Réganon E, Ferrando F, Vila V, Villa P, Martínez-Sales V, Fayos L, Ruano M, Aznar J
Research Center, La Fe University Hospital, Valencia, Spain.
Haemostasis. 1998 Mar-Apr;28(2):99-105. doi: 10.1159/000022419.
This study compares the extent of inhibition of thrombin generation and activity achieved in patients with acute myocardial infarction receiving fibrinolytic treatment (streptokinase SK, or rt-PA) and concomitant intravenous heparin treatment adjusted to the patients' weight with that achieved with the same heparin regimen but without fibrinolytic therapy. The study involved 90 patients, grouped according to their treatment: SK+heparin; rt-PA+heparin, and heparin without thrombolytic agents. Prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT), fibrinopeptide A (FPA) and activated partial thromboplastin time were measured. Patients treated with SK+heparin or rt-PA+heparin and higher F1+2 plasma levels than the patients treated with heparin alone at 12, 48 and 72 h in the case of SK+heparin, and at 12, 24, 48 and 72 h in that of rt-PA+heparin. Compared to baseline, the plasma levels of FPA were decreased in the three treatment groups at 24-48 h. There were no significant changes in TAT and FPA plasma levels among the three treatment groups at the different times. After thrombolytic therapy with both SK and rt-PA, there was an increase in thrombin generation, although high-dose intravenous heparin inhibited the different increases in thrombin associated with the thrombolytic agents to the same extent.
本研究比较了接受纤维蛋白溶解治疗（链激酶SK或rt-PA）并根据患者体重调整静脉注射肝素治疗的急性心肌梗死患者与接受相同肝素治疗方案但未进行纤维蛋白溶解治疗的患者在凝血酶生成抑制程度和活性方面的差异。该研究纳入了90例患者，根据治疗方法分组：SK+肝素组；rt-PA+肝素组，以及未使用溶栓剂的肝素组。检测了凝血酶原片段1+2（F1+2）、凝血酶-抗凝血酶复合物（TAT）、纤维蛋白肽A（FPA）和活化部分凝血活酶时间。SK+肝素组在12、48和72小时时，以及rt-PA+肝素组在12、24、48和72小时时，接受SK+肝素或rt-PA+肝素治疗的患者的F1+2血浆水平高于单独接受肝素治疗的患者。与基线相比，三个治疗组在24至48小时时FPA的血浆水平均下降。三个治疗组在不同时间的TAT和FPA血浆水平均无显著变化。SK和rt-PA溶栓治疗后，凝血酶生成增加，尽管高剂量静脉注射肝素对与溶栓剂相关的不同程度的凝血酶增加具有相同程度的抑制作用。
