Leander K, Wiman B, Hallqvist J, Falk G, De Faire U
Division of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Solna, 171 77 Stockholm, Sweden.
J Intern Med. 2002 Oct;252(4):332-41. doi: 10.1046/j.1365-2796.2002.01041.x.
To elucidate the association between a genetic polymorphism of the fibrinogen Bbeta-gene (G-455A) and plasma fibrinogen levels and myocardial infarction (MI), respectively. In addition, to explore potential synergistic gene-environment interactions involving this polymorphism--until now, these data were unavailable.
This case-referent study of subjects aged 45-70 and living in Stockholm includes 834 men and 346 women with first-time MI and 1034 men and 494 women randomly chosen as referents from the population. The cases were identified between 1992 and 1994 at the 10 emergency hospitals in Stockholm County.
MI and plasma fibrinogen levels.
Crude analyses associated a high level of plasma fibrinogen with an increased risk of MI in both men and women. However, the relative risk decreased after controlling for other risk factors. The multivariate-adjusted odds ratio (OR) (95% confidence interval) was 1.6 (1.2-2.3) for men and 1.5 (0.9-2.6) for women. Presence of the A allele at the G-455A polymorphic site indicated higher plasma fibrinogen levels than the presence of the G allele, but the difference was only statistically significant for male cases. The -455A allele was not associated with an increased risk of MI. Furthermore, there were no strong indications of synergistic interaction between the G-455A polymorphism and any of the environmental exposures considered.
In this large number of MI cases and referents, a high level of plasma fibrinogen was independently associated with increased risk of MI in men but not in women. The presence of the A allele at the G-455A polymorphism of the fibrinogen Bbeta-gene was not associated with increased risk of MI, and no synergistic gene-environment interactions were detected.
分别阐明纤维蛋白原Bβ基因（G-455A）的基因多态性与血浆纤维蛋白原水平及心肌梗死（MI）之间的关联。此外，探究涉及该多态性的潜在基因-环境协同相互作用——目前尚无这些数据。
设计、设置和研究对象：这项针对年龄在45至70岁且居住在斯德哥尔摩的人群的病例对照研究，包括834例首次发生心肌梗死的男性和346例女性，以及从人群中随机选取的1034例男性和494例女性作为对照。病例于1992年至1994年在斯德哥尔摩县的10家急诊医院确诊。
心肌梗死和血浆纤维蛋白原水平。
粗分析表明，男性和女性血浆纤维蛋白原水平升高均与心肌梗死风险增加相关。然而，在控制其他风险因素后，相对风险降低。多因素调整后的比值比（OR）（95%置信区间）男性为1.6（1.2 - 2.3），女性为1.5（0.9 - 2.6）。在G-455A多态性位点存在A等位基因表明血浆纤维蛋白原水平高于存在G等位基因，但差异仅在男性病例中具有统计学意义。-455A等位基因与心肌梗死风险增加无关。此外，没有强烈迹象表明G-455A多态性与所考虑的任何环境暴露之间存在协同相互作用。
在大量心肌梗死病例和对照中，血浆纤维蛋白原水平升高与男性而非女性心肌梗死风险增加独立相关。纤维蛋白原Bβ基因G-455A多态性中A等位基因的存在与心肌梗死风险增加无关，且未检测到基因-环境协同相互作用。
