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慢性心力衰竭患者凝血紊乱的研究

马睿   

  1. 天津医科大学总医院
  • 收稿日期:2012-01-03 修回日期:2012-07-10 出版日期:2013-01-15 发布日期:2013-01-15
  • 通讯作者: 马睿

Study on the disorder of coagulation in the patients with chronic heart failure

  • Received:2012-01-03 Revised:2012-07-10 Published:2013-01-15 Online:2013-01-15

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摘要：

【摘要】 目的对慢性心力衰竭(CHF)患者血管内皮及凝血系统异常改变进行研究,分析其功能紊乱的机制。方法选择CHF患者152例(CHF组)和健康对照150例(对照组),检测所有研究对象血浆血管性血友病因子抗原(vWF∶Ag)含量、组织因子活性(TF∶A)及凝血酶-抗凝血酶复合物(TAT)水平。结果 CHF组的vWF∶Ag、TF∶A、TAT水平均高于对照组,差异有统计学意义(P<0.01)。Ⅱ度心衰患者vWF∶Ag、TF∶A高于Ⅰ度心衰患者,差异有统计学意义(P<0.01),Ⅲ度心衰患者vWF∶Ag、TF∶A、TAT高于Ⅱ度心衰患者(P<0.01)。CHF患者vWF:Ag与TF∶A和TAT无明显相关性(r分别为0.21、0.40,P>0.05),TF∶A与TAT呈正相关(r=0.69,P<0.01)。结论 CHF患者存在严重的血管内皮损伤,凝血系统发生显著活化,导致血栓风险增加。vWF∶Ag、TAT和TF∶A水平变化与患者心衰程度密切相关。 

关键词: 慢性心力衰竭, 功能紊乱, 凝血, 内皮细胞损伤

Abstract: Objective：Study on the function and condition of the vascular endothelial system and coagulation system in the patients with the chronic heart failure(CHF), assay the mechanisms of the dysfunction. Methods：Using the IL ACL-9000 blood coagulation instrument assay the von Willebrand Factor antigen(vWF:Ag). The TF:A was measured by chromogenic substrate method. The TAT was measured by ELISA. Results：Compared the control with the patients group, vWF:Ag, TF:A and TAT were increased significantly in the patients group（P<0.01）. vWF:Ag and TF:A in the HF patients with NYHA Class Ⅱ were remarkably higher than the NYHA Class Ⅰ（P<0.01）. vWF:Ag, TF:A and TAT in the HF patients with NYHA Class Ⅲ were remarkably higher than the NYHA Class Ⅱ（P<0.01）. There was no relationship between the vWF:Ag and the TF:A, the TAT（r=0.2128, r=0.4003, P>0.05）, and the strong positive relationship between the TF:A and the TAT（r=0.6946，P<0.01）. Conclusion：There was severe vascular endothelial cells damage in the patients with HF, and the endothelial injury caused the coagulation system to activate, and brought the worse thrombosis risk. The level of the vWF:Ag, TAT and TF:Ag were closely connected with heart failure progress in CHF patients.

Key words: chronic heart failure, dysfunction, coagulation, endothelial cells damage