title: Independent relation of vital exhaustion and inflammation to fibrinolysis in apparently healthy subjects.
abstract: OBJECTIVE
  Vital exhaustion (VE) and a hypercoagulable state both have been associated with coronary artery disease (CAD). Candidate mechanisms by which VE predicts CAD events are impaired fibrinolysis and inflammatory changes, the latter also affecting hemostasis. We investigated whether VE and inflammation would independently relate to hemostasis.
  
  
  METHODS
  Study participants were 217 (mean age+/-SD, 40+/-9 years) apparently healthy men and women working at an airplane manufacturing plant in Germany who completed the Shortened 9-item VE Maastricht Questionnaire. All subjects had a set of classic cardiovascular risk factors assessed, and plasma levels of fibrin D-dimer, type I plasminogen activator inhibitor (PAI-1) antigen, C-reactive protein (CRP), and tumor necrosis factor (TNF)-alpha were measured.
  
  
  RESULTS
  PAI-1 correlated with VE (r=0.18, p=0.009), CRP (r=0.20, p=0.004), and TNF-alpha (r=0.18, p=0.009); D-dimer correlated with CRP (r=0.16, p=0.018). In linear regression analyses, VE and TNF-alpha independently explained 2 and 1%, respectively, of the variance in PAI-1.
  
  
  CONCLUSIONS
  Our study corroborates previous findings on impaired fibrinolysis in VE. The findings suggest that VE and inflammation may impair fibrinolysis by different pathways, and independently of traditional cardiovascular risk factors.
authors.affiliation: Institute for Behavioral Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. roland.vonkanel@ifv.gess.ethz.ch
authors.forename: Roland
authors.initials: R
authors.lastname: von Känel
authors.forename: Karl
authors.initials: K
authors.lastname: Frey
authors.forename: Joachim
authors.initials: J
authors.lastname: Fischer
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003971:Diastole / Q000502:physiology; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005342:Fibrinolysis / Q000502:physiology*; D005858:Germany; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012016:Reference Values; D012907:Smoking / Q000097:blood / Q000453:epidemiology / Q000503:physiopathology; D013223:Statistics as Topic; D013599:Systole / Q000502:physiology; D014797:Vital Capacity / Q000502:physiology*
chemical_list: D015415:Biomarkers; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005338:Fibrin Fibrinogen Degradation Products; D018836:Inflammation Mediators; D017395:Plasminogen Activator Inhibitor 1; C036309:fibrin fragment D; D002097:C-Reactive Protein