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Changes in platelet function with inflammation in patients undergoing vascular surgery

机译：血管外科患者血小板功能的变化

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摘要

The role of platelets in ischaemic events is well established. Aspirin represents the default antiplatelet and blocks the metabolism of arachidonic acid (AA) at the cyclo-oxygenase enzyme (COX). AA is commonly used as a test of response to aspirin, but recent data raise uncertainty about the validity of this approach. Specifically, in some patients AA-induced clotting is not suppressed, but the level of COX-dependent AA metabolite, thromboxane B2 (TXB2) is negligible. Furthermore, AA-induced whole blood clotting varies dynamically in individuals, who are aspirin responsive according to TXB2 levels. The aim of this study was to assess the level of AA-, ADP- and thrombin-mediated platelet reactivity in patients on aspirin before, during, and after major vascular surgery, which represents a model of on/off vascular inflammation. Firstly, we hypothesized, that in association with this inflammatory episode AA-, ADP- and thrombin-induced clotting would change in a dynamic manner. Secondly, that AA-induced clotting will be modified despite complete suppression of platelet TXB2 production by aspirin throughout the periprocedural period, possibly via a lipoxygenase-mediated mechanism. Fourty patients underwent major vascular surgery (open abdominal aortic aneurysm operation, infrainguinal bypass for subcritical limb ischaemia or peripheral aneurysm repair with bypass). They were all on 75 mg of aspirin prior to and throughout the perioperative period and received 5000 units of unfractionated heparin intraoperatively. AA-, ADP-, and thrombin-induced clotting, AA metabolites (TXB2 and 12-Hyroxyeicosatetraenoic acid (12-HETE)) and inflammatory markers (CRP, IL-6, TNF-alpha and CD40) were measured pre-procedure and at 2, 24, 48 hours, 3 to 5 days and 3 months after surgery. AA-, ADP- and thrombin-induced platelet reactivity was assessed using thrombelastography. TXB2, 12-HETE, IL-6, TNF-alpha, CD40 were determined using the sequential competitive binding Enzyme-Linked ImmunoAssay technique and CRP was determined using an immune-turbidimetric test on human serum. There was a transient rise in inflammatory markers in the early perioperative period (CRP at 24, 48 hours and 3 to 5 days p < 0.001 and IL-6 at 2, 24, 48 hours and 3 to 5 days p < 0.001 as compared to baseline). Patients had negligible levels of TXB2 throughout, confirming a consistent therapeutic response to aspirin. There was a transient rise in thrombin-mediated clotting (MA(Thrombin) at 48 hours p = 0.001 and 3 to 5 days p < 0.001) and a fall in AA- and ADP-induced clotting in the early post op period (both MA(AA) and MA(ADP) p = 0.001 at 2 hours). At 3 months, the level of AA- and ADP-induced clotting was significantly higher than at baseline (p = 0.008 for MA(AA) and p = 0.002 for MA(ADP)), hence demonstrating a rebound effect. These data demonstrate a novel dynamic variation in platelet aggregation with acute vascular inflammation, including AA-induced whole blood clotting which is apparently COX-1 independent.
机译：血小板在缺血事件中的作用得到了很好的成熟。阿司匹林代表默认的抗血小板，并阻断在环氧酶酶（COX）处的花生素酸（AA）的代谢。 AA通常用作对阿司匹林的反应的考验，但最近的数据提高了这种方法的有效性的不确定性。具体地，在一些患者中，不抑制AA诱导的凝血，但COX依赖性AA代谢物的水平可忽略不计。此外，AA诱导的全血液凝固在个体中动态变化，谁根据TXB2水平响应阿司匹林。本研究的目的是评估阿司匹林患者的AA，ADP和凝血酶介导的血小板反应性，在主要血管外科之前，期间和之后代表了血管炎症的模型。首先，我们假设，与这种炎症发作AA - ，ADP-和凝血酶诱导的凝血相关，其将以动态的方式改变。其次，尽管通过在整个百分比时期的阿司匹林完全抑制血小板TxB2生产，但可能通过脂氧基酶介导的机制，仍将改变AA诱导的凝固。四十名患者接受了主要血管外科（开放的腹主动脉瘤操作，针对亚临界肢体缺血或外周动脉瘤修复旁路）。在整个围手术期之前和整个围手术期之前，它们都在75毫克阿司匹林中，并术中接受了5000单位的无机肝素。测量预先序列和炎症标志物（TXB2和12-羟基辛酸（12-HETE））和炎症标记物（CRP，IL-6，TNF-α和CD40）的AA，ADP-和凝血酶诱导的凝血凝血，AA，ADP-和凝血酶诱导的凝血凝血剂，AA代谢物（TXB2和12-氧晶二甲酸（CRP，IL-6，TNF-α和CD40） 2,24,48小时，手术后3至5天和3个月3个月。使用血栓形成评估AA-，ADP和凝血酶诱导的血小板反应性。使用顺序竞争结合酶联免疫测定技术测定TXB2,12-HETE，IL-6，TNF-α，CD40，使用人血清的免疫浊度试验测定CRP。早期围手术期（24,48小时和3至5天P <0.001和IL-6，在2,24,48小时和3至5天P <0.001时，炎症标志物（CRP）存在瞬态升高基线）。患者在整个TXB2水平可忽略不计，确认对阿司匹林的一致治疗反应。凝血酶介导的凝血（MA（凝血酶）在48小时= 0.001和3至5天P <0.001）中存在瞬态升高（MA（凝血酶），并在早期OP期间（MA （AA）和MA（ADP）P = 0.001在2小时）。在3个月内，AA和ADP诱导的凝血水平显着高于基线（MA（AA）的P = 0.008，MA（ADP）的P = 0.002），因此证明了反弹效应。这些数据表明，具有急性血管炎症的血小板聚集的新型动态变异，包括AA诱导的全血液凝固，这显然是COX-1独立的。

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  • 来源
    《Platelets》 |2019年第2期|共9页
  • 作者

    Olechowski Bartosz; Khanna Vikram; Mariathas Mark; Ashby Alexander; Dalton Richard T.; Nordon Ian; Englyst Nicola; Harris Scott; Nicholas Zoe; Thayalasamy Kala; Mahmoudi Michael; Curzen Nick;

  • 作者单位

    Univ Hosp Southampton NHS Fdn Trust Wessex Cardiothorac Ctr Univ Southampton Hants England;

    Univ Hosp Southampton NHS Fdn Trust Wessex Cardiothorac Ctr Univ Southampton Hants England;

    Univ Hosp Southampton NHS Fdn Trust Wessex Cardiothorac Ctr Univ Southampton Hants England;

    Univ Hosp Southampton NHS Fdn Trust Wessex Cardiothorac Ctr Univ Southampton Hants England;

    Univ Hosp Southampton NHS Fdn Trust Wessex Cardiothorac Ctr Univ Southampton Hants England;

    Univ Hosp Southampton NHS Fdn Trust Wessex Cardiothorac Ctr Univ Southampton Hants England;

    Univ Southampton Fac Med Inst Dev Sci Southampton Hants England;

    Univ Hosp Southampton NHS Fdn Trust Wessex Cardiothorac Ctr Univ Southampton Hants England;

    Univ Hosp Southampton NHS Fdn Trust Wessex Cardiothorac Ctr Univ Southampton Hants England;

    Univ Hosp Southampton NHS Fdn Trust Wessex Cardiothorac Ctr Univ Southampton Hants England;

    Univ Hosp Southampton NHS Fdn Trust Wessex Cardiothorac Ctr Univ Southampton Hants England;

    Univ Hosp Southampton NHS Fdn Trust Wessex Cardiothorac Ctr Univ Southampton Hants England;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 基础医学;
  • 关键词

    Aspirin; inflammation; platelets; stent thrombosis; vascular surgery;

    机译：阿司匹林;炎症;血小板;支架血栓形成;血管外科;

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