Does mexiletine have a preferential action (versus healthy myocardium) on the reentrant circuit of ventricular tachycardia?

Abstract

The preferential action (in diseased versus healthy myocardium) of class 1a antiarrhythmic but not class 1b agents has been demonstrated on the reentrant circuit. This study assessed the effect of mexiletine on the fragmented electrogram at the origin of ventricular tachycardia (VT) associated with underlying heart diseases. In 11 consecutive patients, VT of the same morphology was induced, and entrained with rapid pacing during, before, and after mexiletine. The width of the fragmented electrogram, VT cycle length, and the block cycle length (defined as the longest VT-interrupting paced cycle length during entrainment) were measured before and after mexiletine and the findings compared. The effective refractory period (ERP) was measured at the pacing site (normal myocardium) and at the VT origin. To assess the preferential action of mexiletine, changes in fragmented electrogram were examined in relation to QRS duration (defined as the index of global intraventricular conduction). After mexiletine, VT cycle length, block cycle length, and fragmented electrogram were prolonged significantly. The QRS duration was also prolonged significantly, but this change was significantly smaller than that in VT cycle length or in the width of the fragmented electrogram. There was no significant change in ERP either at the pacing site or at the VT origin. Mexiletine was confirmed to preferentially depress conduction in the diseased myocardium at the VT origin, and this action occurred at a higher rate during VT.