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Published on: September 9, 2012
The association between Factor V Leiden with the presence and severity of coronary artery disease
Mohammadali Boroumand1, Leila Pourgholi2, Shayan Ziaee2
1Department of Surgical and Clinical Pathology, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran.
Insights
Factor V Leiden (FVL) is linked to a higher risk of coronary artery disease (CAD). This study found FVL mutation is a significant determinant of CAD occurrence and independently associated with increasing CAD severity.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Thrombosis
Background:
- Factor V Leiden (FVL) is a genetic mutation associated with an increased risk of venous thromboembolism.
- Its role in arterial thrombosis, particularly coronary artery disease (CAD), requires further investigation.
Purpose of the Study:
- To investigate the association between Factor V Leiden mutation and the presence of coronary artery disease (CAD).
- To evaluate the relationship between FVL and the severity of angiographically determined CAD.
Main Methods:
- A case-control study comparing 1083 patients with significant coronary atherosclerosis to control groups.
- CAD severity assessed using vessel score and Gensini score.
- Factor V polymorphisms analyzed via polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP).
Main Results:
- FVL mutation was independently associated with the occurrence of CAD (p=0.020).
- FVL heterozygote and homozygote genotypes showed a trend towards more severe CAD (adjusted ORs 1.85 and 3.70, respectively).
- Gensini scores significantly differed across FVL genotypes (p<0.001), indicating increased severity with mutant alleles.
Conclusions:
- The study confirms FVL mutation as a significant determinant of CAD risk.
- FVL is independently associated with increased severity of coronary artery disease.
Objectives:
The presence of Factor V Leiden (FVL) is proposed to be associated with a higher risk for arterial thrombosis. The aim of this study was to examine a relationship between FVL with the presence and severity of angiographically determined coronary artery disease (CAD).
Design And Methods:
In this case-control study, 1083 patients having angiographic evidence of atherosclerosis with ≥50% luminal stenosis in their epicardial coronary tree were compared with patients with no luminal stenosis (n=320) or with luminal stenosis <50% (n=191) at coronary angiography as reference group. The severity of CAD was determined by vessel score and also a semi-quantitative scoring system (Gensini score). The presence of Factor V polymorphisms was analyzed using polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP).
Results:
FVL was found to be independently associated with the occurrence of CAD (p=0.020). As compared to wild genotype, heterozygote or homozygote mutant genotypes were more likely associated with a trend towards more severe CAD (adjusted OR=1.85, 95% CI=1.26 to 2.72; p=0.002, and adjusted OR=3.70, 95% CI=1.71 to 8.00; p=0.001; respectively). In addition, the median and inter-quartile range for Gensini score were significantly different among the GG (27.8, 3 to 66.5), GA (53.5, 10 to 104.1), and AA (92.8, 48.1 to 125.9) genotypes (p<0.001).
Conclusions:
Our results confirmed the hypothesis that FVL mutation is a significant determinant of CAD risk. Furthermore, we observed that FVL is independently associated with increasing CAD severity.
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