Overview of hemostatic factors involved in atherosclerotic cardiovascular disease
Overview of hemostatic factors involved in atherosclerotic cardiovascular disease
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DOI：
10.1007/s11745-005-1488-8
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发表时间：
2005-12-01
期刊：
影响因子：
1.9
通讯作者：
Kannel, WB
中科院分区：
文献类型：
--
作者：
Kannel, WB
与心血管疾病（CVD）发展相关的止血因子包括纤维蛋白原、血管性血友病因子、组织纤溶酶原激活物（tPA）抗原、纤溶酶原激活物抑制剂-1（派-1）和因子VII。这些的每个SD增量使关联增加24- 30%。大多数止血因子与炎症标志物相互关联[例如，C-反应蛋白（CRP）]和低密度脂蛋白胆固醇。纤维蛋白原似乎是CVD最基本的止血危险因素。Frachial研究再次证实了在两种性别中，年龄、体重指数、吸烟、糖尿病、总胆固醇、HDL胆固醇和TG的纤维蛋白原三分位数（P < 0.001）的显著线性风险因素趋势。纤维蛋白原也可能直接增加CVD风险，因为它在血小板聚集、血浆粘度和纤维蛋白形成中起作用。纤维蛋白原也是一种急性期反应物，在炎症状态下升高。纤维蛋白原介导其他危险因素的血栓形成作用。纤维蛋白原水平随着吸烟数量的增加而增加，并在戒烟后迅速下降。这种快速的纤维蛋白原下降可能是戒烟后CVD风险降低的机制。体重减轻伴随着纤维蛋白原减少。纤维蛋白原和低密度脂蛋白胆固醇之间的相关性表明，脂质引起的CVD风险部分是通过纤维蛋白原介导的。糖尿病患者的高反应性血小板可能部分是由于其增加的纤维蛋白原。不稳定型心绞痛的纤维蛋白原和CRP升高提示急性期反应。患病率、病例对照、血管造影和超声心动图研究表明，止血和炎症标志物是初始和复发CVD的强独立危险因素。研究数据表明，纤维蛋白原每增加一个标准差，风险就增加20%。可以得出结论，纤维蛋白原和CRP测定可能是有用的筛选工具，以确定个人在增加风险的血栓性并发症的CVD。
Hemostatic factors associated with the development of cardiovascular disease (CVD) include fibrinogen, von Willebrand factor, tissue plasminogen activator (tPA) antigen, plasminogen activator inhibitor-1 (PAI-1), and factor VII. Each SD increment of these increases the association by 24-30%. Most hemostatic factors are intercorrelated with inflammatory markers [e.g., C-reactive protein (CRP)] and LDL cholesterol. Fibrinogen seems the most fundamental hemostatic risk factor for CVD. The Framingham Study reaffirms the significant linear risk factor trends across fibrinogen tertiles (P < 0.001) for age, body mass index, smoking, diabetes mellitus, total cholesterol, HDL cholesterol, and TG in both sexes. Fibrinogen may also directly increase CVD risk because of its role in platelet aggregation, plasma viscosity, and fibrin formation. Fibrinogen is also an acute-phase reactant that is elevated in inflammatory states. Fibrinogen mediates the thrombogenic effect of other risk factors. Fibrinogen levels increase with the number of cigarettes smoked and quickly fall after smoking cessation. This rapid fibrinogen decline may be a mechanism for CVD risk reduction after smoking cessation. Weight loss is accompanied by reduced fibrinogen. The correlation between fibrinogen and LDL cholesterol suggests that lipid-imposed CVD risk is mediated partly through fibrinogen. Hyper-reactive platelets of diabetics may result in part from their increased fibrinogen. Elevated fibrinogen and CRP of unstable angina suggest an acute-phase reaction. Prevalence, case-control, angiographic, and echocardiogram investigations incriminate hemostatic and inflammatory markers as strong independent risk factors for initial and recurrent CVD. Framingham Study data indicate that each SD increase in fibrinogen imposes a 20% independent increment in risk. It may be concluded that fibrinogen and CRP determination may be useful screening tools to identify individuals at added risk for thrombotic complications of CVD.