Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication

DOI

10.1016/j.ijcard.2013.07.162

Type

Journal article

Journal

Int J Cardiol

Publication Date

12/10/2013

Volume

168

Pages

4602 - 4607

Keywords

Atherosclerosis, Coagulation, Coronary artery disease, Fibrinogen, Genetic polymorphisms, Angina, Stable, Atherosclerosis, Blood Coagulation, Brachial Artery, DNA, Disease Progression, Endothelium, Vascular, Female, Fibrinogen, Follow-Up Studies, Genotype, Humans, Male, Middle Aged, Polymerase Chain Reaction, Polymorphism, Genetic, Ultrasonography, Doppler, Pulsed, Vasodilation