Dipartimento Cardiovascolare, Policlinico S. Orsola, Bologna, Italy.
Istituto di Patolgia, Policlinico S. Orsola, Bologna, Italy.
PLoS One. 2013 Dec 11;8(12):e81501. doi: 10.1371/journal.pone.0081501. eCollection 2013.
Although ruptured atherosclerotic plaques have been extensively analyzed, the composition of thrombi causing arterial occlusion in patients with ST-segment elevation acute myocardial infarction has been less thoroughly investigated. We sought to investigate whether coagulant active tissue factor can be retrieved in thrombi of patients with STEMI undergoing primary percutaneous coronary intervention.
Nineteen patients with ST-segment elevation acute myocardial infarction referred for primary percutaneous coronary intervention were enrolled in this study. Coronary thrombi aspirated from coronary arteries were routinely processed for paraffin embedding and histological evaluation (4 patients) or immediately snap frozen for evaluation of tissue factor activity using a modified aPTT test (15 patients). Immunoprecipitation followed by immunoblotting was also performed in 12 patients.
Thrombi aspirated from coronary arteries showed large and irregular areas of tissue factor staining within platelet aggregates, and in close contact with inflammatory cells. Some platelet aggregates stained positive for tissue factor, whereas others did not. Monocytes consistently stained strongly for tissue factor, neutrophils had a more variable and irregular tissue factor staining, and red blood cells did not demonstrate staining for tissue factor. Median clotting time of plasma samples containing homogenized thrombi incubated with a monoclonal antibody that specifically inhibits tissue factor-mediated coagulation activity (mAb 5G9) were significantly longer than their respective controls (88.9 seconds versus 76.5 seconds, respectively; p<0.001). Tissue factor was also identified by immunoprecipitation in 10 patients, with significant variability among band intensities.
Active tissue factor is present in coronary artery thrombi of patients with ST-segment elevation acute myocardial infarction, suggesting that it contributes to activate the coagulation cascade ensuing in coronary thrombosis.
尽管已经广泛分析了破裂的动脉粥样硬化斑块，但导致 ST 段抬高型急性心肌梗死患者动脉闭塞的血栓成分尚未得到充分研究。我们旨在研究在接受直接经皮冠状动脉介入治疗的 ST 段抬高型急性心肌梗死患者的血栓中是否可以回收促凝活性组织因子。
本研究纳入了 19 名因 ST 段抬高型急性心肌梗死而接受直接经皮冠状动脉介入治疗的患者。常规处理从冠状动脉抽吸的冠状动脉血栓，用于石蜡包埋和组织学评估（4 例）或立即冷冻用于使用改良的 aPTT 试验评估组织因子活性（15 例）。还对 12 例患者进行了免疫沉淀后免疫印迹分析。
从冠状动脉抽吸的血栓在血小板聚集物内显示出大而不规则的组织因子染色区域，并且与炎症细胞密切接触。一些血小板聚集物呈组织因子阳性，而另一些则呈阴性。单核细胞始终强烈染色组织因子，中性粒细胞的组织因子染色更具变异性和不规则性，而红细胞则没有组织因子染色。含有匀浆血栓的血浆样本的凝血时间明显长于各自的对照（分别为 88.9 秒和 76.5 秒；p<0.001），这些样本用一种特异性抑制组织因子介导的凝血活性的单克隆抗体（mAb 5G9）孵育。在 10 例患者中也通过免疫沉淀鉴定了组织因子，条带强度存在显著差异。
ST 段抬高型急性心肌梗死患者的冠状动脉血栓中存在活性组织因子，提示其有助于激活随后发生的冠状动脉血栓形成的凝血级联反应。
