Long-term intracoronary ethanol administration electrophysiologic and morphologic effects.

The long-term intracoronary infusion of ethanol was used to evaluate the potential of ethanol to produce myocardial injury and cardiac rhythm disturbances. In 22 dogs, electrophysiologic testing was performed 48 hr after cessation of alcohol administration. Multiple premature ventricular beats occurred spontaneously in 3 dogs with spontaneous sustained monomorphic ventricular tachycardia observed in 1 dog. Provocative ventricular pacing produced ventricular tachycardia lasting 20 or more beats in 13 animals with sustained tachycardia observed in 3 animals. Provocative ventricular pacing in the presence of lidocaine or epinephrine produced sustained ventricular tachycardia in an additional 4 dogs. The electrophysiologic properties of Purkinje fibers from the zone receiving ethanol were altered when compared to the control zone. The resting membrane potential was decreased (-76 +/- 2 mV vs. -85 +/- mV, p less than 0.001) with a decrease in action potential amplitude (91 +/- 4 vs. 109 +/- 2 mV, p less than 0.001) and phase 0 upstroke (231 +/- 27 vs. 456 +/- 25 V/sec, p less than 0.02). Prolonged refractoriness was observed in the ethanol zone without a prolongation of action potential duration. Intramural lesions observed within the left circumflex distribution varied from focal acute myofibrillar degeneration and necrosis to severe local scarring. The data suggest that intracoronary ethanol administration at human abuse levels of blood alcohol concentrations produces histologic and electrophysiologic injury in the canine heart. The electrophysiologic ch changes provide a substrate sufficient for the induction and maintenance of ventricular arrhythmia.