Programmed electrical stimulation was used to evaluate the electrophysiologic and antiarrhythmic actions of
methyl lidocaine in both conscious and anesthetized dogs, 4-7 days after
myocardial infarction. When administered to animals demonstrating sustained
ventricular tachycardia (n = 6),
methyl lidocaine (5 and 10 mg/kg i.v.) prevented the induction of the original
ventricular tachycardia in 2 dogs, and in the remaining 4 dogs slowed the
tachycardia (cycle length 163 +/- 18 ms vs. 198 +/- 11 and 219 +/- 11 ms, respectively, p less than 0.05). New morphologic forms of sustained
tachycardia were observed after
drug administration in 4 of 6 experiments. When administered to animals developing only
nonsustained ventricular tachycardia or no arrhythmias with programmed stimulation,
methyl lidocaine administration enabled programmed stimulation to produce monomorphic sustained
ventricular tachycardia in 10 of 13 experiments. The
drug increased activation delays in both normal and ischemically injured epicardium, with larger activation delays always observed in ischemically injured tissue. The
drug increased refractoriness in ischemically injured myocardium without altering refractoriness in normal tissue. The data suggest that the depression of conduction and prolonged refractoriness produced by
methyl lidocaine in ischemically injured tissue may extinguish or slow some forms of ventricular
arrhythmia while promoting the formation of new reentry pathways.