title: The HDL anti-inflammatory function is impaired in myocardial infarction and may predict new cardiac events independent of HDL cholesterol.
abstract: BACKGROUND
  Intrinsic functional properties of high density lipoproteins (HDL) are considered to be physiologically important for atheroprotection. We compared the HDL anti-inflammatory capacity between patients with acute myocardial infarction (MI) and patients with non-cardiac chest pain, and prospectively determined the association of new major adverse cardiovascular events (MACE) with this metric of HDL function.
  
  
  METHODS
  A prospective study was carried out in 93 patients referred for acute chest pain (65 patients with acute MI). The HDL anti-inflammatory capacity was determined as the ability to suppress tumor necrosis factor-α-induced vascular cell adhesion molecule-1 mRNA expression in endothelial cells in vitro.
  
  
  RESULTS
  Acute MI at admission was associated with impaired HDL anti-inflammatory capacity (p=0.001), even after adjustment for HDL cholesterol and apolipoprotein A-I (p=0.003). Twenty nine MACE were ascertained during a median follow-up of 1210 (910-1679) days. New MACE was associated with impaired HDL anti-inflammatory capacity (hazard ratio: 1.80 (1.17-2.77) per SD change, p=0.007) in age, sex, HDL cholesterol and apolipoprotein-AI adjusted analysis.
  
  
  CONCLUSIONS
  The ability of HDL to attenuate endothelial inflammation is impaired in acute MI, and this metric of HDL function may serve as a predictor of new MACE, even independent of HDL cholesterol and apolipoprotein A-I.
authors.affiliation: Department of Endocrinology, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands. Electronic address: r.p.f.dullaart@umcg.nl.
authors.forename: Robin P F
authors.initials: RP
authors.lastname: Dullaart
authors.affiliation: Department of Pediatrics, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
authors.forename: Wijtske
authors.initials: W
authors.lastname: Annema
authors.affiliation: Department of Cardiology, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
authors.forename: René A
authors.initials: RA
authors.lastname: Tio
authors.affiliation: Department of Pediatrics, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands.
authors.forename: Uwe J F
authors.initials: UJ
authors.lastname: Tietge
mesh_terms: D000368:Aged; D002637:Chest Pain / Q000097:blood / Q000175:diagnosis / Q000235:genetics / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis* / Q000235:genetics / Q000378:metabolism*; D011446:Prospective Studies; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics
chemical_list: D008076:Cholesterol, HDL; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1
keywords: Acute coronary syndrome; Atypical chest pain; HDL anti-inflammatory function; Non-STEMI; STEMI