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Published on: April 1, 2019
Prothrombin Gene G20210A Variant in Angiographically Documented Patients with Coronary Artery Stenosis
Leyla Pourgholi1, Hamidreza Goodarzynejad2, Shayan Ziaee1
1Department of Molecular Pathology, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran.
Insights
The prothrombin G20210A variant was not found to be a significant risk factor for coronary artery disease (CAD) or its severity in this study. Further research is needed to clarify the role of this genetic variant in cardiovascular health.
Area of Science:
- Cardiovascular Genetics
- Thrombosis Research
Background:
- Inconclusive evidence links the prothrombin G20210A variant to coronary artery disease (CAD) risk.
- The role of this genetic variant in CAD development and progression requires further investigation.
Purpose of the Study:
- To investigate the association between the prothrombin G20210A variant and the presence and severity of CAD.
- To determine if the G20210A variant influences CAD risk or its clinical manifestation.
Main Methods:
- 1460 patients undergoing elective coronary angiography were enrolled.
- Coronary angiography assessed CAD presence and severity using Gensini and vessel scores.
- Prothrombin G20210A genotypes were determined using PCR-RFLP.
Main Results:
- No statistically significant difference in Gensini scores between wild-type (GG) and mutant (AA+GA) genotypes (P=0.440).
- No significant linear trend observed for the number of diseased vessels (vessel score) in relation to genotype (P=0.765).
Conclusions:
- The study did not confirm the prothrombin G20210A variant as a significant determinant of CAD risk.
- The G20210A variant does not appear to influence the severity of coronary artery disease in this patient cohort.
Abstract:
Background: Studies on the association between the prothrombin G20210A variant and coronary artery disease (CAD) risk are inconclusive. This study aimed to investigate the possible association between the G20210A variant in the prothrombin gene and documented CAD and its severity. Methods: This study enrolled 1460 patients who were consecutively admitted for elective coronary angiography. Via the standard angiographic techniques, coronary angiographies were done and the presence and severity of CAD were determined through the clinical vessel score and the Gensini score. Prothrombin G20210A genotypes were identified using PCR-RFLP. Results: This cross-sectional study was performed on 953 men and 507 women at a mean age of 58.21±10.33 years. The median and the interquartile range for the Gensini score were not statistically significantly different between the wild (GG) and mutant (AA+GA) genotypes (P=0.440). The association between the G20210A polymorphism and the severity of CAD with respect to the vessel score also showed no significant linear trend of higher numbers of diseased vessels (P= 0.765 for the Mantel-Haenszel test of linear trend) in the AA+GA genotype as compared with the GG genotype. Conclusion: Our data failed to confirm the hypothesis that the G20210A variant mutation may be a significant determinant of CAD risk or its severity.
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