LIDOCAINE DOES NOT AFFECT MYOCARDIAL ELECTRICAL HETEROGENEITY - IMPLICATIONS FOR LOW PROARRHYTHMIC ACTIONS

An area of unidirectional conduction block is one requirement for reen trant arrhythmias to occur. Functional block caused by dispersion of r epolarization and refractoriness is the most probable mechanism of dru g-induced unidirectional conduction block. We assessed the effects of lidocaine on spatial dispersion of myocardial repolarization and refra ctoriness in the intact porcine heart. Monophasic action potential dur ation at 90% repolarization, effective refractory period (ERP), and ve ntricular fibrillation cycle length (VFCL) were measured at two endoca rdial and one epicardial sites at baseline and during a treatment phas e with D5W (n=11) or lidocaine 10 mg/kg/hour (n=12). Dispersion was ca lculated as the difference between the maximum and minimum values of t he three recording sites. Lidocaine produced significant changes in ER P, VFCL, paced QRS duration, and intraventricular conduction time. It did not change basal levels of dispersion in repolarization and refrac toriness. Lidocaine produced changes in myocardial electrophysiology t hat are uniform across the myocardium and thus did not change myocardi al electrical heterogeneity. This may be a mechanism of the agent's lo wer proarrhythmic effects compared with other sodium channel blockers that increase myocardial electrical heterogeneity.