Electrophysiologic effects of diltiazem hydrochloride on supraventricular tachycardia.

The effects of intravenous diltiazem hydrochloride (0.25 mg/kg body weight) were studied in eight patients with nine episodes of supraventricular tachycardia. Five episodes of tachycardia were due to atrioventricular (A-V) nodal reentry (group A), two were due to retrograde utilization of a concealed A-V accessory pathway (group B) and two were episodes of atrial fibrillation (group C). Intravenous administration of diltiazem slowed the ventricular rate in eight of nine episodes of tachycardias. Supraventricular tachycardia was terminated within 2 minutes after intravenous diltiazem in four of five patients in group A, and one of two in group B. Cycle length alternation was observed before termination of the arrhythmia in two patients from group A. In group C the ventricular response slowed but also became regular during atrial fibrillation. Although diltiazem depressed both anterograde and retrograde conduction as assessed by programmed stimulation, tachycardia termination or slowing or alternation of cycle length all occurred because of the effects of diltiazem predominantly on anterograde A-V nodal properties during supraventricular tachycardia. Although no statistical conclusions can be made from this limited study, it appears that diltiazem has significant depressant electrophysiologic effects on both anterograde and retrograde A-V nodal function as assessed by programmed stimulation during sinus rhythm. Further electrophysiologic studies are needed before determining the clinical efficacy of this agent for treatment or prophylaxis of recurrent supraventricular tachycardias.