Ileri Mehmet, Alper Aysin, Senen Kubilay, Durmaz Tahir, Atak Ramazan, Hisar Ismet, Yetkin Ertan, Turhan Hasan, Demirkan Deniz
Department of Cardiology, Türkiye Yüksek Ihtisas Hastanesi, Ankara, Turkey.
Am J Cardiol. 2003 Mar 15;91(6):689-92. doi: 10.1016/s0002-9149(02)03405-7.
Inflammation-induced procoagulant changes and alterations in platelet activity appear to play an important role in thromboembolic complications of infective endocarditis (IE). The aim of this study was to investigate systemic coagulation activity, fibrinolytic capacity, and platelet activation in IE patients with and without embolic events by measuring the plasma levels of prothrombin fragment 1 + 2, thrombin-antithrombin III complex, plasminogen activator inhibitor-1, beta-thromboglobulin, and platelet factor 4. The study included 76 consecutive patients with definite IE according to the Duke criteria. Among them, 13 (17.1%) had major embolic events. Plasma concentrations of prothrombin fragment 1 + 2 (3.2 +/- 1.3 vs 1.7 +/- 0.7 and 1.4 +/- 0.7 nmol/L, p <0.001, respectively) and thrombin-antithrombin (7.3 +/- 1.5 vs 2.9 +/- 1.2 and 2.2 +/- 1.1 ng/ml, p <0.001, respectively) were elevated in patients with embolic events compared with both patients without embolic events and control subjects. Similarly, patients with embolic events had increased plasma levels of beta-thromboglobulin (63.3 +/- 10.9 vs 33.1 +/- 11.6 and 19.1 +/- 10.6 ng/ml, p <0.001, respectively) and platelet factor 4 (106.0 +/- 28.7 vs 50.3 +/- 16.7 and 43.0 +/- 15.8 ng/ml, p <0.001, respectively) compared with those without embolic events and the control group. Embolic patients also had higher plasminogen activator inhibitor-1 levels than both nonembolic patients and healthy subjects (14.4 +/- 6.4 vs 8.6 +/- 5.9 and 5.4 +/- 4.3 ng/ml, p = 0.002, respectively). In conclusion, IE patients with subsequent thromboembolism have increased systemic coagulation activation, enhanced platelet activity/damage, and impaired fibrinolysis. The resulting imbalance produces a sustained hypercoagulable state that may contribute to the increased risk of thromboembolic events in this particular group.
炎症诱导的促凝血变化和血小板活性改变似乎在感染性心内膜炎（IE）的血栓栓塞并发症中起重要作用。本研究的目的是通过测量血浆中凝血酶原片段1 + 2、凝血酶 - 抗凝血酶III复合物、纤溶酶原激活物抑制剂 - 1、β - 血小板球蛋白和血小板因子4的水平，调查有无栓塞事件的IE患者的全身凝血活性、纤溶能力和血小板活化情况。该研究纳入了76例根据杜克标准确诊为IE的连续患者。其中，13例（17.1%）发生了主要栓塞事件。与无栓塞事件的患者和对照组相比，发生栓塞事件的患者血浆中凝血酶原片段1 + 2（分别为3.2±1.3 vs 1.7±0.7和1.4±0.7 nmol/L，p<0.001）和凝血酶 - 抗凝血酶（分别为7.3±1.5 vs 2.9±1.2和2.2±1.1 ng/ml，p<0.001）水平升高。同样，与无栓塞事件的患者和对照组相比，发生栓塞事件的患者血浆中β - 血小板球蛋白（分别为63.3±10.9 vs 33.1±11.6和19.1±10.6 ng/ml，p<0.001）和血小板因子4（分别为106.0±28.7 vs 50.3±16.7和43.0±15.8 ng/ml，p<0.001）水平也升高。栓塞患者的纤溶酶原激活物抑制剂 - 1水平也高于非栓塞患者和健康受试者（分别为14.4±6.4 vs 8.6±5.9和5.4±4.3 ng/ml，p = 0.002）。总之，随后发生血栓栓塞的IE患者全身凝血激活增加、血小板活性/损伤增强且纤溶受损。由此产生的失衡导致持续的高凝状态，这可能导致该特定群体血栓栓塞事件风险增加。
