Feindt P, Seyfert U, Volkmer I, Huwer H, Kalweit G, Gams E
Department of Thoracic and Cardiovascular Surgery, Homburg University Hospital, Germany.
Eur J Cardiothorac Surg. 1994;8(6):308-13; discussion 313-4. doi: 10.1016/s1010-7940(05)80091-0.
To determine a possible phase of hypercoagulability after the use of high-dose aprotinin, a prospective randomized double-blind study was performed. Twenty patients undergoing aortocoronary bypass surgery were investigated, a placebo group P (n = 10) was compared to an aprotinin group A (n = 10). Examining parameters of thrombin activation and fibrinolysis, we found during extracorporeal circulation--under continuous aprotinin infusion--a significant inhibition of thrombin activation and fibrinolysis in the aprotinin group (thrombin-antithrombin-III-complexes: 95 +/- 23 micrograms/l, d-dimers: 448 +/- 60 ng/ml, plasminogen activity: 33 +/- 3%, plasminogen activator inhibitor: 98 +/- 14 U/ml) compared to the placebo group (thrombin-antithrombin-III-complexes: 143 +/- 13 micrograms/l, d-dimers: 2755 +/- 430 ng/ml, plasminogen activity: 125 +/- 15%, plasminogen activator inhibitor: 10 +/- 4 U/ml). In contrast, after stopping the aprotinin infusion--from the end of extracorporeal circulation until the morning of the first postoperative day--strong thrombin activation took place in the aprotinin group (d-dimers increased from 472 +/- 90 to 1607 +/- 140 ng/ml), while in the placebo group a decrease could be registered. At this time, the fibrinolysis was still reduced in the aprotinin group (plasminogen activity: 48 +/- 6% vs 85 +/- 16% in the placebo group). In conclusion, interference with the thrombohemorrhagic balance induces hypercoagulability after the use of high-dose aprotinin, with elevated levels of thrombin-antithrombin-III-complexes, d-dimers, and plasminogen and a decreased level of plasminogen activator inhibitor. In our opinion, it is necessary to prevent this counter-regulation.(ABSTRACT TRUNCATED AT 250 WORDS)
为了确定使用大剂量抑肽酶后可能出现的高凝阶段,进行了一项前瞻性随机双盲研究。对20例行主动脉冠状动脉搭桥手术的患者进行了调查,将安慰剂组P(n = 10)与抑肽酶组A(n = 10)进行比较。通过检查凝血酶激活和纤维蛋白溶解的参数,我们发现在体外循环期间——持续输注抑肽酶时——抑肽酶组的凝血酶激活和纤维蛋白溶解受到显著抑制(凝血酶 - 抗凝血酶 - III复合物:95±23微克/升,D - 二聚体:448±60纳克/毫升,纤溶酶原活性:33±3%,纤溶酶原激活物抑制剂:98±14单位/毫升),而安慰剂组的数据为(凝血酶 - 抗凝血酶 - III复合物:143±13微克/升,D - 二聚体:2755±430纳克/毫升,纤溶酶原活性:125±15%,纤溶酶原激活物抑制剂:10±4单位/毫升)。相反,在停止抑肽酶输注后——从体外循环结束到术后第一天早晨——抑肽酶组发生了强烈的凝血酶激活(D - 二聚体从472±90增加到1607±140纳克/毫升),而安慰剂组则出现下降。此时,抑肽酶组的纤维蛋白溶解仍然降低(纤溶酶原活性:48±6%,而安慰剂组为85±16%)。总之,干扰血栓出血平衡会在使用大剂量抑肽酶后诱发高凝状态,表现为凝血酶 - 抗凝血酶 - III复合物、D - 二聚体和纤溶酶原水平升高,纤溶酶原激活物抑制剂水平降低。我们认为,有必要预防这种反调节。(摘要截断于250字)