Why the study?
The relationship between inflammation, coagulation factor VII genetic variation, and myocardial infarction risk remains unclear and requires further elucidation.
Does the R353Q polymorphism in the FVII gene increase the risk of myocardial infarction?
Meta-Analysis (n=10,030)
Does the R353Q polymorphism in the FVII gene increase the risk of myocardial infarction?
Odds Ratio: 1.03 (95% CI 0.92–1.16)
p-value: p=>0.05
The FVII R353Q polymorphism does not appear to be a major independent genetic risk factor for myocardial infarction, though subgroup signals suggest potential relevance depending on ethnicity and BMI.
To further elucidate the connection between inflammation and factor VII (FVII) taking genetic variation in the FVII locus into account, we have examined 387 patients after myocardial infarction and 387 age-matched and sex-matched healthy control individuals. Circulating levels of C-reactive protein, FVII antigen (FVIIag), activated FVII (FVIIa), fibrinogen and interleukin-6 were analysed and all subjects were genotyped for the Arg353Gln polymorphism in the FVII locus. Plasma concentrations of C-reactive protein, fibrinogen, and interleukin-6 were higher among patients than control individuals. FVIIag was lower in the patient group, but for FVIIa there was no difference between the two groups. Among the inflammatory markers, only C-reactive protein indicated a weak nonlinear association with FVII. No significant difference in frequency of the Gln allele was observed between patients and control individuals but the presence of the Gln allele was associated with lower plasma levels of FVIIag and FVIIa in both groups. The low-grade chronic inflammation seen 3 months after myocardial infarction is not of major importance for the variation in plasma concentration of FVII. The presence of the Gln allele in the Arg353Gln polymorphism in the FVII locus did not differ between patients and control individuals but was associated with lower plasma levels of FVIIag and FVIIa that could have a protective effect against myocardial infarction. To further elucidate these facts, a prospective study should be performed to reduce the risk of a possible selection bias due to coronary heart disease death seen in retrospective case-control studies.
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Ekström et al. (2007) conducted a meta-analysis in Myocardial infarction (n=10,030). FVII R353Q polymorphism (R allele) vs. Q allele or QQ genotype was evaluated on Myocardial infarction risk (allele model: R vs Q) (OR 1.03, 95% CI 0.92-1.16, p=>0.05).
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