Abstract

Procaine amide, the amide analogue of procaine, is relatively stable in the body since it is not affected by the enzyme which catalyzes the rapid hydrolysis of procaine. It is rapidly and completely absorbed from the gastrointestinal tract. Plasma levels in man decline only 10 to 20 per cent per hour. Metabolic transformation accounts for part of the decrease but urinary excretion accounts for the larger part. Organ tissues reversibly localize considerable amounts of the drug which are released to the plasma as the drug is lost by metabolic transformation or urinary excretion.

Procaine amide is an effective agent against ventricular arrhythmias. It protects dogs from arrhythmias produced by epinephrine during cyclopropane anesthesia. It suppresses ventricular premature contractions for variable periods in conscious humans. By means of the drug, sustained attacks of ventricular tachycardia have been successfully terminated in thirteen of fifteen patients.

The drug does not usually revert the arrhythmia in chronic auricular flutter and fibrillation but merely slows the auricular rate.

The drug is relatively non-toxic. On intravenous administration in therapeutic dosage, it does not cause the central nervous system stimulation typical of procaine in conscious subjects. With intravenous administration there may be a moderate, though transient, hypotension. In some cases of prolonged ventricular tachycardia where the arterial pressure is low, procaine amide causes a further fall, which disappears promptly with the termination of the tachycardia. Untoward effects have not been seen with daily oral dosage maintained up to three months.

Procaine amide seems more effective and less toxic than quinidine for the treatment of ventricular arrhythmias.