Effect of factor XIII levels and polymorphisms on the risk of myocardial infarction in young patients

Mol Cell Biochem. 2018 Nov;448(1-2):199-209. doi: 10.1007/s11010-018-3326-8. Epub 2018 Feb 26.

Abstract

Factor XIII (FXIII) stabilizes and protects the fibrin network. Its role in myocardial infarction (MI) is still to be clarified. To evaluate the association of FXIII levels with MI in young patients and to investigate how the FXIII-A p.Val34Leu, FXIII-B p.His95Arg, and IVS11, c.1952 + 144 C>G (Intron K) polymorphisms influence FXIII levels and MI risk. Patients with ST elevation MI below 40 years of age (MI, n = 119), age-matched clinical controls (CC, n = 101) without MI and coronary artery disease, and healthy controls (HC, n = 120) were investigated for FXIII activity, FXIII-A2B2, FXIII-B concentrations and for the polymorphisms. FXIII activity and FXIII-A2B2 antigen were significantly elevated in MI. FXIII activity and antigen were significantly elevated in Arg95, while decreased in Intron K "G" carriers. Smoking had an independent increasing effect on FXIII activity and FXIII-A2B2 antigen. Intron K C>G polymorphism significantly decreased the risk of MI in patients with elevated fibrinogen. Among the investigated factors Intron K C>G polymorphism and smoking have the most powerful effect on FXIII levels and on the risk of MI in the young. The effect of smoking on coronary thrombus formation may partially be attributed to its FXIII increasing effect.

Keywords: FXIII polymorphisms; Factor XIII; Myocardial infarction; Smoking.

Publication types

  • Clinical Trial

MeSH terms

  • Adult
  • Factor XIII* / genetics
  • Factor XIII* / metabolism
  • Female
  • Humans
  • Male
  • Polymorphism, Genetic*
  • Risk Factors
  • ST Elevation Myocardial Infarction* / genetics
  • ST Elevation Myocardial Infarction* / metabolism
  • Smoking* / adverse effects
  • Smoking* / genetics
  • Smoking* / metabolism

Substances

  • Factor XIII