title: Acute coronary syndromes do not promote prolonged in vivo FXII-dependent prothrombotic activity.
abstract: BACKGROUND
  Coagulation FXII is activated on contact with lipoprotein particles. It has been suggested that contact with subendothelial tissue provides an alternative biological surface for FXII activation. Our aim was to investigate whether activated FXII (FXIIa) is elevated in patients with coronary atherosclerosis, and whether disease status (acute phase or stable state) affects circulating levels of FXIIa.
  
  
  METHODS
  Circulating FXIIa levels were measured in the peripheral blood of 122 patients with coronary atherosclerosis (32, stable angina; 54, unstable angina; 36, nQ myocardial infarction) and in 45 age-matched subjects (Contr).
  
  
  RESULTS
  FXIIa levels (median, first and third quartiles; ng/ml) were higher in patients than in Contr: 1.61 (1.26-2.02) vs. 1.34 (1.13-1.81) (p<0.01). FXIIa levels were similar among patients with stable angina [1.66 (1.23-1.91)], unstable angina [1.53 (1.21-2.04)], and nQ myocardial infarction [1.75 (1.34-2.03)]. The three groups of patients had similar prevalence for most atherothrombotic risk factors; patients with stable angina had an increased severity of coronary disease, which did not explain the different levels of FXIIa. Fasting levels of triglycerides were the best predictor of FXIIa levels in our patients.
  
  
  CONCLUSIONS
  The finding of similar FXIIa levels among patients in either acute or chronic phases of coronary atherosclerosis suggests that the initial arterial denudation and the acute-phase response associated to acute coronary syndromes are not major determinants for prolonged FXII activation.
authors.affiliation: Division of Cardiology and Laboratory of Cardiovascular Biology, Department of Internal Medicine, University of Genova, Viale Benedetto XV, 6 16132 Genova, Italy.
authors.forename: Paola
authors.initials: P
authors.lastname: Altieri
authors.forename: Emmanuela
authors.initials: E
authors.lastname: Devoto
authors.forename: Paolo
authors.initials: P
authors.lastname: Spallarossa
authors.forename: Pierfranco
authors.initials: P
authors.lastname: Rossettin
authors.forename: Silvano
authors.initials: S
authors.lastname: Garibaldi
authors.forename: Giovanni
authors.initials: G
authors.lastname: Bertero
authors.forename: Manrico
authors.initials: M
authors.lastname: Balbi
authors.forename: Antonio
authors.initials: A
authors.lastname: Barsotti
authors.forename: Claudio
authors.initials: C
authors.lastname: Brunelli
authors.forename: Giorgio
authors.initials: G
authors.lastname: Ghigliotti
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000787:Angina Pectoris / Q000097:blood; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000097:blood; D003327:Coronary Disease / Q000097:blood*; D015956:Factor XIIa / Q000032:analysis*; D006801:Humans; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood; D012307:Risk Factors; D019851:Thrombophilia / Q000209:etiology*; D014280:Triglycerides / Q000097:blood
chemical_list: D014280:Triglycerides; D015956:Factor XIIa