[Drug treatment of a trial fibrillation in patients with Wolff-Parkinson-White syndrome].

In 10 patients with ventricular preexcitation (Kent bundle), in whom atrial fibrillation (A.F.) was present, the effect of some common antiarrhythmic drugs on the conduction through the anomalous pathway, and on the ventricular rate was estimated. Procainamide caused transient complete block in the accessory pathway (disappearance of the aberrant QRS) and marked reduction of the average ventricular rate in all instances. Lidocaine caused incomplete block in the accessory pathway (reduction of the number of the aberrant QRS) and significant reduction of the average ventricular rate in all tested subjects. Amiodarone slowed the ventricular rate (increase of the average and minimum R-R intervals between wide QRS complexes) in two patients, but it did not block the anomalous pathway (all QRS complexes remained aberrant); whereas in 1 patient the ventricular rate became faster and regular and the patient had syncope, while the QRS remained always aberrant. This response was probably due to the change of A.F. into atrial flutter with atrio-ventricular conduction through the anomalous pathway only. Digitalis increased the average ventricular rate and shortened the minimum R-R interval between aberrant QRS complexes 3 out of 3 times. On the basis of our experience and of the data in the literature, we conclude that, in the management of A.F. in patients with W.P.W. syndrome:--the most effective drugs are those of the 1st group of Singh and Hauswirth classification (especially Procainamide and Ajmaline);--Lidocaine is less effective, but not ineffective and its utilization may be recommended whenever the previous drugs may be hazardous;--Amiodarone, although capable of modifying the electrophysiologic properties both of the anomalous pathway and of the A-V node, seems to be less reliable;--the drugs which influence only the A-V node (Verapamil, beta-Blockers, etc.) are quite ineffective;--finally, the Digitalis is not suitable because this drug increases the ventricular rate by decreasing the effective refractory period (ERP) of the anomalous pathway.