title: An increase of C-reactive protein is associated with enhanced activation of endogenous fibrinolysis at baseline but an impaired endothelial fibrinolytic response after venous occlusion.
abstract: OBJECTIVE
  The goal of this study was to determine whether chronic inflammation of the vascular wall may be associated with an impaired activation of the fibrinolytic system.
  
  
  BACKGROUND
  Inflammation plays an important role in the initiation and progression of atherosclerosis, and the fibrinolytic system may prevent local thrombus formation.
  
  
  METHODS
  We included 50 patients six months after their first myocardial infarction. Plasma levels of the inflammatory marker C-reactive protein (CRP) were determined at basal conditions, and the fibrinolytic parameters tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor type-1 (PAI-1) were measured at basal conditions and after a standardized venous occlusion (VO) of the forearm.
  
  
  RESULTS
  Patients with high CRP levels (> or =3 mg/l) showed a significantly higher t-PA activity at baseline compared with patients with medium (1 to 2.9 mg/l) and low (<1 mg/l) CRP levels (p <0.005). In contrast, patients with low CRP levels showed a higher increase of t-PA activity (p <0.05) and a higher reduction of PAI-1 activity during VO (p <0.05) compared with patients with medium and high CRP levels. A multivariate analysis that included cardiovascular risk factors and medical treatment showed that CRP is an independent predictor of the t-PA response after a standardized VO.
  
  
  CONCLUSIONS
  Chronic low-grade inflammation is associated with enhanced activation of endogenous fibrinolysis at baseline but a reduced fibrinolytic response to VO. This impaired endogenous fibrinolytic capacity might be an important contributor to the increased coronary event rate associated with elevated CRP levels.
authors.affiliation: Department of Internal Medicine II, Medical University of Vienna and the Ludwig Boltzmann Foundation for Cardiovascular Research, Vienna, Austria.
authors.forename: Walter Stefan
authors.initials: WS
authors.lastname: Speidl
authors.forename: Andrea
authors.initials: A
authors.lastname: Zeiner
authors.forename: Mariam
authors.initials: M
authors.lastname: Nikfardjam
authors.forename: Alexander
authors.initials: A
authors.lastname: Geppert
authors.forename: Nelli
authors.initials: N
authors.lastname: Jordanova
authors.forename: Alexander
authors.initials: A
authors.lastname: Niessner
authors.forename: Gerlinde
authors.initials: G
authors.lastname: Zorn
authors.forename: Gerald
authors.initials: G
authors.lastname: Maurer
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Schreiber
authors.forename: Johann
authors.initials: J
authors.lastname: Wojta
authors.forename: Kurt
authors.initials: K
authors.lastname: Huber
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000032:analysis*; D003324:Coronary Artery Disease / Q000097:blood*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000097:blood*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010959:Tissue Plasminogen Activator / Q000097:blood
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D002097:C-Reactive Protein; D010959:Tissue Plasminogen Activator