Abstract 15577: Essential Hypertension and Altered Prothrombotic Status: The Role of Fibrinogen Genetic Variability
Background: Essential hypertension (HT) is a risk factor for coronary artery disease (CAD). In addition, fibrinogen genetic polymorphisms have been associated with CAD. In the present study we examined the effect of the G455A polymorphism on fibrinogen, D-dimers, factor V (fV) and factor X (fX) levels in patients with hypertension.
Methods: The study population consisted of 469 HT and 245 non HT. The G455A polymorphism was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique, while circulating levels of fibrinogen were measured by the von Clauss method. D-dimers levels, fV and fX levels were measured by standard coagulometry techniques.
Results: Genotype distribution for non-HT and HT was GG: 50.9%, GA: 41.8%, AA: 9.7% and GG: 51.5%, GA: 37.6%, AA: 10.9% respectively. There was no significant difference in fibrinogen levels (mg/dl) between 455AA homozygotes and 455G allele carriers in non HT patients (448.3±34.6 vs 395.4±9.9, p=NS). Importantly, 455AA genotype presented with significantly more elevated levels of fibrinogen compared to the GG+GA in HT patients (535.4±25.3 vs 414.2±8.0, p<0.001). Moreover, HT 455AA homozygotes had significantly increased D-dimers levels (μ g/l) compared to 455G allele carriers (640.3±83.6 vs 485.5±27.2, p<0.05). No difference was observed for non-HT regarding D-dimers between the 455AA genotype and GG+GA (477.6±74. vs 450.8±40.7, p=NS). Interestingly, 455AA genotype presented with higher fV(%) and fX(%) levels compared to GG+GA in HT patients (133.6±5.8 vs 117.8±3.3, p<0.05, for fV) and (101.9±4.6 vs 92.2±2.4, p<0.05, for fX). However, no difference was observed in fV and fX levels between 455AA and GG+GA (105.8±11.6 vs 118.7±4.4, p=NS for fV and 95.8±8.0 vs 119.4±29.1, p=NS for fX) in non-HT respectively.
Conclusions: The G455A fibrinogen genetic polymorphism has a remarkable effect on the prothrombotic status of patients with hypertension, by modifying fibrinogen, D-dimers, factor V and factor X levels. These findings provide evidence that this polymorphism promotes further the atherosclerotic effects of hypertension through the alterations in the coagulation cascade.
- © 2012 by American Heart Association, Inc.