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静脉注射胺碘酮的急性血流动力学和抗缺血作用。

Acute hemodynamic and antiischemic effects of intravenous amiodarone.

作者信息

Remme W J, Van Hoogenhuyze D C, Krauss X H, Hofman A, Kruyssen D A, Storm C J

出版信息

Am J Cardiol. 1985 Mar 1;55(6):639-44. doi: 10.1016/0002-9149(85)90128-6.

Abstract

The acute hemodynamic and antiischemic properties of amiodarone were investigated in 16 patients with more than 70% diameter reduction of a left coronary artery. Two successive atrial pacing stress tests (APST I and II) were performed, with an interval of 40 minutes in between, and amiodarone, 5 mg/kg/5 min, was infused 30 minutes after APST I. Hemodynamic changes during amiodarone administration consisted of a 20% decrease in left ventricular (LV) systolic pressure, a 13% decrease in systemic vascular resistance and an 18% decrease in stroke work. Coronary vascular resistance was reduced 19% and coronary sinus flow increased 23%. Despite a secondary 14% increase in heart rate, contractility decreased 21%, accompanied by a 45% increase in LV end-diastolic pressure, which persisted until APST II. Although most hemodynamic changes were observed only during the infusion, contractility and LV systolic pressure were still diminished at the beginning of APST II and remained so during pacing, resulting in a reduction in myocardial oxygen demand compared to APST I. Although overall myocardial oxygen consumption and coronary flow were equal during both pacing tests, amiodarone significantly reduced pacing-induced myocardial ischemia. Lactate metabolism remained normal during APST II (lactate extraction 12 +/- 3% vs -28 +/- 8% (APST I) at maximal pacing rates [p less than 0.05]), while ST-segment depression, LV end-diastolic pressure postpacing and angina were also significantly reduced during APST II. Thus, in humans, intravenous amiodarone reduces vascular resistance and contractility and inhibits pacing-induced myocardial ischemia, presumably by reducing myocardial oxygen demand.

摘要

对16例左冠状动脉直径缩小超过70%的患者研究了胺碘酮的急性血流动力学和抗缺血特性。进行了两次连续的心房起搏应激试验(APST I和II),其间间隔40分钟,在APST I后30分钟输注5 mg/kg/5分钟的胺碘酮。胺碘酮给药期间的血流动力学变化包括左心室(LV)收缩压降低20%、全身血管阻力降低13%和每搏功降低18%。冠状动脉血管阻力降低19%,冠状窦血流量增加23%。尽管心率继发性增加14%,但收缩力降低21%,同时左心室舒张末期压力增加45%,直至APST II时仍持续存在。虽然大多数血流动力学变化仅在输注期间观察到,但在APST II开始时收缩力和左心室收缩压仍降低,且在起搏期间保持降低,与APST I相比导致心肌需氧量减少。虽然在两次起搏试验期间总体心肌耗氧量和冠状动脉血流量相等,但胺碘酮显著减少起搏诱导的心肌缺血。在APST II期间乳酸代谢保持正常(在最大起搏率时乳酸摄取为12±3%,而APST I时为-28±8%[p<0.05]),而在APST II期间ST段压低、起搏后左心室舒张末期压力和心绞痛也显著减轻。因此,在人类中,静脉注射胺碘酮可降低血管阻力和收缩力,并抑制起搏诱导的心肌缺血,可能是通过降低心肌需氧量实现的。

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