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目的 观察急性心肌梗死 (AMI)发作期间组织因子途径的变化。方法 6 9例临床确诊的AMI患者和 30例健康中老年人 (作对照 )被纳入研究对象。血浆中的组织因子 (TF)和组织因子途径抑制物 (TFPI)的活性测定采用发色底物法 ,TF和TFPI抗原采用ELISA法。激活的凝血因子Ⅶa采用重组可溶性TF法。凝血因子Ⅶ促凝活性采用活性测定法。结果 与对照组相比 ,AMI患者血浆中TF、TFPI的活性均显著增加 [分别为 5 6 7(1 77～ 5 4 95 )mU/mlvs 2 36 (1 13～ 6 4 2 )mU/ml,P <0 0 1;2 2 4 85 (86 6 5～ 5 12 12 ) %vs 138 75 (5 1 72～ 2 97 2 ) %,P <0 0 1]。同时TF、TFPI的抗原、凝血因子Ⅶa的活性亦有明显升高 ,但凝血因子Ⅶ促凝活性无显著变化。结论 AMI发作期间体内组织因子途径被启动 ,血液呈现高凝状态。
Objective To observe the changes of tissue factor pathway during the onset of acute myocardial infarction (AMI). Methods Sixty-nine clinically diagnosed AMI patients and 30 healthy middle-aged and elderly patients (control group) were included in the study. Tissue Factor (TF) and Tissue Factor Pathway Inhibitor (TFPI) activity in plasma were measured using a chromogenic substrate assay and TF and TFPI antigens were analyzed by ELISA. Activated factor Ⅶ a using recombinant soluble TF method. Prothrombin factor Ⅶ procoagulant activity using activity assay. Results Compared with the control group, the activities of TF and TFPI in plasma of patients with AMI were significantly increased (567 (174-6595) mU / ml vs 36 (13-642) mU / ml, P <0 0 1; 2 2 4 85 (86 6 5 ~ 5 12 12)% vs 138 75 (5 1 72 ~ 2 97 2)%, P 0 01]. At the same time, the antigens of TF and TFPI and the activity of coagulation factor Ⅶ a also increased obviously, but there was no significant change of procoagulant activity of coagulation factor Ⅶ. Conclusion During the course of AMI, the Tissue Factor pathway is activated and the blood is hypercoagulable.