Paired comparisons of efficacy of intravenous and oral procainamide in patients with inducible sustained ventricular tachyarrhythmias

Alberto Interian, Liaqat Zaman, Elsa Velez-Robinson, Patricia Kozlovskis, Agustin Castellanos, Robert J Myerburg

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Abstract

Thirty-eight patients who had inducible sustained ventricular tachycardia during baseline programmed electrical stimulation underwent electrophysiologic testing after both intravenous and oral administration of procainamide. Each had presented clinically with documented sustained ventricular tachycardia or out of hospital cardiac arrest not associated with acute myocardial infarction. In 23 patients (61%) (Group I) the arrhythmia became noninducible during an intravenous infusion of procainamide. Oral procainamide was subsequently administered and retesting was carried out after dose titration to match plasma concentration at the end of the intravenous study. Among the 23 patients in Group I the mean (± SD) plasma procainamide level was 7.2 ± 2.8 μg/ml after intravenous dosing and 7.9 ± 2.5 μg/ml after oral dosing (p = 0.09). In 15 (65%) of the 23 patients, sustained ventricular arrhythmia was inducible on oral therapy with comparable plasma procainamide levels (intravenous = 6.3 ± 2.1 μg/ml, oral = 7.5 ± 2.1 μg/ml). The other eight patients (35%) had concordant responses to repeat testing with comparable intravenous (mean 9.0 ± 3.3 μg/ml) and oral (8.8 ± 3.1 μg/ml) plasma procainamide levels. In the additional 15 patients (Group II) sustained ventricular tachyarrhythmia remained inducible on intravenous procainamide therapy and the patients were retested on oral therapy with similar plasma concentration (p = 0.05). In seven patients (47%) sustained ventricular tachyarrhythmia was noninducible on treatment with oral procainamide (mean plasma level 7.6 ± 2.7 μg/ml) after failure of intravenous procainamide (mean plasma level 10.3 ± 2.3 μg/ml). In conclusion, in patients with inducible ventricular arrhythmia at baseline electrophysiologic study the response to intravenous procainamide does not predict the electrophysiologic effect of subsequent oral administration of procainamide in doses that yield similar or slightly higher plasma concentrations. Thus, there appears to be little advantage to electrophysiologic drug testing with intravenous procainamide.

Original languageEnglish
Pages (from-to)1581-1586
Number of pages6
JournalJournal of the American College of Cardiology
Volume17
Issue number7
DOIs
StatePublished - Jan 1 1991

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Procainamide
Matched-Pair Analysis
Tachycardia
Cardiac Arrhythmias
Ventricular Tachycardia
Oral Administration
Out-of-Hospital Cardiac Arrest
Therapeutics
Intravenous Infusions
Intravenous Administration
Electric Stimulation

ASJC Scopus subject areas

  • Nursing(all)

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Paired comparisons of efficacy of intravenous and oral procainamide in patients with inducible sustained ventricular tachyarrhythmias. / Interian, Alberto; Zaman, Liaqat; Velez-Robinson, Elsa; Kozlovskis, Patricia; Castellanos, Agustin; Myerburg, Robert J.

In: Journal of the American College of Cardiology, Vol. 17, No. 7, 01.01.1991, p. 1581-1586.

Research output: Contribution to journalArticle

Interian, Alberto ; Zaman, Liaqat ; Velez-Robinson, Elsa ; Kozlovskis, Patricia ; Castellanos, Agustin ; Myerburg, Robert J. / Paired comparisons of efficacy of intravenous and oral procainamide in patients with inducible sustained ventricular tachyarrhythmias. In: Journal of the American College of Cardiology. 1991 ; Vol. 17, No. 7. pp. 1581-1586.
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abstract = "Thirty-eight patients who had inducible sustained ventricular tachycardia during baseline programmed electrical stimulation underwent electrophysiologic testing after both intravenous and oral administration of procainamide. Each had presented clinically with documented sustained ventricular tachycardia or out of hospital cardiac arrest not associated with acute myocardial infarction. In 23 patients (61{\%}) (Group I) the arrhythmia became noninducible during an intravenous infusion of procainamide. Oral procainamide was subsequently administered and retesting was carried out after dose titration to match plasma concentration at the end of the intravenous study. Among the 23 patients in Group I the mean (± SD) plasma procainamide level was 7.2 ± 2.8 μg/ml after intravenous dosing and 7.9 ± 2.5 μg/ml after oral dosing (p = 0.09). In 15 (65{\%}) of the 23 patients, sustained ventricular arrhythmia was inducible on oral therapy with comparable plasma procainamide levels (intravenous = 6.3 ± 2.1 μg/ml, oral = 7.5 ± 2.1 μg/ml). The other eight patients (35{\%}) had concordant responses to repeat testing with comparable intravenous (mean 9.0 ± 3.3 μg/ml) and oral (8.8 ± 3.1 μg/ml) plasma procainamide levels. In the additional 15 patients (Group II) sustained ventricular tachyarrhythmia remained inducible on intravenous procainamide therapy and the patients were retested on oral therapy with similar plasma concentration (p = 0.05). In seven patients (47{\%}) sustained ventricular tachyarrhythmia was noninducible on treatment with oral procainamide (mean plasma level 7.6 ± 2.7 μg/ml) after failure of intravenous procainamide (mean plasma level 10.3 ± 2.3 μg/ml). In conclusion, in patients with inducible ventricular arrhythmia at baseline electrophysiologic study the response to intravenous procainamide does not predict the electrophysiologic effect of subsequent oral administration of procainamide in doses that yield similar or slightly higher plasma concentrations. Thus, there appears to be little advantage to electrophysiologic drug testing with intravenous procainamide.",
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AB - Thirty-eight patients who had inducible sustained ventricular tachycardia during baseline programmed electrical stimulation underwent electrophysiologic testing after both intravenous and oral administration of procainamide. Each had presented clinically with documented sustained ventricular tachycardia or out of hospital cardiac arrest not associated with acute myocardial infarction. In 23 patients (61%) (Group I) the arrhythmia became noninducible during an intravenous infusion of procainamide. Oral procainamide was subsequently administered and retesting was carried out after dose titration to match plasma concentration at the end of the intravenous study. Among the 23 patients in Group I the mean (± SD) plasma procainamide level was 7.2 ± 2.8 μg/ml after intravenous dosing and 7.9 ± 2.5 μg/ml after oral dosing (p = 0.09). In 15 (65%) of the 23 patients, sustained ventricular arrhythmia was inducible on oral therapy with comparable plasma procainamide levels (intravenous = 6.3 ± 2.1 μg/ml, oral = 7.5 ± 2.1 μg/ml). The other eight patients (35%) had concordant responses to repeat testing with comparable intravenous (mean 9.0 ± 3.3 μg/ml) and oral (8.8 ± 3.1 μg/ml) plasma procainamide levels. In the additional 15 patients (Group II) sustained ventricular tachyarrhythmia remained inducible on intravenous procainamide therapy and the patients were retested on oral therapy with similar plasma concentration (p = 0.05). In seven patients (47%) sustained ventricular tachyarrhythmia was noninducible on treatment with oral procainamide (mean plasma level 7.6 ± 2.7 μg/ml) after failure of intravenous procainamide (mean plasma level 10.3 ± 2.3 μg/ml). In conclusion, in patients with inducible ventricular arrhythmia at baseline electrophysiologic study the response to intravenous procainamide does not predict the electrophysiologic effect of subsequent oral administration of procainamide in doses that yield similar or slightly higher plasma concentrations. Thus, there appears to be little advantage to electrophysiologic drug testing with intravenous procainamide.

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