To the Editor:

We read with real interest the exhaustive review by Professor Navarro of genetic polymorphisms and coronary artery disease.1 Nonetheless, we would like to further discuss the influence on myocardial infarction of the Val34Leu polymorphism of coagulation factor XIII (FXIII). This polymorphism conditions a change of valine for leucine only 3 amino acids from the site of activation by thrombin. It has been confirmed that it facilitates the activation of FXIII, increasing and accelerating the stabilization of fibrin.2 Nevertheless, paradoxically, it is has been observed that this polymorphism could play a protective role against both venous and arterial thrombosis,3 as Professor Navarro indicates in his review.1

We studied the Val34Leu genotype of FXIII in 180 patients who suffered myocardial infarction before the age of 45 years and in 585 controls.4 We found that the frequency of the Leu/Leu genotype was greater in patients (7.5% vs 3.8%; P=.05). After adjustment for other cardiovascular risk factors, this genotype was found to be an independent risk factor for the development of premature infarction (P=.019; odds ratio [OR], 3.54; 95% confidence interval [CI], 1.22-10.22).

Recently we analyzed the possible influence of this polymorphism on response to fibrinolytic treatment in premature myocardial infarction.5 We observed that patients with the Val/Val genotype more frequently met criteria for non-invasive reperfusion (P=.006; OR, 5.11; 95% CI, 1.28-21.12). Therefore, the results of our study demonstrate the existence of clinical manifestations of the type suggested by the results of experimental studies.6 These findings enhance the interest of this polymorphism in myocardial infarction and should be examined in prospective multicenter studies. It is even more important to know the influence this polymorphism has on fibrinolytic treatment in populations where it has been shown to be a mutation that protects against the development of thrombotic phenomena.