The HDL anti-inflammatory function is impaired in myocardial infarction and may predict new cardiac events independent of HDL cholesterol

Clin Chim Acta. 2014 Jun 10:433:34-8. doi: 10.1016/j.cca.2014.02.026. Epub 2014 Mar 5.

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.

Keywords: Acute coronary syndrome; Atypical chest pain; HDL anti-inflammatory function; Non-STEMI; STEMI.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Chest Pain / blood
  • Chest Pain / diagnosis
  • Chest Pain / genetics
  • Chest Pain / metabolism
  • Cholesterol, HDL / blood
  • Cholesterol, HDL / metabolism*
  • Female
  • Gene Expression Regulation / drug effects
  • Humans
  • Inflammation / metabolism
  • Male
  • Middle Aged
  • Myocardial Infarction / blood
  • Myocardial Infarction / diagnosis*
  • Myocardial Infarction / genetics
  • Myocardial Infarction / metabolism*
  • Prospective Studies
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Risk Factors
  • Tumor Necrosis Factor-alpha / pharmacology
  • Vascular Cell Adhesion Molecule-1 / genetics

Substances

  • Cholesterol, HDL
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1