The effect of procaine amide (pronestyl) in clinical auricular fibrillation and flutter.

Procaine amide (Pronestyl) was administered to patients with auricular fibrillation and flutter in an attempt to restore sinus rhythm. Thirteen of 20 patients with auricular fibrillation had sinus rhythm re-established. Several of the patients who were not converted with procaine amide were later restored to sinus rhythm with quinidine. OR MANY YEARS the restoration of sinus rhythm in patients with auricular fibrillation and auricular flutter has been limited primarily to the use of quinidine and its allies. Other agents have occasionally been used without too satisfactory clinical effects. In animal experiments, procaine hydro-chloride has been shown to exert a markedly depressant action on conduction of the cardiac impulse'. Procaine hydrochloride has been employed locally and parenterally in treating cardiac arrhythmias arising during surgical procedures in anesthetized patients and has been tried in various clinical instances of spontaneous cardiac irregularities'. While sometimes useful under the former circumstances, its central stimulating effects have precluded its application in the unanesthetized patient. Recently a procaine derivative, the amide analogue of procaine has been introduced3. This agent, procaine amide (Pronestyl), is free of central nervous stimulating effects in the dosages used and is applicable in unanesthetized patients. The experimental data of Newman and Clark4' demonstrated that procaine amide exerts a slowing effect on conduction and produces a decrease of irritability of auricular muscle of the rabbit and the dog. These observations have led us to explore the sphere of usefulness of the drug in the conversion of 41 auricular fibrillation and flutter to sinus rhythm in clinical instances of these arrhythmias. MATERIAL AND METHODS Our material and the therapy used are listed in table 1. There were 20 patients with auricular fibrillation; of these, 13 had chronic auricular fibril-lation. The latter term was arbitrarily applied to those patients who were known to have auricular fibrillation for two weeks or more. Their ages ranged from 37 to 71 years and the duration of the ar-rhythmia from 16 days to more than three years. Five of these patients had rheumatic heart disease and seven had hypertensive and/or arteriosclerotic heart disease. Of seven patients with paroxysmal auricular fibril-lation, five had hypertensive and/or arteriosclerotic heart disease and one patient (case 2) with no previous evidence of heart disease developed au-ricular fibrillation one day following an appendec-tomy. All three patients with auricular flutter had arteriosclerotic heart disease; in two the auricular flutter was paroxysmal while the duration of the arrhythmia …