Electrophysiological and cardiovascular effects of pirmenol, a new class 1 antiarrhythmic drug

Pirmenol, a new antiarrhythmic agent, has been studied in the pithed rat and in the sinoatrial (SA) node, atrium, atrioventricular (AV) node, Purkinje cells, and ventricular muscle of the isolated rabbit heart. It resembles disopyramide chemically and in its electrophysiologic effects. Pirmenol decreased the maximum rate of depolarization (MRD) and overshoot potential in isolated rabbit atrium, Purkinje cells, and ventricle. Pirmenol caused bradycardia in pithed rats and isolated rabbit SA nodes. In the latter, repolarization was delayed, but there was little change in MRD or in the slope of the slow diastolic depolarization. Like disopyramide, but unlike lidocaine, pirmenol lengthened APD in all cardiac tissues studied. The above effects were dose-related and were reversed on washout. Pirmenol did not lengthen conduction time within the AV node. Unlike disopyramide, pirmenol had no negative inotropic action, and did not alter the relation between contractile force and extracellular calcium concentration. This suggests, as does the absence of effect on sinoatrial MRD or AV conduction, that pirmenol does not block calcium channels.