Author + information
- Received April 10, 1984
- Revision received June 12, 1984
- Accepted June 22, 1984
- Published online December 1, 1984.
- Francis E. Marchlinski, MD, FACC*,1,2,
- Alfred E. Buxton, MD, FACC1,2,
- Joseph A. Vassallo, MD1,
- Harvey L. Waxman, MD, FACC1,
- Dennis M. Cassidy, MD1,3,
- John U. Doherty, MD1 and
- Mark E. Josephson, MD, FACC1
- ↵*Address for reprints:Francis E. Marchlinski, MD, Hospital of the University of Pennsylvania, Ravdin Building, Room 656B, 3400 Spruce Street. Philadelphia, Pennsylvania 19104.
Thirty-three patients with sustained ventricular arrhythmias underwent electrophysiologic testing after intravenous 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 μg/ml difference after intravenous (mean 8.6 ± 2.7) and oral (mean 8.8 ± 2.7) procainamide administration, with mean N-acetylpro-cainamide concentrations of 1.0 ± 0.6 and 6.2 ± 2.8 μg/ml, respectively. Group 2 included 18 patients with discordant serum procainamide concentrations after intravenous (mean 9.5 ± 5.9 μ/ml and oral (mean 14.1 ± 5.2 μ/ml) procainamide, with mean iV-acetylprocainamide concentrations of 0.9 ± 0.5 and 10.7 ± 5.7 μ/ml, respectively.
In group 1, response to programmed stimulation was the same after intravenous 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 intravenous compared with 7 of 18 patients after oral procainamide administration. There was a different response to programmed stimulation after oral compared with intravenous procain- amide 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 five of the six patients with a discordant response, and the effective route of administration was oral in five of the six patients. The change in ventricular refractoriness in group 1 was similar after intravenous (28 ± 23 ms) and oral (29 ± 19 ms) procainamide, whereas in group 2, refractoriness was increased more after oral (33 ± 21 ms) than intravenous (20 ± 17 ms) procainamide administration and paralleled the difference in procainamide concentration.
In conclusion, intravenous 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 intravenous 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 μg/ml can be achieved.
- Received April 10, 1984.
- Revision received June 12, 1984.
- Accepted June 22, 1984.
- American College of Cardiology Foundation