Paradoxical effects of procainamide--facilitation of the induction of sustained reciprocating tachycardia after procainamide administration in Wolff-Parkinson-White syndrome.

Abstract

The effects of procainamide on the refractory periods of the accessory and normal pathways in the antegrade and retrograde directions with reference to the reciprocating tachycardia were studied in 31 patients with Wolff-Parkinson-White (WPW) syndrome. Right atrial, left atrial and right ventricular pacing (incremental pacing and extrastimulus technique) were performed to induce reciprocating tachycardia and to measure antegrade and retrograde effective refractory periods (A-ERP and R-ERP) of the accessory pathway (AP) and the A-V node (AVN). Atrial extrastimulus technique was performed at 2 or more basic cycle lengths and repeated after an intravenous administration of procainamide (600 mg). Prior to the procainamide administration reciprocating tachycardias were induced in 10 of the 31 patients. After procainamide, induction of the tachycardia became impossible in 2 of these 10 patients. In 3 patients, procainamide decreased the tachycardia zone, while procainamide widened the tachycardia zone in the other 4 patients. In the remaining one, procainamide had no significant effect on the tachycardia was induced in 21 of the 31 patients. In 15 of these 21, no tachycardia was induced after procainamide. However, in 6 of the 21 patients, sustained reciprocating tachycardias were induced after procainamide. All reciprocating tachycardias that occurred in these patients were characterized by narrow QRS complexes, and demonstrated circus movement with antegrade conduction via the normal pathway and retrograde conduction via the accessory pathway. In 10 of the 31 patients (32%), induction of the tachycardia by an atrial premature beat after procainamide was shown while prior to its administration no tachycardia could be initiated, or the tachycardia zone was widened on procainamide administration. In these patients, procainamide could not block retrograde conduction over the AP and altered the relationship between the A-ERPAP and the A-ERPAVN by lengthening the A-ERPAP with shortening the A-ERPAVN, i.e., after procainamide the A-ERPAP became longer than the A-ERPAVN, and, by shortening the A-ERPAVN, procainamide did augment the differences in length of the ERP of the 2 A-V pathways, so that sustained reciprocating tachycardia could be induced by atrial stimulation. In conclusion, we consider that in some patients with WPW syndrome procainamide may facilitate the induction of sustained reciprocating tachycardia by prolonging the A-ERPAP and, at the same time, by shortening the A-ERPAVN but by only minimally increasing the R-ERPAP.