title: Activation of the contact system in patients with a first acute myocardial infarction.
abstract: BACKGROUND
  The contribution of the contact system to arterial thrombosis is unclear, results of clinical studies are conflicting. Particularly, little is known about the involvement of the contact system in the progression of arterial thrombosis. Therefore, we investigated the activation of the contact system during an acute myocardial infarction (AMI) and 3 and 6 months following the acute event.
  
  
  METHODS
  Plasma of patients with a first AMI was collected on admission and 3 and 6 months after the AMI. The levels of complexes of activated factor XI (FXIa), FXIIa and kallikrein with C1 esterase inhibitor (C1INH) and the levels of complexes of FXIa with α1-antitrypsin (AT) were measured in these plasmas. Recurrent cardiovascular events were recorded during a one year period after the AMI.
  
  
  RESULTS
  We observed that the levels of FXIa-C1INH were elevated during the acute phase compared to the steady-phase 3 and 6 months after the AMI. The levels of FXIa-AT, FXIIa-C1INH and kallikrein-C1INH did not change over time. The levels of FXIa-C1INH, FXIa-AT, FXIIa-C1INH and kallikrein-C1INH were not predictive for a recurrent event.
  
  
  CONCLUSIONS
  We observed that during an AMI, the activation of FXI was increased. The levels of FXIIa-C1INH were not elevated, suggesting that activation of FXI during the acute phase did not result from contact activation. The levels of the enzyme inhibitor complexes were not predictive for a recurrent event one year after the first AMI.
authors.affiliation: Laboratory for Clinical Thrombosis and Haemostasis, Department of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University Medical Centre, Maastricht, The Netherlands. J.Konings@maastrichtuniversity.nl
authors.forename: Joke
authors.initials: J
authors.lastname: Konings
authors.forename: José W P
authors.initials: JW
authors.lastname: Govers-Riemslag
authors.forename: Henri M H
authors.initials: HM
authors.lastname: Spronk
authors.forename: Johannes L
authors.initials: JL
authors.lastname: Waltenberger
authors.forename: Hugo
authors.initials: H
authors.lastname: ten Cate
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001777:Blood Coagulation; D050718:Complement C1 Inhibitor Protein / Q000032:analysis* / Q000378:metabolism; D004789:Enzyme Activation; D015945:Factor XIa / Q000032:analysis* / Q000378:metabolism; D005260:Female; D006801:Humans; D007610:Kallikreins / Q000097:blood* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000378:metabolism; D000515:alpha 1-Antitrypsin / Q000097:blood* / Q000378:metabolism
chemical_list: D050718:Complement C1 Inhibitor Protein; D000515:alpha 1-Antitrypsin; D007610:Kallikreins; D015945:Factor XIa
keywords: A.U; AMI; Acute myocardial infarction; C1 esterase inhibitor; C1-esterase inhibitor; C1INH; CABG; CAD; CHD; CI; CV; Coagulation factor XI; Coagulation factor XII; Contact system; ELISA; F; F1.2; IQR; LMWH; OR; PCI; Prekallikrein; SD; STI; acute myocardial infarction; arbitrary units; coagulation factor; coefficient variation; confidence interval; coronary artery bypass grafting; coronary artery disease; coronary heart disease; enzyme-linked immunosorbent assays; interquartile range; low-molecular-weight-heparin; odds ratio; percutaneous coronary intervention; prothrombin fragment 1.2; soybean trypsin inhibitor; standard deviation