A Study of the Effect of Procaine Amide Hydrochloride in Supraventricular Arrhythmias

Abstract

The effect of the intravenous administration of procaine amide in 25 patients with supraventricular arrhythmias is reported. The data, including six conversions of auricular fibrillation, indicate a pronounced effect of this drug on the auricles as well as on the heart as a whole. Special attention is directed to the finding of frequent and undesirable electrocardiographic and hypotensive effects of this drug.

The peri‐operative management of atrial fibrillation

“…Procainamide is negatively inotropic, especially in patients with left ventricular dysfunction, and may also cause conduction disturbances. It has been used to convert atrial fibrillation for over 40 years [48]. In two uncontrolled studies, an intravenous infusion of procainamide was effective in restoring sinus rhythm in 43% and 58% of patients [49,50].…”

The Effect of Procaine Amide (Pronestyl) in Clinical Auricular Fibrillation and Flutter

“…However, six of the 13 patients with chronic auricular fibrillation were also restored to sinus rhythm. This result is somewhat better than anticipated since a number of observers5' 7, [8][9][10][11][12][13] have reported the absence of conversions in patients with chronic auricular fibrillation given intravenous procaine amide. It is quite likely that the greater success in more recent investigations using oral procaine amidels' 15 and in the present study was a result of the higher dosage schedules employed.…”

Iatrogenic ‘torsade de pointes’ ventricular tachycardia

“…The drugs which, so far, have been implicated to induce torsade de pointes ventricular tachycardia are cardioactive agents such as quinidine (Rainier-Pope et al, 1962;Seizer andWray, 1964), procainamide (McCord andTaguchi, 1951;Castellanos and Salhanick, 1967), and lignocaine (Krikler and Curry, 1976a), antianginal drugs such as prenylamine (Puritz et al, 1977) and amiodarone (Bens et al, 1973), psychotropic agents (Fowler et al, 1976), such as phenothiazines (chlorpromazine, thioridazine, trifluoperazine, mesoridazine) and tricyclic antidepressants (amitriptyline, imipramine, protriptiline, nortriptyline,) diuretics, corticosteroids and glycyrrhizin (Bens et al, 1973), which induce hypokalaemia. Torsade de pointes can complicate (Krikler and Curry, 1976) myocardial ischaemia (Prinzmetal's variant angina, myocardial infarction), electrolytic deficits (hypokalaemia, hypomagnesaemia), acquired heart disease (myocarditis, coronary arteriosclerosis), slow basic rhythm (sino-atrial disease, high degree AV block), electrical ventricular stimulation and congenital disorders with deafness (Jervell-Lange-Nielsen syndrome, Romano-Ward-Barlow syndrome) with apparent (or only after exercise as a forme fruste) QT prolongation (Bernuth et al, 1973).…”