FIBRINOGEN GENETIC VARIABILITY AND COAGULATION PROCESS MEDIATE ATHEROSCLEROSIS MANIFESTATIONS AND AFFECT THE EXTENT OF THE DISEASE
(Abstract release date: 05/19/16)
EHA Library. Pallantza Z. 06/09/16; 133103; E1554
Dr. Zoi Pallantza
Contributions
Contributions
Abstract
Abstract: E1554
Type: Eposter Presentation
Aims
Evidence suggests that altered coagulation and fibrinogen genetic variability may contribute to atherogenesis. Therefore, we examined the combined effects of the rs1800790, rs2070011 fibrinogen polymorphisms on coagulation and endothelial function as well as the effect of coagulation on atherosclerotic manifestations.
Methods
In the present study we enrolled 422 patients with stable angina (SA) and 277 controls. The rs1800790 (G455A) and the rs2070011 (G58A) polymorphisms were detected by appropriate genotyping. Fibrinogen and D-Dimer levels, as well as factors (f) V, X activity were measured by standard coagulometry techniques. Flow-mediated dilation (FMD) was assessed by brachial ultrasound.
Results
We have shown that the 455AA homozygosity was associated with increased fibrinogen levels in both groups (p=0.035 controls and p<0.001 SA). In addition, homozygotes for the 58A allele had lower fibrinogen levels in controls (p=0.038). Both the 58AA (p=0.027) and 455AA homozygotes (p=0.022) had higher levels of D-Dimer in the SA group. The 455AA homozygotes had also increased fV activity in the SA group (p=0.048). No effects were observed on fX activity and FMD. Further analysis revealed that fibrinogen levels were strongly associated with SA (1.005 [1.003–1.007], p<0.001) as well as the presence of myocardial infarction (MI) (1.003 [1.001–1.005], p=0.001). Similarly, D-Dimer levels were also strong predictors of CAD (1.001 [1.001–1.002], p<0.001), but not of MI (1.000 [1.001–1.001], p=0.083). Surprisingly, when fV and fX activities were examined for possible associations with clinical presentations, we found that fV activity was associated with increased number of diseased vessels (1.016 [1.001–1.030], p=0.037), while fX activity was strongly related to MI (0.985 [0.973–0.997], p=0.013).
Conclusion
Our results demonstrate that the rs1800790 variant increases significantly fibrinogen, D-Dimers levels and fV activity, contributing to atherogenesis. Moreover, fibrinogen and D-Dimers levels are strong predictors of SA and MI. Interestingly, in our study we have shown for the first time that fV and fX are associated with the number of diseased vessels and the risk of MI respectively.
Session topic: E-poster
Type: Eposter Presentation
Aims
Evidence suggests that altered coagulation and fibrinogen genetic variability may contribute to atherogenesis. Therefore, we examined the combined effects of the rs1800790, rs2070011 fibrinogen polymorphisms on coagulation and endothelial function as well as the effect of coagulation on atherosclerotic manifestations.
Methods
In the present study we enrolled 422 patients with stable angina (SA) and 277 controls. The rs1800790 (G455A) and the rs2070011 (G58A) polymorphisms were detected by appropriate genotyping. Fibrinogen and D-Dimer levels, as well as factors (f) V, X activity were measured by standard coagulometry techniques. Flow-mediated dilation (FMD) was assessed by brachial ultrasound.
Results
We have shown that the 455AA homozygosity was associated with increased fibrinogen levels in both groups (p=0.035 controls and p<0.001 SA). In addition, homozygotes for the 58A allele had lower fibrinogen levels in controls (p=0.038). Both the 58AA (p=0.027) and 455AA homozygotes (p=0.022) had higher levels of D-Dimer in the SA group. The 455AA homozygotes had also increased fV activity in the SA group (p=0.048). No effects were observed on fX activity and FMD. Further analysis revealed that fibrinogen levels were strongly associated with SA (1.005 [1.003–1.007], p<0.001) as well as the presence of myocardial infarction (MI) (1.003 [1.001–1.005], p=0.001). Similarly, D-Dimer levels were also strong predictors of CAD (1.001 [1.001–1.002], p<0.001), but not of MI (1.000 [1.001–1.001], p=0.083). Surprisingly, when fV and fX activities were examined for possible associations with clinical presentations, we found that fV activity was associated with increased number of diseased vessels (1.016 [1.001–1.030], p=0.037), while fX activity was strongly related to MI (0.985 [0.973–0.997], p=0.013).
Conclusion
Our results demonstrate that the rs1800790 variant increases significantly fibrinogen, D-Dimers levels and fV activity, contributing to atherogenesis. Moreover, fibrinogen and D-Dimers levels are strong predictors of SA and MI. Interestingly, in our study we have shown for the first time that fV and fX are associated with the number of diseased vessels and the risk of MI respectively.
Session topic: E-poster
Abstract: E1554
Type: Eposter Presentation
Aims
Evidence suggests that altered coagulation and fibrinogen genetic variability may contribute to atherogenesis. Therefore, we examined the combined effects of the rs1800790, rs2070011 fibrinogen polymorphisms on coagulation and endothelial function as well as the effect of coagulation on atherosclerotic manifestations.
Methods
In the present study we enrolled 422 patients with stable angina (SA) and 277 controls. The rs1800790 (G455A) and the rs2070011 (G58A) polymorphisms were detected by appropriate genotyping. Fibrinogen and D-Dimer levels, as well as factors (f) V, X activity were measured by standard coagulometry techniques. Flow-mediated dilation (FMD) was assessed by brachial ultrasound.
Results
We have shown that the 455AA homozygosity was associated with increased fibrinogen levels in both groups (p=0.035 controls and p<0.001 SA). In addition, homozygotes for the 58A allele had lower fibrinogen levels in controls (p=0.038). Both the 58AA (p=0.027) and 455AA homozygotes (p=0.022) had higher levels of D-Dimer in the SA group. The 455AA homozygotes had also increased fV activity in the SA group (p=0.048). No effects were observed on fX activity and FMD. Further analysis revealed that fibrinogen levels were strongly associated with SA (1.005 [1.003–1.007], p<0.001) as well as the presence of myocardial infarction (MI) (1.003 [1.001–1.005], p=0.001). Similarly, D-Dimer levels were also strong predictors of CAD (1.001 [1.001–1.002], p<0.001), but not of MI (1.000 [1.001–1.001], p=0.083). Surprisingly, when fV and fX activities were examined for possible associations with clinical presentations, we found that fV activity was associated with increased number of diseased vessels (1.016 [1.001–1.030], p=0.037), while fX activity was strongly related to MI (0.985 [0.973–0.997], p=0.013).
Conclusion
Our results demonstrate that the rs1800790 variant increases significantly fibrinogen, D-Dimers levels and fV activity, contributing to atherogenesis. Moreover, fibrinogen and D-Dimers levels are strong predictors of SA and MI. Interestingly, in our study we have shown for the first time that fV and fX are associated with the number of diseased vessels and the risk of MI respectively.
Session topic: E-poster
Type: Eposter Presentation
Aims
Evidence suggests that altered coagulation and fibrinogen genetic variability may contribute to atherogenesis. Therefore, we examined the combined effects of the rs1800790, rs2070011 fibrinogen polymorphisms on coagulation and endothelial function as well as the effect of coagulation on atherosclerotic manifestations.
Methods
In the present study we enrolled 422 patients with stable angina (SA) and 277 controls. The rs1800790 (G455A) and the rs2070011 (G58A) polymorphisms were detected by appropriate genotyping. Fibrinogen and D-Dimer levels, as well as factors (f) V, X activity were measured by standard coagulometry techniques. Flow-mediated dilation (FMD) was assessed by brachial ultrasound.
Results
We have shown that the 455AA homozygosity was associated with increased fibrinogen levels in both groups (p=0.035 controls and p<0.001 SA). In addition, homozygotes for the 58A allele had lower fibrinogen levels in controls (p=0.038). Both the 58AA (p=0.027) and 455AA homozygotes (p=0.022) had higher levels of D-Dimer in the SA group. The 455AA homozygotes had also increased fV activity in the SA group (p=0.048). No effects were observed on fX activity and FMD. Further analysis revealed that fibrinogen levels were strongly associated with SA (1.005 [1.003–1.007], p<0.001) as well as the presence of myocardial infarction (MI) (1.003 [1.001–1.005], p=0.001). Similarly, D-Dimer levels were also strong predictors of CAD (1.001 [1.001–1.002], p<0.001), but not of MI (1.000 [1.001–1.001], p=0.083). Surprisingly, when fV and fX activities were examined for possible associations with clinical presentations, we found that fV activity was associated with increased number of diseased vessels (1.016 [1.001–1.030], p=0.037), while fX activity was strongly related to MI (0.985 [0.973–0.997], p=0.013).
Conclusion
Our results demonstrate that the rs1800790 variant increases significantly fibrinogen, D-Dimers levels and fV activity, contributing to atherogenesis. Moreover, fibrinogen and D-Dimers levels are strong predictors of SA and MI. Interestingly, in our study we have shown for the first time that fV and fX are associated with the number of diseased vessels and the risk of MI respectively.
Session topic: E-poster
{{ help_message }}
{{filter}}