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Effect Of Procaine Amide, Quinidine, And Ajmaline In The Wolff-Parkinson-White Syndrome

HEIN J.J. WELLENS, DIRK DURRER

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Using the single test stimulus method, atrioventricular (A-V) conduction, ventriculo-atrial conduction, the refractory period of right atrium and right ventricle, and the mechanism of tachycardia were studied in 16 patients with the Wolff-Parkinson-White syndrome. The same studies were repeated at least four times during the hour following intra-atrial administration of 10 mg procaine amide/kg body weight (six patients), 4 mg quinidine gluconate/kg body weight (six patients), or 50 mg ajmaline (four patients). Following procaine amide the refractory period of the accessory pathway increased in all patients, with temporary complete block of the accessory pathway in four patients. There was an increase in H-V interval during antegrade conduction through the A-V node-His pathway. The effective refractory period of the A-V node showed no appreciable change. In three of four patients tachycardia could not be produced by pacing in contrast to the pacing effect found prior to procaine amide. Quinidine gluconate increased the refractory period of the accessory pathway in four patients, causing temporary complete block in two patients. The H-V interval increased in three patients. The refractory period of the A-V node showed no change in three patients, lengthened in one, and shortened in the other two. Quinidine gluconate prevented pacing-induced initiation of tachycardia in two out of four patients. Ajmaline * increased the refractory period of the accessory pathway in all four patients, with temporary complete block in three patients. The H-V interval also lengthened. No change was observed in the refractory period of the A-V node. Ajmaline prevented initiation of tachycardia in one out of two patients. In the other patient tachycardias could still be initiated despite disappearance of pre-excitation during atrial pacing. In one patient in each group tachycardia could be produced during pacing following drug administration where no tachycardia could be produced under control conditions. In two patients re-entry in the A-V node during ventricular pacing caused this phenomenon. In the other patient administration of the drug prevented atrial re-entry during atrial pacing. This re-entrant beat had previously created refractoriness in the atrial part of the tachycardia pathway. The changes following procaine amide, quinidine gluconate, and ajmaline were clearly short term; their effects disappeared after one hour in 15 of the 16 patients studied.