Summary:In patients with malignant ventricular arrhythmias, antiarrhythniic therapy is known to c x y a substantial risk of proarrhythmia. This risk is usually considered to be low when supraventricular arrhythmias or benign ventricular arrhythmias are considered. We were able to collect data on four patients without a history of life-threatening arrhythmias. in whom witiarrhythmic therapy was used and resulted in documented ventriculx fibrillation or torsade de pointes. In Cases No. 1 and 2.amal fibrillation was treated with either quinidine or quinidine and sotalol in combination. In both patients Holter monitoring, 4-I2 h :]tier conversion to sinus rhythm, documented the spmtaneous Occurrence of toixade de pointes degenerating into ventriculm fibrillation and requiring DC shock for termination. In Case No. 3, atrial fibrillation was treated with sotalol and amiodarone for 2 months when incessant episodes of torsade de pointes were documented. In Case No. 4, frequent but unsustained ventricular arrhythmias were treated with amiodarone in a patient sutfering dilative cardiomyopathy. After 6 days of treatment at a hem rate of 54 beats/inin, a mdrked QT increase was associated with the occurrence of repetitive episodes of polymorphic ventricular tachycardia degenerating into ventricular fibrillalion. None of the patients presented significant electrolyte abnormalities in the laboratory. A pathologic increase of' the QTc-lime was documented in Cases No. 1,3, and 4. In all pati en r s an ti m h yt hmic therapy was withdrawn after the proarrhythmic event and the patient became free of malignant tachyan-hythnuas. Antiarrhythmic therapy also carries a considerable risk of proarrhythmia when "benign" cardiac mhythtnias are treated. The risk seems to be lower than in patients with malignant arrhythmias, however it includes the occurrence of lethal tachyarrhythmias. Special attention should be paid to the selection ofantiarrhythmic agents when used in combination.