Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure

K. M. Kessler, D. S. Kayden, D. M. Estes, P. L. Koslovskis, R. Sequeira, R. G. Trohman, A. R. Palomo, Robert J Myerburg

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Abnormal procainamide pharmacokinetics (prolonged half-life and decreased volume of distribution) and pharmacodynamics (decreased threshold for the suppression of premature ventricular complexes) have been suggested in patients with acute myocardial infarction or congestive heart failure, or both. To better define procainamide kinetics, 37 patients in the acute care setting received intravenous procainamide (25 mg/min, median dose 750 mg) with peak and hourly blood samples taken over 6 hours. Compared with the 10 control patients, the 12 patients with acute myocardial infarction and the 15 patients with congestive heart failure had normal procainamide pharmacokinetics with respect to half-life (2.3 ± 1.0, 2.5 ± 0.9 and 2.6 ± 0.8 hours, respectively), volume of distribution (1.9 ± 0.7, 1.8 ± 0.4 and 1.8 ± 0.5 liters/kig, respectively), clearance (11.3 ± 7.5, 9.3 ± 3.6 and 9.1 ± 3.5 ml/min per kg, respectively) and unbound drug fraction (66 ± 9, 66 ± 9 and 69 ± 4%, respectively). Low thresholds for greater than 85% premature ventricular complex suppression were confirmed in these patients (median 4.7 μg/ml in patients with acute myocardial infarction and 3.3 μg/ml in patients with congestive heart failure). Thus, differences in the response of premature ventricular complexes to procainamide reflect electropharmacologic differences dependent on clinical setting rather than pharmacokinetic abnormalities. Furthermore, the reduction of procainamide dosing in patients with acute myocardial infarction or congestive heart failure, based solely on prior kinetic data, may result in inappropriate antiarrhythmic therapy.

Original languageEnglish
Pages (from-to)1131-1139
Number of pages9
JournalJournal of the American College of Cardiology
Volume7
Issue number5
StatePublished - Jul 9 1986

Fingerprint

Procainamide
Heart Failure
Pharmacokinetics
Myocardial Infarction
Ventricular Premature Complexes
Half-Life

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Kessler, K. M., Kayden, D. S., Estes, D. M., Koslovskis, P. L., Sequeira, R., Trohman, R. G., ... Myerburg, R. J. (1986). Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure. Journal of the American College of Cardiology, 7(5), 1131-1139.

Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure. / Kessler, K. M.; Kayden, D. S.; Estes, D. M.; Koslovskis, P. L.; Sequeira, R.; Trohman, R. G.; Palomo, A. R.; Myerburg, Robert J.

In: Journal of the American College of Cardiology, Vol. 7, No. 5, 09.07.1986, p. 1131-1139.

Research output: Contribution to journalArticle

Kessler, KM, Kayden, DS, Estes, DM, Koslovskis, PL, Sequeira, R, Trohman, RG, Palomo, AR & Myerburg, RJ 1986, 'Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure', Journal of the American College of Cardiology, vol. 7, no. 5, pp. 1131-1139.
Kessler KM, Kayden DS, Estes DM, Koslovskis PL, Sequeira R, Trohman RG et al. Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure. Journal of the American College of Cardiology. 1986 Jul 9;7(5):1131-1139.
Kessler, K. M. ; Kayden, D. S. ; Estes, D. M. ; Koslovskis, P. L. ; Sequeira, R. ; Trohman, R. G. ; Palomo, A. R. ; Myerburg, Robert J. / Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure. In: Journal of the American College of Cardiology. 1986 ; Vol. 7, No. 5. pp. 1131-1139.
@article{d08d24ba893c45e0972ef38b35f80851,
title = "Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure",
abstract = "Abnormal procainamide pharmacokinetics (prolonged half-life and decreased volume of distribution) and pharmacodynamics (decreased threshold for the suppression of premature ventricular complexes) have been suggested in patients with acute myocardial infarction or congestive heart failure, or both. To better define procainamide kinetics, 37 patients in the acute care setting received intravenous procainamide (25 mg/min, median dose 750 mg) with peak and hourly blood samples taken over 6 hours. Compared with the 10 control patients, the 12 patients with acute myocardial infarction and the 15 patients with congestive heart failure had normal procainamide pharmacokinetics with respect to half-life (2.3 ± 1.0, 2.5 ± 0.9 and 2.6 ± 0.8 hours, respectively), volume of distribution (1.9 ± 0.7, 1.8 ± 0.4 and 1.8 ± 0.5 liters/kig, respectively), clearance (11.3 ± 7.5, 9.3 ± 3.6 and 9.1 ± 3.5 ml/min per kg, respectively) and unbound drug fraction (66 ± 9, 66 ± 9 and 69 ± 4{\%}, respectively). Low thresholds for greater than 85{\%} premature ventricular complex suppression were confirmed in these patients (median 4.7 μg/ml in patients with acute myocardial infarction and 3.3 μg/ml in patients with congestive heart failure). Thus, differences in the response of premature ventricular complexes to procainamide reflect electropharmacologic differences dependent on clinical setting rather than pharmacokinetic abnormalities. Furthermore, the reduction of procainamide dosing in patients with acute myocardial infarction or congestive heart failure, based solely on prior kinetic data, may result in inappropriate antiarrhythmic therapy.",
author = "Kessler, {K. M.} and Kayden, {D. S.} and Estes, {D. M.} and Koslovskis, {P. L.} and R. Sequeira and Trohman, {R. G.} and Palomo, {A. R.} and Myerburg, {Robert J}",
year = "1986",
month = "7",
day = "9",
language = "English",
volume = "7",
pages = "1131--1139",
journal = "Journal of the American College of Cardiology",
issn = "0735-1097",
publisher = "Elsevier USA",
number = "5",

}

TY - JOUR

T1 - Procainamide pharmacokinetics in patients with acute myocardial infarction or congestive heart failure

AU - Kessler, K. M.

AU - Kayden, D. S.

AU - Estes, D. M.

AU - Koslovskis, P. L.

AU - Sequeira, R.

AU - Trohman, R. G.

AU - Palomo, A. R.

AU - Myerburg, Robert J

PY - 1986/7/9

Y1 - 1986/7/9

N2 - Abnormal procainamide pharmacokinetics (prolonged half-life and decreased volume of distribution) and pharmacodynamics (decreased threshold for the suppression of premature ventricular complexes) have been suggested in patients with acute myocardial infarction or congestive heart failure, or both. To better define procainamide kinetics, 37 patients in the acute care setting received intravenous procainamide (25 mg/min, median dose 750 mg) with peak and hourly blood samples taken over 6 hours. Compared with the 10 control patients, the 12 patients with acute myocardial infarction and the 15 patients with congestive heart failure had normal procainamide pharmacokinetics with respect to half-life (2.3 ± 1.0, 2.5 ± 0.9 and 2.6 ± 0.8 hours, respectively), volume of distribution (1.9 ± 0.7, 1.8 ± 0.4 and 1.8 ± 0.5 liters/kig, respectively), clearance (11.3 ± 7.5, 9.3 ± 3.6 and 9.1 ± 3.5 ml/min per kg, respectively) and unbound drug fraction (66 ± 9, 66 ± 9 and 69 ± 4%, respectively). Low thresholds for greater than 85% premature ventricular complex suppression were confirmed in these patients (median 4.7 μg/ml in patients with acute myocardial infarction and 3.3 μg/ml in patients with congestive heart failure). Thus, differences in the response of premature ventricular complexes to procainamide reflect electropharmacologic differences dependent on clinical setting rather than pharmacokinetic abnormalities. Furthermore, the reduction of procainamide dosing in patients with acute myocardial infarction or congestive heart failure, based solely on prior kinetic data, may result in inappropriate antiarrhythmic therapy.

AB - Abnormal procainamide pharmacokinetics (prolonged half-life and decreased volume of distribution) and pharmacodynamics (decreased threshold for the suppression of premature ventricular complexes) have been suggested in patients with acute myocardial infarction or congestive heart failure, or both. To better define procainamide kinetics, 37 patients in the acute care setting received intravenous procainamide (25 mg/min, median dose 750 mg) with peak and hourly blood samples taken over 6 hours. Compared with the 10 control patients, the 12 patients with acute myocardial infarction and the 15 patients with congestive heart failure had normal procainamide pharmacokinetics with respect to half-life (2.3 ± 1.0, 2.5 ± 0.9 and 2.6 ± 0.8 hours, respectively), volume of distribution (1.9 ± 0.7, 1.8 ± 0.4 and 1.8 ± 0.5 liters/kig, respectively), clearance (11.3 ± 7.5, 9.3 ± 3.6 and 9.1 ± 3.5 ml/min per kg, respectively) and unbound drug fraction (66 ± 9, 66 ± 9 and 69 ± 4%, respectively). Low thresholds for greater than 85% premature ventricular complex suppression were confirmed in these patients (median 4.7 μg/ml in patients with acute myocardial infarction and 3.3 μg/ml in patients with congestive heart failure). Thus, differences in the response of premature ventricular complexes to procainamide reflect electropharmacologic differences dependent on clinical setting rather than pharmacokinetic abnormalities. Furthermore, the reduction of procainamide dosing in patients with acute myocardial infarction or congestive heart failure, based solely on prior kinetic data, may result in inappropriate antiarrhythmic therapy.

UR - http://www.scopus.com/inward/record.url?scp=0022580932&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022580932&partnerID=8YFLogxK

M3 - Article

VL - 7

SP - 1131

EP - 1139

JO - Journal of the American College of Cardiology

JF - Journal of the American College of Cardiology

SN - 0735-1097

IS - 5

ER -