title: Haemostatic factors and the risk of cardiovascular death in patients with coronary artery disease: the AtheroGene study.
abstract: OBJECTIVE
  To get a better insight into the role of hemostasis in coronary artery disease (CAD), we assessed the impact of von Willebrand factor (vWF), fibrinogen, thrombin-antithrombin (TAT) complexes, D-dimers, and plasmin-antiplasmin (PAP) complexes on the risk of cardiovascular event in a prospective cohort of CAD patients.
  
  
  RESULTS
  The prospective Atherogene cohort includes 1057 individuals with an angiographically proven coronary artery disease at baseline. After a median follow-up of 6.6 years, 135 individuals died from a cardiovascular cause and 97 had a nonfatal cardiovascular event. Higher levels of all 5 hemostatic markers at baseline were associated with an increased risk of cardiovascular death, but not of nonfatal event. Except for vWF, these associations remained significant after adjustment for conventional cardiovascular risk factors and C-reactive protein (CRP) levels (P for trend according to increasing tertiles=0.20, 0.011, 0.026, 0.019, and 0.01 for vWF, fibrinogen, TAT, D-Dimer, and PAP, respectively). When including the 5 hemostatic markers in a stepwise Cox regression analysis where conventional risk factors and CRP were forced into the model, fibrinogen and D-dimers remained independently associated with the risk of cardiovascular death. Adjusted hazard ratios (95% CI) associated with one SD increase of fibrinogen and D-dimers were 1.27 (1.04 to 1.55) and 1.29 (1.09 to 1.53), respectively.
  
  
  CONCLUSIONS
  In patients with coronary artery disease, fibrinogen and D-dimer levels are independent predictors of subsequent cardiovascular death. Our data support a role of impaired coagulation/fibrinolysis process in the complications of coronary artery disease.
authors.affiliation: INSERM UMR S 525 and Université Pierre et Marie Curie-Paris 6, Paris, France. pmorange@ap-hm.fr
authors.forename: P E
authors.initials: PE
authors.lastname: Morange
authors.forename: C
authors.initials: C
authors.lastname: Bickel
authors.forename: V
authors.initials: V
authors.lastname: Nicaud
authors.forename: R
authors.initials: R
authors.lastname: Schnabel
authors.forename: H J
authors.initials: HJ
authors.lastname: Rupprecht
authors.forename: D
authors.initials: D
authors.lastname: Peetz
authors.forename: K J
authors.initials: KJ
authors.lastname: Lackner
authors.forename: F
authors.initials: F
authors.lastname: Cambien
authors.forename: S
authors.initials: S
authors.lastname: Blankenberg
authors.forename: L
authors.initials: L
authors.lastname: Tiret
mesh_terms: D000368:Aged; D000990:Antithrombin III / Q000235:genetics; D002097:C-Reactive Protein / Q000235:genetics / Q000378:metabolism; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000235:genetics / Q000378:metabolism* / Q000401:mortality* / Q000503:physiopathology; D018450:Disease Progression; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000235:genetics / Q000378:metabolism*; D005340:Fibrinogen / Q000235:genetics / Q000378:metabolism*; D005341:Fibrinolysin / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000235:genetics; D006487:Hemostasis / Q000235:genetics / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000097:blood / Q000235:genetics; D011446:Prospective Studies; D012044:Regression Analysis; D012307:Risk Factors; D000979:alpha-2-Antiplasmin / Q000235:genetics / Q000378:metabolism; D014841:von Willebrand Factor / Q000235:genetics / Q000378:metabolism
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C037742:plasmin-plasmin inhibitor complex; D014841:von Willebrand Factor; D000990:Antithrombin III; D005340:Fibrinogen; D002097:C-Reactive Protein; D010447:Peptide Hydrolases; D005341:Fibrinolysin