Electrophysiologic effects and mechanisms of termination of supraventricular tachycardia by intravenous amiodarone

Abstract

Electrophysiologic studies were performed in nine patients with reentrant paroxysmal supraventricular tachycardia (PSVT) during a control period and following 5 mg/kg body weight of intravenous amiodarone (Cordarone, Labaz) administered as a slow continuous infusion over 15 to 20 minutes. All nine patients had induction of sustained PSVT during control studies. In seven of nine patients (group 1) the tachycardia was due to atrioventricular (AV) nodal reentry, and in two of nine patients (group 2) a concealed retrograde bypass tract was incorporated in the reentrant process. In group 1, following amiodarone, all seven patients lost the ability to sustain PSVT with either absence of atrial echoes (one patient) or induction of ≤3 echo beats (six patients) with termination of PSVT in the antegrade pathway (three patients) or retrograde pathway (two patients) or both (one patient). In group 2, following amiodarone, both patients lost the ability to sustain PSVT with absence of atrial echoes (one patient) on induction of a single echo beat (one patient) with block in the retrograde pathway (i.e., the concealed retrograde bypass tract). Amiodarone significantly increased (1) atrial cycle length for AV nodal Wenckebach block, (2) antegrade functional refractory period of the AV node, (3) antegrade effective refractory period of the AV node, (4) ventricular paced cycle length for ventricular atrial block, and (5) the retrograde functional refractory period of the ventricular-atrial conducting system. Thus intravenous-amiodarone inhibited induction of sustained reentrant PSVT by inducing block in the antegrade or retrograde or both limbs of the reentrant circuit and was shown to have significant depressant effects on both antegrade and retrograde AV nodal conduction and refractory periods.