Interian A, Zaman L, Velez-Robinson E, Kozlovskis P, Castellanos A, Myerburg R J
Department of Medicine, University of Miami School of Medicine, Florida 33101.
J Am Coll Cardiol. 1991 Jun;17(7):1581-6. doi: 10.1016/0735-1097(91)90651-o.
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 micrograms/ml after intravenous dosing and 7.9 +/- 2.5 micrograms/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 micrograms/ml, oral = 7.5 +/- 2.1 micrograms/ml). The other eight patients (35%) had concordant responses to repeat testing with comparable intravenous (mean 9.0 +/- 3.3 micrograms/ml) and oral (8.8 +/- 3.1 micrograms/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 micrograms/ml) after failure of intravenous procainamide (mean plasma level 10.3 +/- 2.3 micrograms/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
38例在基础程控电刺激时可诱发持续性室性心动过速的患者,在静脉及口服普鲁卡因酰胺后接受了电生理检查。每例患者临床上均表现为记录在案的持续性室性心动过速或与急性心肌梗死无关的院外心脏骤停。23例患者(61%)(第I组)在静脉输注普鲁卡因酰胺期间心律失常变得不可诱发。随后给予口服普鲁卡因酰胺,并在剂量滴定以匹配静脉研究结束时的血浆浓度后再次进行检测。在第I组的23例患者中,静脉给药后普鲁卡因酰胺的平均(±标准差)血浆水平为7.2±2.8μg/ml,口服给药后为7.9±2.5μg/ml(p = 0.09)。在23例患者中的15例(65%),口服治疗时可诱发持续性室性心律失常,且血浆普鲁卡因酰胺水平相当(静脉=6.3±2.1μg/ml,口服=7.5±2.1μg/ml)。另外8例患者(35%)对重复检测的反应一致,静脉和口服时的血浆普鲁卡因酰胺水平相当(平均分别为9.0±3.3μg/ml和8.8±3.1μg/ml)。在另外15例患者(第II组)中,静脉应用普鲁卡因酰胺治疗时持续性室性快速心律失常仍可诱发,且这些患者在口服治疗时再次进行检测,血浆浓度相似(p = 0.05)。在7例患者(47%)中,静脉应用普鲁卡因酰胺失败(平均血浆水平10.3±2.3μg/ml)后,口服普鲁卡因酰胺治疗(平均血浆水平7.6±2.7μg/ml)时持续性室性快速心律失常不可诱发。(摘要截短于250字)