首页> 外文期刊>Journal of the American College of Cardiology >Overestimation of platelet aspirin resistance detection by thrombelastograph platelet mapping and validation by conventional aggregometry using arachidonic acid stimulation.
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Overestimation of platelet aspirin resistance detection by thrombelastograph platelet mapping and validation by conventional aggregometry using arachidonic acid stimulation.

机译:血栓弹力描记器血小板作图法高估了血小板阿司匹林抵抗力,而花生四烯酸刺激则通过常规的凝集法进行了验证。

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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% at24 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.
机译:目的:本研究试图通过直接指示血小板环氧合酶抑制程度的方法确定血小板阿司匹林耐药性的发生率。背景:血小板的阿司匹林耐药性可能会因无法分离环氧合酶活性的非特异性实验室测量而被高估。方法:在接受325 mg阿司匹林治疗之前和之后24 h,对健康受试者(n = 6)的血液进行花生四烯酸(AA)诱导的透光性血小板聚集(LTA)和血栓弹性成像(TEG)血小板作图。接受长期每日阿司匹林治疗依从性的患者(n = 203接受经皮介入治疗[PCI],n = 20,有支架血栓形成史)。阿司匹林耐药性定义为:LTA聚集> 20%,TEG聚集> 50%。结果:在健康受试者中,AA诱导的AA聚集在阿司匹林之前为82 +/- 10%,在阿司匹林后24小时为2 +/- 1%(p <0.001),而TEG所引起的聚集为86 +/- 14%。阿司匹林治疗24小时后为5 +/- 7%(p <0.001)。在依从性患者中,AA引起的LTA聚集在PCI前为3 +/- 2%,在PCI之后为3 +/- 2%(p = NS),而TEG在PCI之前为5 +/- 9%,且6 + PCI后14%(p = NS)。七名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例患者中,只有1例(约0.4%)对阿司匹林治疗有抗药性。结论:通过直接表明抑制环氧合酶的方法评估的血小板阿司匹林耐药性在冠心病患者中很少见。

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