COMPARATIVE ELECTROPHYSIOLOGIC EFFECTS OF INTRAVENOUS AND ORAL PROCAINAMIDE IN PATIENTS WITH SUSTAINED VENTRICULAR ARRHYTHMIAS

[摘要] Thirty-three patients with sustained ventricular arrhythmias underwent electrophysiologic testing after i.v. and again after oral procainamide administration. Two groups were identified: group 1 included 15 patients with concordant serum procainamide concentrations with less than a 3 .mu.g/ml difference after i.v. (mean 8.6 .+-. 2.7) and oral (mean 8.8 .+-. 2.7) procainamide administration, with mean N-acetylprocainamide administrations of 1.0 .+-. 0.6 and 6.2 .+-. 2.8 .mu.g/ml, respectively. Group 2 included 18 patients with discordant serum procainamide concentrations after i.v. (mean 9.5 .+-. 5.9 .mu.g/ml) and oral (mean 14.1 .+-. 5.2 .mu.g/ml) procainamide, with mean N-acetylprocainamide concentrations of 0.9 .+-. 0.5 and 10.7 .+-. 5.7 .mu.g/ml, respectively. In group 1, response to programmed stimulation was the same after i.v. and oral procainamide administration, with no inducible ventricular arrhythmia in 5 of 15 patients. In group 2, 3 of 18 patients had no inducible arrhythmia after i.v. compared with 7 of 18 patients after oral procainamide administration. There was a different response to programmed stimulation after oral compared with i.v. procainamide in 6 of 18 patients in group 2 but in none of 15 patients in group 1 (P = 0.02). The effective procainamide concentration was greater than the ineffective concentration in 5 of the 6 patients with a discordant response, and the effective route of administration was oral in 5 of the 6 patients. The change in ventricular refractoriness in group 1 was similar after i.v. (28 .+-. 23 ms) and oral (29 .+-. 19 ms) procainamide, whereas in group 2, refractoriness was increased more after oral (33 .+-. 21 ms) than i.v. (20 .+-. 17 ms) procainamide administration and paralleled the difference in procainamide concentration. Evidently, i.v. procainamide closely predicts the electrophysiologic effects of oral procainamide when similar serum procainamide concentrations are achieved, and N-acetylprocainamide contributes little to the electrophysiologic effects of procainamide at the observed concentrations. If i.v. procainamide fails to prevent ventricular arrhythmia induction, repeat testing to determine the effect of oral therapy appears to be indicated only if increased procainamide serum concentrations of at least greater than 3 .mu.g/ml can be achieved.