The electrophysiologic actions of pirmenol, an investigational class I antiarrhythmic agent, were evaluated in eight anesthetized dogs, 5 to 10 days after anterior myocardial infarction. Before administration of the drug, programmed ventricular stimulation failed to initiate nonsustained or sustained ventricular tachyarrhythmias (VT) in any of the postinfarction dogs. After the cumulative administration of 2.5, 5.0, and 10.0 mg/kg pirmenol, programmed stimulation initiated sustained VT in six of the eight postinfarction dogs tested, with one additional dog responding with reproducible nonsustained VT (15 to 20 monomorphic complexes) after pirmenol administration. Only one of eight postinfarction dogs tested remained noninducible throughout the pirmenol dosing schedule. Administration of pirmenol tended to increase ventricular excitation thresholds, relative (p less than 0.05 after 10 mg/kg) and effective refractory periods in ischemically injured ventricular myocardium, and increased the difference or disparity in relative (p less than 0.05 after 5.0 and 10.0 mg/kg) and effective (p less than 0.01 after 2.5, 5, and 10, mg/kg) refractory periods between ischemically injured and normal noninjured ventricular myocardium. These findings suggest a potential for the provocation or aggravation of ventricular arrhythmias by pirmenol in the setting of recent myocardial infarction.