have the opposite effect of exacerbating or provoking arrhythmias, a phenomenon that is termed proarrhythmia when such an event is specifically due to the drug in use. Early proarrhythmic events (within 30 days of initiation of drug use) have been reasonably well characterized and are predicted by either type of drug employed or the nature of the patient's cardiac disease and arrhythmia type. Late proarrhythmic events, as defined by placebo-controlled trials, have now been recognized as an increased risk of arrhythmic death in patients on antiarrhythmic drugs after many months of therapy. Initially, this late proarrhythmic event was identified with encainide and flecainide, but now several new studies have demonstrated that the risk of late proarrhythmia of comparable magnitude may be present in patients subjected to commonly used drugs, such as quinidine, mexelitine, etc. At present, only moricizine and the class II drugs (beta-adrenergic blockers) appear not to have this potential late proarrhythmic response. Therefore, before instituting antiarrhythmic drug therapy, the physician must be able to quantitate the degree of proarrhythmia and other risks of such therapy, as compared to their potential benefit, to define the proper indications for these agents.