High FV:C and FVII:C were independent risk factors for myocardial infarction (P<0.0001), whereas the prothrombin gene 20210G-->A transition (OR 0.1; 95% CI 0.01-1.1) and factor V Leiden were not.
Case-Control (n=300)
Are increased levels of hemostatic factors and genetic mutations of coagulation proteins associated with an increased risk of myocardial infarction?
High clotting activity of factors V and VII are independent risk factors for myocardial infarction, while prothrombin 20210G-->A and factor V Leiden mutations are not.
Effect estimate: OR 0.1 (95% CI 0.01 to 1.1)
Absolute Event Rate: 0.6% vs 4.5%
Increased levels of hemostatic factors and genetic mutations of proteins involved in coagulation may play a role in the pathogenesis of coronary artery disease. We investigated clotting activity of factors II (FII:C), V (FV:C), VII (FVII:C), and X (FX:C), the prothrombin gene 20210G-->A transition, and the factor V Leiden mutation in 200 survivors of myocardial infarction and in 100 healthy controls. FV:C (PA transition (odds ratio OR, 0.1; 95% confidence interval CI, 0.01 to 1.1) nor the factor V Leiden mutation (OR, 1.0; 95% CI, 0.4 to 2.8) were associated with an increased relative risk for myocardial infarction. In conclusion, our data indicate that neither the prothrombin gene 20210G-->A transition nor the factor V Leiden mutation are risk factors for myocardial infarction. High FVII:C was confirmed to be an independent risk factor for myocardial infarction. Moreover, we describe for the first time that high FV:C is an independent risk factor for myocardial infarction.
Redondo et al. (1999) conducted a case-control in Myocardial infarction (n=300). Prothrombin gene 20210G-->A transition and factor V Leiden mutation vs. Healthy controls was evaluated on Myocardial infarction (OR 0.1, 95% CI 0.01 to 1.1). High FV:C and FVII:C were independent risk factors for myocardial infarction (P<0.0001), whereas the prothrombin gene 20210G-->A transition (OR 0.1; 95% CI 0.01-1.1) and factor V Leiden were not.