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A Methodological Approach to Non-invasive Assessments of Vascular Function and Morphology
Published on: February 7, 2015
Absence of association between polymorphisms in the hemostatic factor pathway genes and carotid intimal medial
Caroline S Fox1, Martin G Larson, Diane Corey
1National Heart, Lung and Blood Institute's Framingham Heart Study, Framingham, Mass, USA.
Insights
This study found no link between common genetic variations in hemostatic factor genes and carotid intima-media thickness (IMT), a measure of atherosclerosis. Further research is needed to explore other genetic variants and their impact on subclinical cardiovascular disease.
Area of Science:
- Cardiovascular Genetics
- Atherosclerosis Research
- Hemostasis and Thrombosis
Background:
- Cardiovascular disease is linked to key coagulation proteins like fibrinogen and plasminogen activator inhibitor-1.
- Gene polymorphisms can influence plasma levels of these hemostatic factors.
- Carotid intima-media thickness (IMT) is a heritable marker for atherosclerosis and a predictor of cardiovascular events.
Purpose of the Study:
- To investigate the association between carotid IMT and polymorphisms in well-characterized hemostatic factor genes.
- To determine if genetic variations in coagulation pathways contribute to subclinical atherosclerosis.
Main Methods:
- The Framingham offspring cohort (867 men, 911 women, mean age 57) underwent carotid ultrasonography to measure IMT.
- Analysis included factor V Leiden, factor VII Arg/Gln, fibrinogen HindIII beta-148, PAI-1 4G/5G, and Pl(A2) polymorphisms.
- Linear regression models, adjusted for age, sex, and other variables, assessed the association with log-transformed CCA and ICA IMT.
Main Results:
- Mean internal carotid artery (ICA) IMT was 0.58 mm; mean common carotid artery (CCA) IMT was 0.60 mm.
- No statistically significant differences in ICA or CCA IMT were observed based on genotype for any of the studied hemostatic factor gene polymorphisms.
- These findings held true across unadjusted, age/sex-adjusted, and multivariable-adjusted models.
Conclusions:
- This study provides no evidence supporting an association between common, well-studied polymorphisms in hemostatic factor genes and carotid IMT.
- The role of other common genetic variants within these hemostatic factor genes in subclinical atherosclerosis requires further investigation.
Background And Purpose:
Fibrinogen, plasminogen activator inhibitor-1, and other key proteins in the coagulation cascade have been implicated in the origin of cardiovascular disease. Polymorphisms in genes encoding these proteins have been associated with variability in plasma levels of these proteins. Carotid intimal medial thickness (IMT) is a heritable, quantitative measure of atherosclerosis that is predictive of subsequent myocardial infarction and stroke. We sought to test whether carotid IMT is associated with polymorphisms in several well-characterized genes in the hemostatic factor pathways.
Methods:
Here, 867 men and 911 women (mean age, 57 years) in the Framingham offspring cohort underwent B-mode carotid ultrasonography to determine the mean internal (ICA) and common carotid artery (CCA) IMT. Age-, sex-, and multivariable-adjusted linear regression was used to estimate the association of the following variants with log-transformed CCA and ICA IMT: factor V Leiden, factor VII Arg/Gln, fibrinogen HindIII beta-148, plasminogen activator inhibitor-1 4G/5G, and the glycoprotein IIIa Pl(A2) polymorphism.
Results:
Mean ICA IMT was 0.58 mm; mean CCA IMT was 0.60 mm. There were no differences in ICA or CCA IMT by genotype for any of the candidate genes in unadjusted, age- or sex-adjusted, and multivariable-adjusted models.
Conclusions:
There is no evidence for an association between well-studied polymorphisms in the hemostatic factor genes and carotid IMT. Whether other common genetic variants in hemostatic factor genes are associated with subclinical atherosclerosis remains to be determined.
