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急性心肌梗死的中心血流动力学。自然病史、与酶释放的关系及美托洛尔的作用。

Central haemodynamics in acute myocardial infarction. Natural history, relation to enzyme release and effects of metoprolol.

作者信息

Held P

出版信息

Acta Med Scand Suppl. 1986;709:1-47.

PMID:3532697
Abstract

The aim of this investigation was to study central haemodynamics in initially uncomplicated acute myocardial infarction (AMI) with respect to natural history, relation to enzyme estimated infarct size, mortality and effects of metoprolol. A total of 212 patients with AMI but without clinical signs of serious heart failure or hypotension and with a mean delay from onset of pain to study entry of about 7 hours were studied. They were randomised to placebo or metoprolol (15 mg i.v. + 50 mg orally q.i.d.) treatment. Central pressures and cardiac output were evaluated by repeated measurements over 24 hours by means of pulmonary artery catheters. The pharmacokinetics of metoprolol were studied in further 20 patients with AMI. The natural history, as reflected by the placebo group, was observed to be a gradual significant fall in systemic artery pressures, pulmonary capillary wedge pressure (PCWP; 13.6-10.5 mmHg) and stroke volume, while heart rate increased, leaving cardiac output unchanged. The decrease in PCWP was confined to the group with baseline pressure above the median of 13 mmHg and was of equal magnitude in the group given concomitant medication to that of those who required no such therapy. Significant but weak correlations between the peak serum aspartate aminotransferase level and the baseline PCWP (r = 0.28) and stroke volume (r = 0.22) were found. Non-survivors had a significant baseline depression of cardiac output and stroke volume, while PCWP was increased. However, the overlap with survivors was large. The dosage of metoprolol used resulted in mean plasma levels of about 200 nmol/l, which should induce a rapid and sustained degree of beta-blockade. The patients randomised to placebo or metoprolol were assessed according to initial heart rate. The haemodynamic changes induced by metoprolol were similar but were more pronounced in patients with high heart rate compared to those with low rate. In patients with heart rate greater than 65 beats/min, the metoprolol treated group, in comparison to the placebo group, was characterised by a decrease of 10-20% in systolic artery pressure and heart rate, suggesting a decreased myocardial oxygen consumption. Cardiac index (2.9-2.2 l/min/m2) and stroke volume index (36-32 ml/beat/m2) decreased to a minimum after 30 minutes and gradually rose thereafter. The PCWP increased from 13.7 to 15.4 mmHg, 30 minutes after the injection of metoprolol. This increase was confined to the group with baseline low pressure and the difference compared to the placebo group disappeared after 8 hours.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

本研究旨在探讨初发无并发症急性心肌梗死(AMI)患者的中心血流动力学情况,包括其自然病程、与酶学估算梗死面积的关系、死亡率以及美托洛尔的作用。共研究了212例AMI患者,这些患者无严重心力衰竭或低血压的临床体征,从疼痛发作到研究开始的平均延迟时间约为7小时。他们被随机分为安慰剂组或美托洛尔组(静脉注射15 mg + 口服50 mg,每日4次)进行治疗。通过肺动脉导管在24小时内重复测量来评估中心压力和心输出量。另外对20例AMI患者研究了美托洛尔的药代动力学。安慰剂组所反映的自然病程显示,体动脉压、肺毛细血管楔压(PCWP;从13.6降至10.5 mmHg)和每搏量逐渐显著下降,而心率增加,心输出量不变。PCWP的下降仅限于基线压力高于中位数13 mmHg的组,且接受联合用药组的下降幅度与无需此类治疗组相同。发现血清天冬氨酸转氨酶峰值水平与基线PCWP(r = 0.28)和每搏量(r = 0.22)之间存在显著但较弱的相关性。非幸存者的心输出量和每搏量基线显著降低,而PCWP升高。然而,与幸存者的重叠范围较大。所用美托洛尔剂量导致平均血浆水平约为200 nmol/l,这应能诱导快速且持续的β受体阻滞程度。根据初始心率对随机分为安慰剂组或美托洛尔组的患者进行评估。美托洛尔诱导的血流动力学变化相似,但与心率低的患者相比,心率高的患者变化更明显。在心率大于65次/分钟的患者中,与安慰剂组相比,美托洛尔治疗组的收缩动脉压和心率降低了10 - 20%,提示心肌氧耗减少。心脏指数(从2.9降至2.2 l/min/m²)和每搏量指数(从36降至32 ml/搏/m²)在30分钟后降至最低,此后逐渐上升。注射美托洛尔30分钟后,PCWP从13.7 mmHg升至15.4 mmHg。这种升高仅限于基线压力低的组,与安慰剂组的差异在8小时后消失。(摘要截断于400字)

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