Kannel William B
Boston University School of Medicine/Framingham Heart Study, Framingham, Massachusetts 01702-5827, USA.
Lipids. 2005 Dec;40(12):1215-20. doi: 10.1007/s11745-005-1488-8.
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. Hyperreactive 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.
与心血管疾病（CVD）发生相关的止血因子包括纤维蛋白原、血管性血友病因子、组织型纤溶酶原激活剂（tPA）抗原、纤溶酶原激活剂抑制剂-1（PAI-1）和因子VII。这些因子每增加1个标准差，关联度就会增加24%-30%。大多数止血因子与炎症标志物[如C反应蛋白（CRP）]和低密度脂蛋白胆固醇相互关联。纤维蛋白原似乎是CVD最基本的止血危险因素。弗雷明汉姆研究再次证实，在年龄、体重指数、吸烟、糖尿病、总胆固醇、高密度脂蛋白胆固醇和甘油三酯方面，纤维蛋白原三分位数之间存在显著的线性危险因素趋势（P<0.001），男女皆是如此。纤维蛋白原还可能因其在血小板聚集、血浆黏度和纤维蛋白形成中的作用而直接增加CVD风险。纤维蛋白原也是一种急性期反应物，在炎症状态下会升高。纤维蛋白原介导其他危险因素的血栓形成作用。纤维蛋白原水平随吸烟量增加而升高，戒烟后迅速下降。这种纤维蛋白原的快速下降可能是戒烟后CVD风险降低的一种机制。体重减轻伴随着纤维蛋白原减少。纤维蛋白原与低密度脂蛋白胆固醇之间的相关性表明，脂质引发的CVD风险部分是通过纤维蛋白原介导的。糖尿病患者血小板反应性过高可能部分源于其纤维蛋白原增加。不稳定型心绞痛患者纤维蛋白原和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均表明，止血和炎症标志物是初始和复发性CVD的强有力独立危险因素。弗雷明汉姆研究数据表明，纤维蛋白原每增加1个标准差，风险就会独立增加20%。可以得出结论，纤维蛋白原和CRP检测可能是识别CVD血栓形成并发症额外风险个体的有用筛查工具。
