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先前的阿司匹林治疗可抑制急性心肌梗死患者的基线血小板活性。GUSTO-III血小板亚研究。

Antecedent aspirin therapy inhibits baseline platelet activity in patients presenting with acute myocardial infarction. The GUSTO-III Platelet Substudy.

作者信息

Serebruany V L, Bahr R D, O'Connor C M, Lowry D R, Gurbel P A

机构信息

Emergency Departments and Critical Care Units, St. Agnes and Union Memorial Hospitals, Baltimore, MD 21215, USA.

出版信息

Cardiology. 1998 Jul;90(1):37-42. doi: 10.1159/000006814.

DOI:10.1159/000006814
PMID:9693169
Abstract

Aspirin therapy and platelet inhibition reduce the risk for the development of acute myocardial infarction (AMI). However, the effects of aspirin on baseline platelet activity in patients presenting with AMI are not known. We determined the effect of long-term aspirin use on baseline platelet activity in patients presenting with AMI, enrolled in the GUSTO-III Platelet Study. Platelet characteristics were investigated by aggregometry, flow cytometry and enzyme-linked immunosorbent assay in 23 patients before thrombolysis. Sixteen AMI patients were aspirin free, and 7 patients were using aspirin (81-500 mg/daily). The aspirin-treated patients exhibited a mild but consistent reduction of platelet activity which reached significance for 5 microM (p = 0.02), and 10 microM (p = 0.01) adenosine diphosphate induced aggregation. The surface expression of P-selectin (p = 0.02) and PECAM-1 (p = 0.03) and the plasma level of soluble P-selectin (p = 0.02) were also reduced. As previously observed in normal humans and patients with stable coronary artery disease, long-term aspirin therapy is also associated with diminished platelet activation in patients presenting with AMI. Long-term aspirin therapy mildly reduces baseline platelet activity; however, this degree of relative platelet inhibition does not appear to be cardioprotective.

摘要

阿司匹林治疗和血小板抑制可降低急性心肌梗死(AMI)的发生风险。然而,阿司匹林对AMI患者基线血小板活性的影响尚不清楚。我们在参与GUSTO-III血小板研究的AMI患者中,确定了长期使用阿司匹林对基线血小板活性的影响。在23例患者溶栓前,通过凝集测定法、流式细胞术和酶联免疫吸附测定法研究血小板特征。16例AMI患者未使用阿司匹林,7例患者正在使用阿司匹林(81 - 500毫克/日)。接受阿司匹林治疗的患者血小板活性呈现轻度但持续的降低,对于5微摩尔(p = 0.02)和10微摩尔(p = 0.01)二磷酸腺苷诱导的聚集具有显著意义。P-选择素(p = 0.02)和PECAM-1(p = 0.03)的表面表达以及可溶性P-选择素的血浆水平(p = 0.02)也降低。如先前在正常人和稳定型冠状动脉疾病患者中所观察到的,长期阿司匹林治疗也与AMI患者血小板活化减弱有关。长期阿司匹林治疗可轻度降低基线血小板活性;然而,这种程度的相对血小板抑制似乎并无心脏保护作用。

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