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通过血栓弹力图血小板功能分析高估血小板阿司匹林抵抗检测,并使用花生四烯酸刺激的传统血小板聚集试验进行验证。

Overestimation of platelet aspirin resistance detection by thrombelastograph platelet mapping and validation by conventional aggregometry using arachidonic acid stimulation.

作者信息

Tantry Udaya S, Bliden Kevin P, Gurbel Paul A

机构信息

Sinai Center for Thrombosis Research, Baltimore, Maryland 21215, USA.

出版信息

J Am Coll Cardiol. 2005 Nov 1;46(9):1705-9. doi: 10.1016/j.jacc.2005.05.090. Epub 2005 Oct 10.

Abstract

OBJECTIVES

This study sought to determine the prevalence of platelet aspirin resistance using methods that directly indicate the degree of platelet cyclooxygenase inhibition.

BACKGROUND

Aspirin resistance in platelets may be overestimated by nonspecific laboratory measurements that do not isolate cyclooxygenase activity.

METHODS

Arachidonic acid (AA)-induced light-transmittance platelet aggregation (LTA) and thrombelastography (TEG) platelet mapping were performed on the blood of healthy subjects (n = 6) before and 24 h after receiving 325 mg aspirin, and on 223 patients reporting compliance with long-term daily aspirin treatment (n = 203 undergoing percutaneous intervention [PCI] and n = 20 with a history of stent thrombosis). Aspirin resistance was defined as >20% aggregation by LTA or >50% aggregation by TEG.

RESULTS

In healthy subjects, AA-induced aggregation by LTA was 82 +/- 10% before and 2 +/- 1% at 24 h after aspirin (p < 0.001), and aggregation by TEG was 86 +/- 14% before and 5 +/- 7% at 24 h after aspirin (p < 0.001). In compliant patients, AA-induced aggregation by LTA was 3 +/- 2% before PCI and 3 +/- 2% after PCI (p = NS), and aggregation by TEG was 5 +/- 9% before PCI and 6 +/- 14% after PCI (p = NS). Seven PCI patients were noncompliant, and all were aspirin sensitive after in-hospital aspirin treatment. Among 223 patients, only one patient ( approximately 0.4%) was resistant to aspirin treatment.

CONCLUSIONS

Platelet aspirin resistance assessed by methods that directly indicate inhibition of cyclooxygenase is rare in compliant patients with coronary artery disease.

摘要

目的

本研究旨在采用直接反映血小板环氧化酶抑制程度的方法来确定血小板阿司匹林抵抗的发生率。

背景

血小板阿司匹林抵抗可能会被未分离环氧化酶活性的非特异性实验室检测方法高估。

方法

对6名健康受试者在服用325毫克阿司匹林前及服药后24小时的血液进行花生四烯酸(AA)诱导的透光率血小板聚集(LTA)和血栓弹力图(TEG)血小板图谱分析,同时对223名报告长期每日服用阿司匹林依从性良好的患者(203名接受经皮冠状动脉介入治疗[PCI],20名有支架血栓形成病史)进行同样分析。阿司匹林抵抗定义为LTA检测下聚集率>20%或TEG检测下聚集率>50%。

结果

在健康受试者中,LTA检测下AA诱导的聚集率在服用阿司匹林前为82±10%,服药后24小时为2±1%(p<0.001);TEG检测下的聚集率在服用阿司匹林前为86±14%,服药后24小时为5±7%(p<0.001)。在依从性良好的患者中,LTA检测下AA诱导的聚集率在PCI术前为3±2%,术后为3±2%(p=无显著性差异);TEG检测下的聚集率在PCI术前为5±9%,术后为6±14%(p=无显著性差异)。7名PCI患者不依从,所有患者在院内接受阿司匹林治疗后均对阿司匹林敏感。在223名患者中,只有1名患者(约0.4%)对阿司匹林治疗有抵抗。

结论

在依从性良好的冠心病患者中,采用直接反映环氧化酶抑制的方法评估的血小板阿司匹林抵抗很少见。

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