title: Chronic dysfunction of the endothelium is associated with mortality in acute coronary syndrome patients.
abstract: BACKGROUND
  Platelet activation and endothelium dysfunction are determinants of atherothrombosis in acute coronary syndrome (ACS) patients. The aim of this study was to investigate the relationship between platelet and endothelial cell activation markers and mortality in patients presenting with ACS.
  
  
  METHODS
  Plasma levels of RANTES, Neutrophil Activating Protein-2 (NAP-2), Thrombospondin-1 (TSP-1), Von Willebrand Factor (VWF), Von Willebrand Factor Propeptide (VWF:pp) and Osteoprotegerin (OPG) were measured in a cohort study of 339 consecutive ACS patients who underwent percutaneous coronary interevention (PCI). The primary endpoint was 4-year mortality.
  
  
  RESULTS
  There were 46 deaths during the follow up. Median values of VWF (12.2μg/mL versus 7.86μg/mL, P=0.001) and VWF:pp (7.34nM versus 6.17nM, P=0.011) were higher in non-survivors compared to survivors. High levels of OPG were found in 37 patients: 27 of them were survivors (9.2%) and 10 were non-survivors (21.7%, P=0.011). Kaplan-Meier estimates of mortality for VWF were 7.5% in the first quartile (n=6 deaths), 12.2% in the second quartile (n=10 deaths), 11.2% in the third quartile (n=9 deaths) and 25% in the fourth quartile (n=21 deaths) of VWF (P=0.004). There was a 27.8% of probability of mortality when high OPG was measured versus 12.4% when low OPG was measured (P=0.007). No relationship between baseline platelet activation markers and mortality was found.
  
  
  CONCLUSIONS
  In patients with ACS undergoing PCI, increased chronic endothelial cell activation and dysfunction is associated with an increased risk of long-term mortality.
authors.affiliation: Department of Clinical Chemistry and Haematology, University Medical Center Utrecht, The Netherlands. a.hyseni@umcutrecht.nl
authors.forename: Agon
authors.initials: A
authors.lastname: Hyseni
authors.forename: Mark
authors.initials: M
authors.lastname: Roest
authors.forename: Siegmund L
authors.initials: SL
authors.lastname: Braun
authors.forename: Arjan D
authors.initials: AD
authors.lastname: Barendrecht
authors.forename: Philip G
authors.initials: PG
authors.lastname: de Groot
authors.forename: Gjin
authors.initials: G
authors.lastname: Ndrepepa
authors.forename: Adnan
authors.initials: A
authors.lastname: Kastrati
mesh_terms: D054058:Acute Coronary Syndrome / Q000401:mortality* / Q000473:pathology*; D000368:Aged; D001792:Blood Platelets / Q000166:cytology*; D018946:Chemokine CCL5 / Q000378:metabolism; D003331:Coronary Vessels / Q000473:pathology; D042783:Endothelial Cells / Q000166:cytology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009687:Nuclear Proteins / Q000378:metabolism; D053244:Osteoprotegerin / Q000378:metabolism; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects*; D011379:Prognosis; D019700:Thrombospondin 1 / Q000378:metabolism; D013997:Time Factors
chemical_list: C483024:CCL5 protein, human; D018946:Chemokine CCL5; C104356:NAP1L4 protein, human; D009687:Nuclear Proteins; D053244:Osteoprotegerin; D019700:Thrombospondin 1