Lidocaine (10 mg/kg/hour) produced uniform changes in myocardial electrophysiology across the intact porcine heart without altering basal levels of dispersion in repolarization and refractoriness.
Does lidocaine affect spatial dispersion of myocardial repolarization and refractoriness in an intact porcine heart model?
Lidocaine produces uniform changes in myocardial electrophysiology without altering electrical heterogeneity, potentially explaining its lower proarrhythmic risk compared to other sodium channel blockers.
An area of unidirectional conduction block is one requirement for reentrant arrhythmias to occur. Functional block caused by dispersion of repolarization and refractoriness is the most probable mechanism of drug-induced unidirectional conduction block. We assessed the effects of lidocaine on spatial dispersion of myocardial repolarization and refractoriness in the intact porcine heart. Monophasic action potential duration at 90% repolarization, effective refractory period (ERP), and ventricular fibrillation cycle length (VFCL) were measured at two endocardial and one epicardial sites at baseline and during a treatment phase with D5W (n=11) or lidocaine 10 mg/kg/hour (n=12). Dispersion was calculated as the difference between the maximum and minimum values of the three recording sites. Lidocaine produced significant changes in ERP, VFCL, paced QRS duration, and intraventricular conduction time. It did not change basal levels of dispersion in repolarization and refractoriness. Lidocaine produced changes in myocardial electrophysiology that are uniform across the myocardium and thus did not change myocardial electrical heterogeneity. This may be a mechanism of the agent's lower proarrhythmic effects compared with other sodium channel blockers that increase myocardial electrical heterogeneity.
Sims et al. (1997) studied Myocardial electrical heterogeneity (n=23). Lidocaine vs. D5W was evaluated on Spatial dispersion of myocardial repolarization and refractoriness. Lidocaine (10 mg/kg/hour) produced uniform changes in myocardial electrophysiology across the intact porcine heart without altering basal levels of dispersion in repolarization and refractoriness.