Procainamide: clinical pharmacology and efficacy against ventricular arrhythmias.
Procainamide (PA) has been a mainstay of treatment against acute and chronic supraventricular and ventricular arrhythmias for more than 30 years. PA's clinical pharmacology has been studied extensively and its bioavailability (75-95%); volume of distribution (1.5-2.5 liters per kg), plasma protein-binding (15-25%), half-time for elimination (3-7 hours), and metabolism are known. PA's efficacy against acute ventricular arrhythmias and chronic stable VPDs is associated with plasma drug concentrations of 4 to 10 micrograms per ml; but much higher plasma concentrations may be required against sustained ventricular arrhythmias. From 30 to 60% of a PA dose is excreted as the metabolite, N-acetylprocainamide (NAPA), and PA's metabolism is determined genetically (fast or slow acetylation phenotype). Studies in patients with VPDs indicate that NAPA is also antiarrhythmic, although the contribution of NAPA to the antiarrhythmic effect after PA is not known. Studies in patients with the systemic lupus-like syndrome from PA show that NAPA is not associated with this. Investigations comparing efficacy and adverse effects of PA with those of new antiarrhythmic agents available for clinical trials are indicated in the future.
D000120:Acecainide / Q000494:pharmacology; D000284:Administration, Oral; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000188:drug therapy*; D004562:Electrocardiography; D006321:Heart / Q000187:drug effects; D006801:Humans; D007275:Injections, Intravenous; D007700:Kinetics; D008180:Lupus Erythematosus, Systemic / Q000139:chemically induced; D011342:Procainamide / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use*
D000120:Acecainide; D011342:Procainamide