Effect of Procainamide, Mexiletine, and Propranolol on Ventricular Activation Time Recorded at Cardiac Mapping in Chronic Canine Myocardial Infarction

Delayed potentials detected during sinus rhythm appear to be markers for ventricular tachyarrhyth mias associated with ch ronic myocardial infarction. This study investigated whether intravenous Class I and Class II antiarrhythmic drugs could affect delayed potentials detected at cardiac mapping in dogs studied 1–2 weeks after anterior myocardial infarction. Procainamide at therapeutic serum levels (17–34 μmol/L) caused prolongation of delayed potentials (first degree block), the mean change in duration of ventricular activation being + 19.4 ± 5.0 msec (n = 4, p <0.05). At serum levels above the therapeutic range, procainamide caused first degree block in delayed potentials in three of six animals tested (50%), second degree block (Wenckebach, 2:1 or 3:1 block) in another two animals, and third degree block (complete abolition of delayed potentials) in the remaining animal. Mexiletine at therapeutic serum levels (3.5–9.0 μmol/L, caused no significant change in delayed potential duration (+3.1 ± 5.7 msec, n = 4). At serum levels above the therapeutic range, first degree block occurred in four of five animals tested (80%), there being no change in the fifth animal. After propranolol (0.2 mg/kg), there was no significant change in delayed potential duration (−2.5 ± 2.5 msec, n = 4). conclusion: (1) at standard doses, mexiletine and propranolol have no effect on delayed potentials, but procainamide causes first degree block; (2) at serum levels above the therapeutic range, mexiletine typically causes first degree block, while procainamide causes either first degree or high grade block; (3) ventricular tachyarrhythmias may still be inducible after drugs if delayed potentials persist unchanged or with first degree block.