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微粒相关组织因子活性及凝血酶活性增加在ST段抬高型心肌梗死纤溶功能衰竭中起潜在作用。

Microparticle-linked tissue factor activity and increased thrombin activity play a potential role in fibrinolysis failure in ST-segment elevation myocardial infarction.

作者信息

Huisse Marie-Geneviève, Ajzenberg Nadine, Feldman Laurent, Guillin Marie-Claude, Steg Philippe Gabriel

机构信息

Department of Haematology, AP-HP, Hôpital Bichat, Paris, France.

出版信息

Thromb Haemost. 2009 Apr;101(4):734-40.

PMID:19350119
Abstract

Fibrinolysis for acute ST-segment elevation MI achieves early recanalisation of the infarct artery in approximately 60% of cases. The aim of the study was to determine whether failure to achieve recanalisation was associated with differences in haemostasis biomarkers compared to patients with successful fibrinolysis. Fourty-three patients were prospectively enrolled in a case-control study. All patients had received tenecteplase (TNK-tPA) together with aspirin (500 mg) and heparin (5,000 IU). Emergency angiography within 90 minutes of bolus TNK-tPA identified 13 TIMI 0-2 patients (cases) and 30 TIMI 3 patients (controls). Blood samples were collected before angiography to determine tissue factor activity associated with microparticles (TF-MP); soluble platelet glycoprotein V (sGPV) and thrombin-antithrombin complexes (TAT) as markers of thrombin generation; tissue plasminogen activator (endogenous tPA+ TNK-tPA), plasminogen activator inhibitor (PAI-1) and plasmin-antiplasmin complexes (PAP) as markers of plasmin generation. The baseline characteristics of the two patients' groups were similar with respect to sex, age, and risks factors. Cases differed from controls by higher TF-MP levels (1.9 [1-13] vs. 1 [0.6-1.3] pM), sGPV (67 [51-126] vs. (48 [39-72] ng/ml), p = 0.039 and TAT (10 [4-37.5] vs. 4 [2.9-7.2] ng/ml), p = 0.035. TAT correlated with TF-MP (r = 0.51, p = 0.0064) and sGPV (r = 0.51, p = 0.0018). No significant difference was observed in tPA or PAI-1 levels. PAP were lower in cases (18.83 [14.83-40.43] mug/ml) than in controls (35.83 [27.9-43.94] mug/ml), p = 0.045. In conclusion, fibrinolysis failure in AMI is characterised by a higher procoagulant state associated with TF-MP and a lower plasmin generation.

摘要

急性ST段抬高型心肌梗死进行纤溶治疗时,约60%的病例梗死相关动脉可实现早期再通。本研究旨在确定与纤溶成功的患者相比,未实现再通是否与止血生物标志物的差异有关。43例患者前瞻性纳入一项病例对照研究。所有患者均接受了替奈普酶(TNK - tPA)联合阿司匹林(500mg)和肝素(5000IU)治疗。在推注TNK - tPA后90分钟内进行急诊血管造影,确定了13例TIMI 0 - 2级患者(病例组)和30例TIMI 3级患者(对照组)。在血管造影前采集血样,以测定与微粒相关的组织因子活性(TF - MP);可溶性血小板糖蛋白V(sGPV)和凝血酶 - 抗凝血酶复合物(TAT)作为凝血酶生成的标志物;组织型纤溶酶原激活剂(内源性tPA + TNK - tPA)、纤溶酶原激活剂抑制剂(PAI - 1)和纤溶酶 - 抗纤溶酶复合物(PAP)作为纤溶酶生成的标志物。两组患者在性别、年龄和危险因素方面的基线特征相似。病例组与对照组相比,TF - MP水平较高(1.9[1 - 13]对1[0.6 - 1.3]pM)、sGPV水平较高(67[51 - 126]对48[39 - 72]ng/ml,p = 0.039)以及TAT水平较高(10[4 - 37.5]对4[2.9 - 7.2]ng/ml,p = 0.035)。TAT与TF - MP(r = 0.51,p = 0.0064)和sGPV(r = 0.51,p = 0.0018)相关。tPA或PAI - 1水平未观察到显著差异。病例组的PAP水平(18.83[14.83 - 40.43]μg/ml)低于对照组(35.83[27.9 - 43.94]μg/ml),p = 0.045。总之,急性心肌梗死纤溶治疗失败的特征是与TF - MP相关的促凝状态较高且纤溶酶生成较低。

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