Woodward M, Lowe G D, Rumley A, Tunstall-Pedoe H
Cardiovascular Epidemiology Unit, University of Dundee, Scotland.
Eur Heart J. 1998 Jan;19(1):55-62. doi: 10.1053/euhj.1997.0573.
Fibrinogen was measured in 5095 men and 4860 men aged 40-59 in a random population sample from 25 districts of Scotland recruited during 1984-87: the Scottish Heart Health Study. Fibrinogen was then related to the chance of fatal and non-fatal coronary events and death from any cause during a subsequent follow-up period of around 8 years.
Fibrinogen was measured by the Clauss assay. The effect of fibrinogen on coronary heart disease and death was assessed through age-adjusted means and Cox proportional hazards regression models, accounting for age, cotinine (a measure of tobacco smoke inhalation) and 11 other major coronary risk factors. Fibrinogen was found to be an important risk factor for coronary heart disease in men and women, with and without pre-existing coronary heart disease. There appears to be a threshold effect, with those in the highest fifth of the distribution having a much increased risk. Estimated age-adjusted hazard ratios by sex and pre-existing coronary heart disease group for the highest to lowest fifth of fibrinogen range between 1.93 and 4.86. Fibrinogen is also important as a risk factor for coronary death and all-causes mortality, with a similar threshold effect. Comparing the two extreme fifths, the hazard ratios for coronary death are 3.01 and 3.42, and for all-cause mortality are 2.59 and 2.20, for men and women respectively. Adjustment for cotinine reduces the hazard ratios, but further adjustment for the other 11 risk factors has little effect for coronary heart disease events. After full adjustment there is a remaining significant (P < 0.05) hazard ratio for coronary death and death from any cause and for a coronary heart disease event for those free of coronary heart disease at baseline, amongst men, comparing the highest to the lowest fifth.
Fibrinogen is a strong predictor of coronary heart disease, fatal or non-fatal, new or recurrent, and of death from an unspecified cause, for both men and women. Its effect is only partially attributable to other coronary risk factors, the most important of which is smoking.
在1984年至1987年从苏格兰25个地区招募的随机人群样本中，对5095名40至59岁男性和4860名女性进行纤维蛋白原测量：即苏格兰心脏健康研究。随后在大约8年的后续随访期内，将纤维蛋白原与致命和非致命性冠心病事件以及任何原因导致的死亡几率相关联。
采用Clauss法测量纤维蛋白原。通过年龄调整均值和Cox比例风险回归模型评估纤维蛋白原对冠心病和死亡的影响，该模型考虑了年龄、可替宁（衡量吸入烟草烟雾的指标）以及其他11种主要冠心病风险因素。结果发现，无论男性还是女性，无论是否已有冠心病，纤维蛋白原都是冠心病的重要风险因素。似乎存在阈值效应，处于分布最高五分位数的人群风险大幅增加。按性别和已有冠心病组划分，纤维蛋白原范围从最高五分位数到最低五分位数的估计年龄调整风险比在1.93至4.86之间。纤维蛋白原作为冠心病死亡和全因死亡率的风险因素也很重要，具有类似的阈值效应。比较两个极端五分位数，男性和女性冠心病死亡的风险比分别为3.01和3.42，全因死亡率的风险比分别为2.59和2.20。对可替宁进行调整会降低风险比，但对其他11种风险因素进一步调整对冠心病事件影响不大。在进行全面调整后，对于基线时无冠心病的男性，比较最高五分位数和最低五分位数，冠心病死亡、任何原因导致的死亡以及冠心病事件仍存在显著（P<0.05）风险比。
纤维蛋白原是男性和女性致命或非致命、新发或复发冠心病以及不明原因死亡的有力预测指标。其影响仅部分归因于其他冠心病风险因素，其中最重要的是吸烟。
