title: Total cholesterol content of erythrocyte membranes is increased in patients with acute coronary syndrome: a new marker of clinical instability?
abstract: OBJECTIVE
  We hypothesized that cholesterol content is increased in the circulating erythrocytes of patients with acute coronary syndrome (ACS) and may be a marker of clinical instability. We therefore sought to investigate whether cholesterol content differs in erythrocyte membranes of patients presenting with ACS compared to patients with chronic stable angina (CSA).
  
  
  BACKGROUND
  Plaque rupture in ACS depends at least partly on the volume of the necrotic lipid core. Histopathologic studies have suggested that cholesterol transported by erythrocytes and deposited into the necrotic core of atheromatous plaques contributes to lipid core growth.
  
  
  METHODS
  Consecutive angina patients were prospectively assessed; 120 had CSA (83 men, age 64 +/- 11 years) and 92 ACS (67 men, 66 +/- 11 years). Total cholesterol content in erythrocyte membranes (CEM) was measured using an enzymatic assay, and protein content was assessed by the Bradford method.
  
  
  RESULTS
  The CEM (median and interquartile range) was higher (p < 0.001) in ACS patients (184 microg/mg; range 130.4 to 260.4 microg/mg) compared with CSA patients (81.1 microg/mg; range 53.9 to 109.1 microg/mg) (analysis of covariance). Total plasma cholesterol concentrations did not correlate with CEM levels (r = -0.046, p = 0.628).
  
  
  CONCLUSIONS
  This study shows, for the first time, that CEM is significantly higher in patients with ACS compared with CSA patients. These findings suggest a potential role of CEM as a marker of atheromatous plaque growth and vulnerability. Large ad hoc studies are required to establish the clinical importance and pathogenic significance of CEM measurement.
authors.affiliation: Cardiovascular Biology Research Centre, Division of Cardiac and Vascular Sciences, St. George's, University of London, London, United Kingdom.
authors.forename: Dimitrios N
authors.initials: DN
authors.lastname: Tziakas
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Kaski
authors.forename: Georgios K
authors.initials: GK
authors.lastname: Chalikias
authors.forename: Carlos
authors.initials: C
authors.lastname: Romero
authors.forename: Salim
authors.initials: S
authors.lastname: Fredericks
authors.forename: Ioannis K
authors.initials: IK
authors.lastname: Tentes
authors.forename: Alexandros X
authors.initials: AX
authors.lastname: Kortsaris
authors.forename: Dimitrios I
authors.initials: DI
authors.lastname: Hatseras
authors.forename: David W
authors.initials: DW
authors.lastname: Holt
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000097:blood* / Q000188:drug therapy; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood*; D017023:Coronary Angiography; D004910:Erythrocyte Membrane / Q000378:metabolism*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy; D011446:Prospective Studies
chemical_list: D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002097:C-Reactive Protein; D002784:Cholesterol