Viscoelastic measurements of platelet function, not fibrinogen function, predicts sensitivity to tissue-type plasminogen activator in trauma patients.
Viscoelastic measurements of platelet function, not fibrinogen function, predicts sensitivity to tissue-type plasminogen activator in trauma patients.
复制标题
血小板功能的粘弹性测量，而不是纤维蛋白原功能可以预测创伤患者中对组织型纤溶酶原激活剂的敏感性。
DOI：
10.1111/jth.13067
复制
发表时间：
2015-10
期刊：
影响因子：
--
通讯作者：
Silliman CC
中科院分区：
文献类型：
--
作者：
Moore HB;Moore EE;Chapman MP;Gonzalez E;Slaughter AL;Morton AP;D'Alessandro A;Hansen KC;Sauaia A;Banerjee A;Silliman CC
全身性纤溶亢进是创伤引起的凝血病的致命表型。其发病机制尚不清楚。最近的研究支持血小板在止血和纤维蛋白溶解调节中的核心作用，这意味着血小板损伤是损伤后全身纤维蛋白溶解亢进的发展不可或缺的一部分。本研究的目的是确定血小板功能是否与血凝块对纤溶的敏感性相关。我们假设 ADP 通路的血小板损伤与创伤患者的纤溶敏感性相关。对城市创伤中心符合最高激活水平标准的患者进行了一项前瞻性观察研究。使用天然血栓弹力图 (TEG) 和 ADP 通路的 TEG 血小板图谱 (ADP-MA) 测量与血小板功能相关的粘弹性参数（最大振幅 [MA]）。使用 TEG（角度）和 TEG 功能性纤维蛋白原 (FF) 测定 (FF-MA) 测量纤维蛋白原对凝血的贡献。另一种含有组织型纤溶酶原激活剂 (t-PA) (75 ng mL−1) 的 TEG 测定通过使用 30 分钟 (LY30) 变量的 TEG 裂解来评估凝块对外源纤溶刺激的敏感性。使用多元线性回归来确定哪个 TEG 变量与 t-PA-LY30（纤维蛋白溶解敏感性的量化）相关。分析中包括 58 名创伤患者，中位损伤严重程度评分为 17，碱基缺陷为 6 mEq L−1。显着预测 t-PA-LY30 的 TEG 参数与血小板功能相关（ADP-MA，P = 0.001；MA，P < 0.001），但与纤维蛋白原无关（FF-MA，P = 0.773；角度，P = 0.083）。血小板 ADP 损伤的临床预测因素包括钙水平 (P = 0.001)、碱缺乏 (P = 0.001) 和损伤严重程度 (P = 0.001)。 ADP 通路的血小板损伤与 t-PA 敏感性增加相关。血小板中 ADP 途径的抑制可能是全身纤溶亢进发病机制的早期步骤。
Systemic hyperfibrinolysis is a lethal phenotype of trauma-induced coagulopathy. Its pathogenesis is poorly understood. Recent studies have support a central role of platelets in hemostasis and in fibrinolysis regulation, implying that platelet impairment is integral to the development of postinjury systemic hyperfibrinolysis. The objective of this study was to identify if platelet function is associated with blood clot sensitivity to fibrinolysis. We hypothesize that platelet impairment of the ADP pathway correlates with fibrinolysis sensitivity in trauma patients. A prospective observational study of patients meeting the criteria for the highest level of activation at an urban trauma center was performed. Viscoelastic parameters associated with platelet function (maximum amplitude [MA]) were measured with native thrombelastography (TEG), and TEG platelet mapping of the ADP pathway (ADP-MA). The contribution of fibrinogen to clotting was measured with TEG (angle) and the TEG functional fibrinogen (FF) assay (FF-MA). Another TEG assay containing tissue-type plasminogen activator (t-PA) (75 ng mL−1) was used to assess clot sensitivity to an exogenous fibrinolytic stimulus by use of the TEG lysis at 30 min (LY30) variable. Multivariate linear regression was used to identify which TEG variable correlated with t-PA-LY30 (quantification of fibrinolysis sensitivity). Fifty-eight trauma patients were included in the analysis, with a median injury severity score of 17 and a base deficit of 6 mEq L−1. TEG parameters that significantly predicted t-PA-LY30 were related to platelet function (ADP-MA, P = 0.001; MA, P < 0.001) but not to fibrinogen (FF-MA, P = 0.773; angle, P = 0.083). Clinical predictors of platelet ADP impairment included calcium level (P = 0.001), base deficit (P = 0.001), and injury severity (P = 0.001). Platelet impairment of the ADP pathway is associated with increased sensitivity to t-PA. ADP pathway inhibition in platelets may be an early step in the pathogenesis of systemic hyperfibrinolysis.