Procainamide



Electrophysiological effects of procainamide re­semble those of quinidine. Procainamide exerts less intense anticholinergic effects than disopyr-amide and quinidine. It has a major metabolite, N-acetyl procainamide (NAPA), that exhibits much weaker electrophysiological effects than does procainamide. In patients with renal failure, NAPA levels increase more than procainamide levels and must be monitored to prevent toxicity. A sustained-release form is available that can be administered every 6 hours instead of every 3 to 4 hours; the total daily dose of both procainamide and the sustained release form of procainamide should be the same. Procainamide depresses my­ocardial contractility only in high doses. It may produce peripheral vasodilation, probably via a mild ganglionic blocking action. The clinical in­dications for procainamide are very similar to those for quinidine. Although the effects of both drugs are similar, an arrhythmia not suppressed by one drug may be suppressed by the other. Con­duction disturbances and ventricular tachyar­rhythmias similar to those caused by quinidine can occur.

Procainamide does not increase serum digoxin levels. A systemic lupus erythematosus-like syn­drome including arthralgia, fever, pleuropericar-ditis, hepatomegaly, and hemorrhagic pericardial effusion with tamponade has been described. The brain and kidneys are usually spared and hema­tologic complications are unusual. Sixty to 70 per cent of patients who receive procainamide de­velop antinuclear antibodies, but clinical symp­toms occur in 20 to 30 per cent and are reversible when the drug is stopped. A positive ANA is not necessarily a reason to stop procainamide ther­apy.