Sato Hideo, Yamamoto Koji, Kakinuma Akihito, Nakata Yoshinori, Sawamura Shigehito
Department of Anesthesia, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo, 173-8605, Japan.
Department of Transfusion Medicine and Cell Therapy, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan.
J Cardiothorac Surg. 2015 Jun 23;10:84. doi: 10.1186/s13019-015-0295-9.
Any form of surgery or tissue damage causes release of tissue factor into the circulation. This may lead to the accelerated consumption of coagulation factors, resulting in severe consumptive coagulopathy. In this study, we compared the molecular markers involved in coagulation activation during cardiopulmonary bypass (CPB) between patients who underwent aortic replacement surgery and those who underwent valve surgery.
This prospective observational study was performed in each 14 patients who underwent aortic replacement surgery or valve surgery. We evaluated the differences in the levels of fibrinogen, activated factor VII (FVIIa), thrombin-antithrombin complex (TAT), and soluble fibrin monomer complex (SFMC) during surgery between these two groups.
The change in fibrinogen levels showed no difference between the groups. The magnitude of increase in TAT was much larger in patients who underwent aortic replacement surgery than in those who underwent valve surgery (173.6 vs. 49.4 ng/mL; p = 0.0001). More importantly, the elevation of FVIIa was significantly higher in patients who underwent aortic replacement (28.5 vs. 19.0 mU/mL; p = 0.0122). The magnitude of increase in SFMC was also larger in the aortic replacement surgery.
The activation of coagulation during CPB was dramatically higher in the aortic replacement surgery compared with the valve surgery, probably owing to the activation of the extrinsic coagulation pathway in the former. This could potentially exacerbate consumptive coagulopathy after CPB termination in patients who underwent aortic replacement, possibly resulting in massive hemorrhage due to impaired hemostasis.
任何形式的手术或组织损伤都会导致组织因子释放进入循环系统。这可能会导致凝血因子加速消耗,从而引发严重的消耗性凝血病。在本研究中,我们比较了接受主动脉置换手术的患者和接受瓣膜手术的患者在体外循环(CPB)期间参与凝血激活的分子标志物。
本前瞻性观察性研究对14例接受主动脉置换手术或瓣膜手术的患者进行。我们评估了两组患者手术期间纤维蛋白原、活化因子VII(FVIIa)、凝血酶 - 抗凝血酶复合物(TAT)和可溶性纤维蛋白单体复合物(SFMC)水平的差异。
两组之间纤维蛋白原水平的变化无差异。接受主动脉置换手术的患者中TAT的增加幅度远大于接受瓣膜手术的患者(173.6对49.4 ng/mL;p = 0.0001)。更重要的是,接受主动脉置换的患者中FVIIa的升高明显更高(28.5对19.0 mU/mL;p = 0.0122)。主动脉置换手术中SFMC的增加幅度也更大。
与瓣膜手术相比,主动脉置换手术期间CPB期间的凝血激活明显更高,这可能是由于前者的外源性凝血途径被激活。这可能会在主动脉置换患者CPB结束后加剧消耗性凝血病,可能导致止血功能受损而大量出血。