Electrophysiologic mechanisms of adverse effects of class I antiarrhythmic drugs (cibenzoline, pilsicainide, disopyramide, procainamide) in induction of atrioventricular re-entrant tachycardia

Summary

We evaluated the electrophysiological mechanisms of adverse effects of class I antiarrhythmic drugs (cibenzoline in seven patients, pilsicainide in two, and disopyramide in two, and procainamide in three) in the induction of orthodromic atrioventricular re-entrant tachycardia (AVRT). In 14 patients (10 males, 4 females; mean age 37±18 years) who had inducible AVRT despite the administration of class I drugs, electrophysiological effects of class I antiarrhythmic drugs were evaluated using programmed electrical stimulation techniques. In 4 out of 6 patients with a manifest accessory pathway, class I drugs induced unidirectional conduction block of the accessory pathway (antegrade conduction block associated with preserved retrograde conduction) and enhanced the induction of AVRT with atrial extrastimulation. In eight patients with a concealed accessory pathway, the outward or inward expansion of the tachycardia induction zone was observed in patients who had greater prolongation of the conduction time than the refractory period of the retrograde accessory pathway after class I drugs. During ventricular extrastimulation, the induction of bundle branch reentry after class I drugs initiated the AVRT in patients with either manifest or concealed accessory pathways. We conclude that the adverse effects of class I drugs are mainly due to induction of unidirectional retrograde conduction of the manifest accessory pathway and the greater prolongation of the retrograde conduction time of the concealed accessory pathway than the refractory period, regardless of the subclassification of class I drugs.