THE ANTIARRHYTHMIC EFFECT OF VERAPAMIL ON ATRIOVENTRICULAR REENTRY INTHE WOLFF-PARKINSON-WHITE SYNDROME - A COMPUTER-MODEL STUDY

Verapamil is supposed to suppress the initiation of circus movement su praventricular tachycardia by affecting the atrioventricular node. In electrophysiological tests, programmed stimulation is usually performe d by using the same location for pacing and premature stimulus. Sponta neous ectopic activity starts from a different location than the sinus node and can therefore find altered re-entry conditions. In this stud y a 3D computer model based on Huygen's principle is used for simulati on of the spread of excitation in the human heart in combination with a posterobasal, right or left lateral accessory pathway (AP). The effe ct bf verapamil on properties of the atrioventricular node were modell ed by prolonging the effective refractory period and basal conduction time. For each of the three APs, ectopic foci at the atrial base and b etween sinus node and AP were modelled at various coupling intervals f or investigating re-entrant activation. In the control state (without verapamil) only orthodromic echoes were found. The maximum echo zone ( EZ) range was found near the AP. If stimuli were selected further away from the AP on the atrial basis, the EZ range decreased until no EZ w as found. The EZ range decreased from it's maximum value near the AP, towards the difference of the effective refractory periods between AP and AV-node near the sinus node. Verapamil abolished the EZ in case of a posteroseptal AP. For a lateral AP the administration of verapamil resulted in an orthodromic and antidromic EZ depending on the atrial p remature activation site. A maximum orthodromic EZ was found for prema ture stimuli near the AP. As stimulus site moved away from the AP, the EZ range first decreased continuously to zero leading eventually to a n antidromic EZ. These findings suggest the important influence of the site of premature stimuli with respect to the accessory pathway and A V-node on the inducibility of atrial re-entry.