Mutation in the Factor V Gene and the Risk of Myocardial Infarction

Abstract

Ridker and colleagues (April 6 issue)¹ demonstrated that the mutation resulting in the substitution of glutamine for arginine at position 506 in the gene coding for coagulation factor V is not associated with an increased risk of myocardial infarction or stroke but is strongly associated with the occurrence of deep venous thrombosis. This study fully confirms the results of three of four previous studies^2-5 that assessed the relation between myocardial infarction and this mutation, which is responsible for resistance to activated protein C. In the largest series, there was no statistically significant difference in the prevalence of the factor V mutation between the 609 men who had had myocardial infarction (5.1 percent) and the 692 age-matched controls (4.6 percent).² Nevertheless, these results cannot be extrapolated to people who are homozygous for this trait. Finally, these results suggest that a local event, such as a plaque rupture that triggers platelets and coagulation factors, may be more important in arterial thrombosis than the existence of a permanent and systemic procoagulant state.