Increased levels of coagulation factors such as FVII and FXIII have been associated with acute myocardial Infarction (AMI). Molecular biology studies have identified several mutations in the genes of FVII and FXIII and observe its influence on the levels of these and their possible association and risk of AMI. Methods: We studied 186 patients with documented AMI and 201 controls with no history of cardiovascular disease. We performed a case-control study. It was determined the FXIII Val34Leu polymorphisms, FVII IVS7, FVII R353Q, according to the procedures described. This research followed the guidelines of institutional bioethics. Results: The mean age of patients was 46.2 years (147 men / 39 women), and controls was 46 years (141 men / 60 women). The prevalence of mutations obtained in patients as controls were: FVII IVS7 OR: 0.60 (0.26 to 1.38) p = 0.193 and FVIIR353Q OR: 0.81 (0.61 to 1.08) p = 0.729 , respectively. It is observed that the phenotype Leu/Leu is more common in controls than in patients, and after adjustment for cardiovascular risk factors, was shown to be a protective factor for the development of AMI OR: 0.66 (0.47 - 0.93) p = 0.01. The traditional risk factors were statistically significant. In FVII, were found in the FVII IVS, new variants * (4 and 8), not previously described. Conclusion: FXIII Val34Leu was found as protector factor but neither FVII polymorphisms were associated as risk factors for AMI. FXIII Val34Leu, had been described as a facilitator of the activation of factor XIII, during the final stages of coagulation, increasing and accelerating stabilization of the fibrin, conferring mayor resistance to fibrinolysis. Increase the interest of this polymorphism in AMI and especially for patients who were subjected to antifibrinolytic therapy.

Acute myocardial infarction; polymorphisms; coagulation; fibrinogen; FXIIIVal34Leu; FVII IVS7; FVIIR353Q