The role of factor XIIIVal34Leu in cardiovascular disease

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Abstract
Blood coagulation factor XIII (also called fibrin-stabilizing factor1) plays an important role in clot stabilization by crosslinking fibrin chains.2 Factor XIII (FXIII) was discovered over 70 years ago by Barkan et al., who observed the insolubility of fibrin clots in the presence of calcium.3 Most studies on FXIII have been carried out in patients with FXIII deficiency which results in a serious bleeding diathesis, defective wound healing and a high risk of miscarriage in the deficient female.4,5 Most of these subjects show no plasma FXIII activity because of a complete absence of the A-subunit in plasma, platelets and monocytes.6 Little is known about the role of FXIII in vascular diseases. Although Kloczko et al. showed increased levels of FXIII A-subunit antigen in patients with obliterative atherosclerosis of the lower limbs and in patients with diabetic angiopathy, small patient numbers make the interpretation of these data difficult.7,8 However, increased plasma concentration of cross-linked fibrin polymers in acute myocardial infarction has been described, assuming the presence of increased plasma FXIII plasma activity in patients with coronary artery disease.9 Results from our laboratory add further support in the involvement of FXIII in cardiovascular diseases.10,11 Here we discuss some new insights regarding the role of FXIII in vascular disease, with emphasis on a common polymorphism in the A-subunit gene of FXIII (FXIIIVal34Leu) and its association with myocardial infarction, stroke and venous thromboembolism.

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