Effects of procainamide on atrioventricular nodal re-entrant paroxysmal tachycardia.

Abstract

Electrophysiological effects of 750 mg i.v. procainamide were studied in 14 patients with dual pathway atrioventricular (A-V) nodal re-entrant paroxysmal tachycardia (PSVT). All patients utilized an A-V nodal slow pathway for antegrade and an A-V nodal fast pathway for retrograde conduction during PSVT. In all 14 patients, procainamide depressed retrograde fast pathway conduction, manifest by increase in mean .+-. SEM [standard error of the mean] ventricular paced cycle length (CL) producing V-A block from .ltoreq. 295 .+-. 25 to 385 .+-. 17 ms (P < 0.001). Antegrade fast and slow pathway properties were unchanged with procainamide. Of the 14 patients, 11 had induction of sustained PSVT before procainamide. Eight of these lost ability to induce or sustain PSVT after procainamide, reflecting depression of retrograde fast pathway conduction with either absence of atrial echoes (4) or induction of nonsustained PSVT, with termination of PSVT occurring after QRS (retrograde block in fast pathway) (4). In 3 of these 11 patients, sustained PSVT was inducible before and after procainamide (mean CL of 395 .+-. 38 and 395 .+-. 40, respectively). Three patients had induction of nonsustained PSVT before procainamide. In 2, induction of sustained PSVT occurred after procainamide due to enhanced antegrade slow pathway conduction, while in the other PSVT remained nonsustained. Procainamide inhibited induction of sustained A-V nodal re-entrant PSVT in most patients, reflecting selective depression of retrograde A-V nodal fast pathway conduction. In a minority of patients, vagolytic effects of procainamide potentiated induction of sustained PSVT.