Effects of Procainamide on Atrioventricular Nodal Re-entrant

amide 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 con-duction, manifest by increase in mean ± SEM ventricular paced cycle length (CL) producing V-A block from 5 295 ± 25 to 385 ± 17 msec (P < 0.001). Antegrade fast and slow pathway properties were unchanged with procainamide. Eleven of the 14 patients 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 ELECTROPHYSIOLOGICAL STUDIES have dem-onstrated atrioventricular (A-V) nodal re-entrance to be the most common mechanism of paroxysmal supraventricular tachycardia (PSVT).1-8 The ability to induce and terminate A-V nodal re-entrant PSVT in the catheterization laboratory has allowed evaluation of drug effects on induc-tion of this arrhythmia.3 4-1 Previous studies have been concerned with the effects of intravenous ouabain, propranolol, and verapamil on the induction of A-V nodal re-entrant PSVT. Both quinidine and procainamide have been recom-mended for treatment of the acute attack and for preven-tion of PSVT.12 Despite these recommendations, little is known about the effects of these agents upon the induction and maintenance of A-V nodal re-entrant PSVT. In this study, we thus examine the acute electrophysiological effects of procainamide on induction and maintenance of A-V nodal re-entrant PSVT. In addition, observations are made concerning the effects of procainamide on antegrade and retrograde A-V nodal fast and slow pathway proper-ties.3 ' , 13-2