title: Evidence of contact activation in patients suffering from ST-elevation myocardial infarction.
abstract: BACKGROUND
  Factor (F) XIIa is an attractive target for anticoagulation in arterial thrombosis. The aim of this study is to investigate the degree of involvement of the contact system in cardiac infarctions.
  
  
  METHODS
  165 patients suffering from ST-elevation myocardial infarction (STEMI) and 100 healthy controls were included in the study. Samples were drawn at admission before percutaneous intervention (PCI), 1-3days post-percutaneous intervention (PCI) and, in one-third of the patients, 3months after PCI. In order to investigate the degree of Factor XII (FXII) activation, changes in FXIIa/AT and FXIIa/C1INH complex levels were quantified by ELISA.
  
  
  RESULTS
  FXIIa/AT levels at admission (0.89±0.50; p<0.01) were significantly higher than those in normal individuals (0.39±0.28), but the levels after 1-3days (0.33±0.33; p<0.05) were essentially normalized. In contrast, the FXII/C1INH levels at admission (1.40±0.72; p<0.001) and after 1-3days (0.83±0.59; p<0.001) were both significantly higher than those in normal individuals (0.40±0.30). FXIIa/AT and FXIIa/C1INH complexes at admission (p<0.001; p<0.001) and after 1-3days (p<0.02; p<0.001) were significantly different from those at 3months. No significant differences were observed when the data were stratified for patency (open/closed culprit lesions).
  
  
  CONCLUSIONS
  Both FXIIa/AT and FXIIa/C1INH complexes were significantly increased and reflected the activation of FXII in STEMI patients at admission. In particular, FXIIa/AT complex elevations support the hypothesis that clot propagation-mediated FXII activation had occurred, and this activation may be a target for anticoagulation in patients with cardiac infarction. Based on previous studies, the FXIIa/C1INH complex levels were primarily interpreted to reflex endothelial cell activation.
authors.affiliation: Department of Cardiology, Örebro University Hospital, Sweden; Linnæus Center for Biomaterials Chemistry, Linnæus University, SE-391 82 Kalmar, Sweden.
authors.forename: Kjeld
authors.initials: K
authors.lastname: Christensen
authors.affiliation: Department of Immunology, Genetics and Pathology, Rudbeck Laboratory C5:3, Uppsala University, S-751 85, Sweden; Linnæus Center for Biomaterials Chemistry, Linnæus University, SE-391 82 Kalmar, Sweden.
authors.forename: Huda
authors.initials: H
authors.lastname: Kozarcanin
authors.affiliation: Department of Immunology, Genetics and Pathology, Rudbeck Laboratory C5:3, Uppsala University, S-751 85, Sweden; Linnæus Center for Biomaterials Chemistry, Linnæus University, SE-391 82 Kalmar, Sweden.
authors.forename: Kristina N
authors.initials: KN
authors.lastname: Ekdahl
authors.affiliation: Department of Immunology, Genetics and Pathology, Rudbeck Laboratory C5:3, Uppsala University, S-751 85, Sweden; Linnæus Center for Biomaterials Chemistry, Linnæus University, SE-391 82 Kalmar, Sweden. Electronic address: bo.nilsson@igp.uu.se.
authors.forename: Bo
authors.initials: B
authors.lastname: Nilsson
mesh_terms: D000368:Aged; D058833:Antithrombin Proteins / Q000032:analysis; D001777:Blood Coagulation; D003174:Complement C1 Inactivator Proteins / Q000032:analysis; D050718:Complement C1 Inhibitor Protein; D015956:Factor XIIa / Q000032:analysis*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*
chemical_list: D058833:Antithrombin Proteins; D003174:Complement C1 Inactivator Proteins; D050718:Complement C1 Inhibitor Protein; C469952:SERPING1 protein, human; D015956:Factor XIIa
keywords: AT; C1INH; Contact system; FXII; STEMI