Antiarrhythmic agents can worsen existing arrhythmias by increasing their duration or frequency, increasing the number of premature complexes or couplets, altering the rate of the arrhythmia or causing new, previously unexperienced arrhythmias. QT prolongation occurs in many settings, not all of which are associated with increased arrhythmia development. Arrhythmogenesis in the setting of a long QT interval may be related to marked asynchrony of repolarization. The role of afterdepolarizations is still being investigated. No correlation has been established between the occurrence of torsades de pointes, a specific degree of QT prolongation and either the dose or serum concentration of any of the antiarrhythmic agents. In 30 patients who experienced drug-induced ventricular fibrillation, the median time to ventricular fibrillation was only 3 days after drug treatment began. Significant caution must be exercised in determining the need for antiarrhythmic therapy and in monitoring patients after treatment has begun.