Aprindine for treatment of supraventricular tachycardias. With particular application to Wolff-Parkinson-White syndrome

Ten patients with recurrent or continuous Supraventricular tachycardia difficult to control with conventional antiarrhythmic agents were treated with aprindine, a new antiarrhythmic drug. Nine patients had Wolff-Parkinson-White syndrome. An electrophysiologic study was performed before and during oral administration of aprindine. At the time of the first study, circus movement Supraventricular tachycardia was initiated in Patients 1 to 8. During administration of aprindine, circus movement Supraventricular tachycardia could no longer be initiated in Patients 1 to 4 but was initiated with difficulty in Patients 5 and 6 and with greater ease in Patients 7 and 8. In Patient 9, aprindine therapy slowed the ventricular response during atrial flutter from 1:1 conduction over the accessory pathway to 2:1 conduction over the normal pathway; in Patient 10, it slowed the ventricular rate during atrial fibrillation from 140-180 to 80-100 beats/min. Patients 1 to 6, 9 and 10 had an excellent clinical response, but treatment with aprindine was discontinued in Patients 7 and 8. Electrophysiologic evaluation revealed that aprindine produced complete block or increased refractoriness of the accessory pathway in an antegrade direction in all patients and in a retrograde direction in all but two (Patients 7 and 8) tested. Aprindine also slowed conduction in the accessory pathway and, when Supraventricular tachycardia could still be initiated, it occurred at a slower rate. Neurologic side effects occurred primarily during the initial administration and dose adjustment of aprindine.