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Recent studies that show a depressant effect of procainamide (PA) on retrograde conduction in patients with atrioventricular (AV) nodal reentrant tachycardia (RT) have suggested possible incorporation of AV nodal bypass tracts. Electrophysiologic effects of i.v. PA, 10 mg/kg, on retrograde AV nodal conduction were examined in 13 patients without RT, demonstrable AV nodal refractory period curves, or accessory pathways. Ventriculoatrial (VA) conduction was recorded before and after PA using intracardiac electrograms, incremental ventricular pacing and extrastimulation. With incremental pacing during the control, VA block occurred at a mean cycle length (CL) of 364.6 +/- 87.9 msec. After PA, VA conduction was abolished in five of 13 patients due to onset of retrograde block in the AV node; in seven of 13, VA block occurred at a longer paced CL after PA (344.2 +/- 51.2 msec vs 477.1 +/- 93.2 msec). In one patient, PA did not affect VA conduction. PA invariably produced prolongation in the VA interval at comparable CL of pacing. With ventricular premature stimulation, the retrograde H2A2 intervals during the control period were short (less than 50 msec) in seven of 13, intermediate (60-100 msec) in three of 13 and long (greater than 100 msec) in three of 13 cases. PA either abolished H2A2 conduction (H2 but no A2) or prolonged the H2A2 intervals by 5-20 msec in most cases in this series. The data suggest that i.v. PA almost uniformly depresses retrograde AV nodal conduction in the intact human heart. This depressant response to PA is not indicative of presence of partial or complete AV nodal bypass tracts.

Procainamide and retrograde atrioventricular nodal conduction in man.