Effect of propranolol, procainamide, and lidocaine on ventricular automaticity and reentry in experimental myocardial infarction.

The importance of two arrhythmogenic mechanisms, ventricular reentry and automaticity, was assessed after coronary ligation in 35 cats. Automaticity was estimated by the frequency of ventricular escape beats after intravenous acetylcholine, and reentry was estimated by the number of repetitive beats induced by premature ventricular stimuli. Increased automaticity only was present after coronary ligation in two studies; increased reentry only was noted in 24; and both increased automaticity and reentry were seen in nine studies. Incremental doses of lidocaine (2-4 mg/kg), propranolol (0.1-0.3 mg/kg), or procainamide (5-15 mg/kg) consistently returned automaticity to normal. Procainamide abolished repetitive beats in 12 of 13 studies, propranolol did so in eight of 11, but lidocaine did so in only six of 17. Repetitive beats actually increased in six studies after lidocaine, at a time when lidocaine blood levels were in the lower therapeutic range. A persistent arrhythmia appeared after coronary ligation in 12 studies; in 10 the disappearance or persistence of the arrhythmia after drug administration matched the disappearance or persistence of repetitive beats. We conclude that both reentry and increased ventricular automaticity appear during myocardial infarction but that reentry seems of greater importance in the genesis of arrhythmias. These drugs are more reliable in normalizing automaticity than in abolishing reentry; the failure of a drug may thus be related to its failure to abolish reentry. Moreover, lidocaine may accentuate ventricular reentry, especially at the lower blood levels.