Mechanisms of verapamil-induced conduction block in anomalous atrioventricular bypass tracts

Abstract

Verapamil, a calcium channel blocking agent, has been demonstrated to have depressive effects on the atrioventricular (AV) node but not anomalous AV bypass tracts. Of 39 patients with AV reciprocating tachycardia utilizing left-sided bypass tracts for retrograde conduction, intravenous infusion of verapamil (0.15 mg/kg) terminated the tachycardia in 31 patients. Verapamil interrupted the tachycardia circuit by inducing retrograde conduction block in the bypass tract rather than the AV node in 5 of these 31 patients. Electrophysiologic studies in these five patients revealed that verapamil-induced conduction block in the bypass tract could be accounted for by two distinctly different mechanisms. In three patients, verapamil induced alternating slow and fast AV nodal conduction resulting in alternating long and short cycle lengths during the tachycardia; consequently, development of the Ashman phenomenon in the bypass tract terminated the tachycardia. In the remaining two patients, the bypass tract exhibited properties similar to those of the AV node; verapamil prolonged the effective refractory period of the bypass tract, thereby terminating the tachycardia. Thus, depending on the functional properties of the bypass tract, verapamil may interrupt an AV reciprocating tachycardia circuit by exerting either a direct or indirect depressive action on the bypass tract.