title: Myeloperoxidase predicts progression of carotid stenosis in states of low high-density lipoprotein cholesterol.
abstract: OBJECTIVE
  We investigated the effect of myeloperoxidase (MPO) on progression of carotid stenosis in states of high and low high-density lipoprotein-cholesterol (HDL-C) and low-density lipoprotein-cholesterol (LDL-C) levels.
  
  
  BACKGROUND
  Myeloperoxidase is pivotally involved in the pathogenesis of atherosclerosis. In vitro data suggest that MPO exerts deleterious effects via oxidative modulation of lipoproteins.
  
  
  METHODS
  We prospectively studied 1,019 of 1,268 consecutive patients who were asymptomatic with respect to carotid artery disease. Patients underwent serial carotid ultrasound investigations at baseline and after a follow-up interval of median 7.5 months (range 6 to 9 months), categorizing carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed or occluded. The MPO, HDL-C, and LDL-C levels were measured at baseline, grouped by medians, and correlated with progression of carotid atherosclerosis.
  
  
  RESULTS
  Progression of carotid atherosclerosis was found in 100 of 1,019 patients (9.8%). Myeloperoxidase (p = 0.014) but not HDL-C (p = 0.95) or LDL-C (p = 0.30) were associated with progressive disease. However, MPO > or =310 ng/ml was significantly associated with progressive disease (adjusted odds ratio [OR] 2.57, 95% confidence interval [CI] 1.39 to 4.75) only in patients with HDL-C levels <49 mg/dl. Otherwise, in patients with higher HDL-C levels (> or =49 mg/dl), MPO > or =310 ng/ml did not predict disease progression (adjusted OR 1.42, 95% CI 0.72 to 2.78). No interaction of MPO with LDL-C was observed.
  
  
  CONCLUSIONS
  Myeloperoxidase was associated with progression of carotid atherosclerosis in patients with HDL cholesterol levels below 49 mg/dl.
authors.affiliation: Department of Medical and Chemical Laboratory Diagnostics, Medical University Vienna, Vienna, Austria.
authors.forename: Markus
authors.initials: M
authors.lastname: Exner
authors.forename: Erich
authors.initials: E
authors.lastname: Minar
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Mlekusch
authors.forename: Schila
authors.initials: S
authors.lastname: Sabeti
authors.forename: Jasmin
authors.initials: J
authors.lastname: Amighi
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Lalouschek
authors.forename: Gerald
authors.initials: G
authors.lastname: Maurer
authors.forename: Christian
authors.initials: C
authors.lastname: Bieglmayer
authors.forename: Heidi
authors.initials: H
authors.lastname: Kieweg
authors.forename: Oswald
authors.initials: O
authors.lastname: Wagner
authors.forename: Martin
authors.initials: M
authors.lastname: Schillinger
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D016893:Carotid Stenosis / Q000097:blood* / Q000000981:diagnostic imaging*; D008076:Cholesterol, HDL / Q000097:blood*; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007249:Inflammation / Q000097:blood; D008297:Male; D008875:Middle Aged; D009195:Peroxidase / Q000097:blood*; D011237:Predictive Value of Tests; D011446:Prospective Studies; D014463:Ultrasonography
chemical_list: D008076:Cholesterol, HDL; D002097:C-Reactive Protein; D009195:Peroxidase