@article{3159068,
    title = "Combined effects of fibrinogen genetic variability on atherosclerosis in
patients with or without stable angina pectoris: Focus on the
coagulation cascade and endothelial function",
    author = "Papageorgiou, Nikolaos and Tousoulis, Dimitris and Miliou, Antigoni and and Hatzis, George and Kozanitou, Maria and Androulakis, Emmanuel and and Charakida, Marietta and Antonopoulos, Alexios and Antoniades, and Charalambos and Briasoulis, Alexandros and Giolis, Anastasios and and Bouras, George and Pallantza, Zoi and Stefanadis, Christodoulos",
    journal = "International Journal of Cardiology",
    year = "2013",
    volume = "168",
    number = "5",
    pages = "4602-4607",
    publisher = "Elsevier Ireland Ltd",
    issn = "0167-5273",
    doi = "10.1016/j.ijcard.2013.07.162",
    keywords = "Fibrinogen; Genetic polymorphisms; Atherosclerosis; Coronary artery
disease; Coagulation",
    abstract = "Background: Fibrinogen is a coagulation/inflammatory biomarker strongly
associated with atherogenesis. Data have reported that the genetic
variability on fibrinogen chains may affect the atherosclerotic process
and the risk of coronary artery disease (CAD). We examined the combined
effects of the G455A and the G58A fibrinogen genetic polymorphisms on
prothrombotic profile, endothelial function and the risk of CAD in a
Caucasian population.
Methods: We recruited 422 patients with angiographically documented CAD
and 277 controls matched for age and gender. The two polymorphisms were
genotyped by polymerase chain reaction and restriction endonuclease
digestion. Fibrinogen and D-Dimers levels, as well as factors’ (f) V, X
activity were measured by standard coagulometry techniques. Endothelial
function was assessed by the flow mediated dilatation (FMD) of the
brachial artery.
Results: The two polymorphisms had no significant effect on the risk for
CAD. Although the 58AA subjects had not significantly different levels
of fibrinogen compared with the 58GG + GA in both groups (p = NS), we
importantly found that the 455AA homozygosity was associated with
increased fibrinogen levels not only in the control group (p = 0.035),
but also in the CAD group (p < 0.001) compared to the G allele carriers.
Moreover, both the 58AA (p = 0.016) and 455AA homozygotes (p = 0.022)
presented with higher levels of D-Dimers in the CAD group.
Interestingly, the 455AA homozygotes had increased fV activity in the
CAD group (p = 0.048). However, no significant effects were observed on
fX activity and FMD.
Conclusions: Both fibrinogen polymorphisms are capable to modify the
atherosclerotic process via their effects on the coagulation cascade.
(C) 2013 Elsevier Ireland Ltd. All rights reserved."
}