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普鲁卡因胺在人类室性心动过速的诱发和持续中的作用。

Procainamide in the induction and perpetuation of ventricular tachycardia in man.

作者信息

Kang P S, Gomes J A, El-Sherif N

出版信息

Pacing Clin Electrophysiol. 1982 May;5(3):311-22. doi: 10.1111/j.1540-8159.1982.tb02237.x.

Abstract

The effects of a single intravenous infusion of 750 mg of procainamide was studied in 12 patients with symptomatic chronic recurrent ventricular tachycardia in whom arrhythmias could reproducibly be initiated and terminated by programmed electrical stimulation of the heart. Sustained ventricular tachycardia was induced in 6 patients and non-sustained tachycardia was induced in the remaining 6 patients during control studies. Following procainamide (plasma level 10.3 +/- 3.7 mcg/ml), ventricular tachycardia could be induced in 10/12 patients, sustained in 4 patients and non-sustained in the remaining 6 patients. In 8/12 patients (66%), induction of ventricular tachycardia was facilitated as demonstrated by: (1) tachycardia zone was widened in 4 patients and was unchanged in another 3 patients; (2) non-sustained ventricular tachycardia was sustained ventricular tachycardia in one patient. the ventricular tachycardia had a faster rate and a different QRS morphology; (3) in 4 patients tachycardia was inducible with a lesser number of extrastimuli and/or by spontaneously occurring ventricular premature depolarization and; (4) increase of the number of induced ventricular responses of non-sustained ventricular tachycardia. In 4/12 patients (33%), procainamide abolished or modified the induction of ventricular tachycardia as demonstrated by: (1) inability to induce ventricular tachycardia in 2 patients; (2) narrowing of the tachycardia zone and conversion from sustained into non-sustained ventricular tachycardia (one patient) and; (3) decrease in the number of induced ventricular responses in one patient. The response to procainamide could not be predicted from rates of spontaneous ventricular tachycardia, induced ventricular tachycardia during control studies, degree of slowing of ventricular tachycardia or from prolongation of the coupling interval after procainamide. These results suggest that instead of abolishing the arrhythmia, procainamide in frequently employed doses in patients with chronic recurrent ventricular tachycardia can facilitate its initiation sometimes at even faster rates. Patients not responsive to the usual doses of procainamide should undergo acute drug trials to determine the optimal dose/drug levels.

摘要

对12例有症状的慢性复发性室性心动过速患者进行了研究,这些患者的心律失常可通过心脏程控电刺激反复诱发和终止。单次静脉输注750毫克普鲁卡因酰胺的效果在这些患者中得到了研究。在对照研究期间,6例患者诱发出持续性室性心动过速,其余6例患者诱发出非持续性心动过速。给予普鲁卡因酰胺后(血浆水平为10.3±3.7微克/毫升),12例患者中有10例可诱发出室性心动过速,其中4例为持续性,其余6例为非持续性。在12例患者中有8例(66%),室性心动过速的诱发得到促进,表现为:(1)4例患者心动过速区增宽,另3例患者无变化;(2)1例患者的非持续性室性心动过速转变为持续性室性心动过速,室性心动过速速率更快且QRS形态不同;(3)4例患者用较少的额外刺激和/或通过自发出现的室性早搏去极化即可诱发出心动过速;(4)非持续性室性心动过速诱发的室性反应数量增加。在12例患者中有4例(33%),普鲁卡因酰胺消除或改变了室性心动过速的诱发,表现为:(1)2例患者无法诱发出室性心动过速;(2)心动过速区变窄,持续性室性心动过速转变为非持续性室性心动过速(1例患者);(3)1例患者诱发的室性反应数量减少。从自发性室性心动过速的速率、对照研究期间诱发的室性心动过速、室性心动过速的减慢程度或普鲁卡因酰胺后耦联间期的延长情况,均无法预测对普鲁卡因酰胺的反应。这些结果表明,对于慢性复发性室性心动过速患者,常用剂量的普鲁卡因酰胺非但不能消除心律失常,反而有时会以更快的速率促进其发作。对常规剂量普鲁卡因酰胺无反应的患者应进行急性药物试验,以确定最佳剂量/药物水平。

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