Folsom A R, Pankow J S, Williams R R, Evans G W, Province M A, Eckfeldt J H
Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis 55454-1015, USA.
Thromb Haemost. 1998 Feb;79(2):400-4.
Several studies have linked higher plasma fibrinogen and plasminogen activator inhibitor (PAI-1) concentrations with increased risk of cardiovascular disease. We studied whether members of families with increased occurrence of coronary heart disease (CHD) have increased levels of fibrinogen and PAI-1 and whether subclinical carotid atherosclerosis is associated with these two hemostatic factors. Contrary to our hypothesis, fibrinogen and PAI-1 antigen levels were not different between high CHD risk families versus random families. Adjusted for age and family type, fibrinogen and PAI-1 were both associated positively with carotid intima-media thickness assessed by B-mode ultrasound. However, adjustment for lifestyle and medical covariates essentially eliminated these associations. These data suggest 1) elevated fibrinogen and PAI-1 do not explain clustering of CHD in families and 2) fibrinogen and PAI-1 may partly mediate the effects of other risk factors on carotid atherosclerosis, though the data are also consistent with them playing no causal role.
多项研究已将较高的血浆纤维蛋白原和纤溶酶原激活物抑制剂（PAI-1）浓度与心血管疾病风险增加联系起来。我们研究了冠心病（CHD）发病率增加的家族成员的纤维蛋白原和PAI-1水平是否升高，以及亚临床颈动脉粥样硬化是否与这两种止血因子相关。与我们的假设相反，高冠心病风险家族与随机家族之间的纤维蛋白原和PAI-1抗原水平并无差异。在对年龄和家族类型进行校正后，纤维蛋白原和PAI-1均与通过B型超声评估的颈动脉内膜中层厚度呈正相关。然而，对生活方式和医学协变量进行校正后，这些关联基本消失。这些数据表明：1）纤维蛋白原和PAI-1升高并不能解释家族性冠心病的聚集现象；2）纤维蛋白原和PAI-1可能部分介导了其他危险因素对颈动脉粥样硬化的影响，尽管这些数据也与它们不发挥因果作用一致。
