title: Intensive lipid-lowering therapy ameliorates novel calcification markers and GSM score in patients with carotid stenosis.
abstract: OBJECTIVE
  Carotid plaque echogenicity quantified by the Gray-Scale Median (GSM) score has been associated with plaque vulnerability. The aim of this study was to assess whether intensive lipid-lowering treatment with atorvastatin in patients with carotid artery stenosis ameliorates novel vascular calcification inhibitors, such as osteopontin (OPN) and osteoprotegerin (OPG), and improves GSM score.
  
  
  METHODS
  Ninety-seven patients with carotid stenosis (>40%), but without indication for intervention, were treated for 6 months with atorvastatin (10mg-80mg) to target LDL<100mg/dl. Fifty-two age-and sex-matched healthy individuals served as the control group. Blood samples and GSM were obtained at the beginning and after 6 months.
  
  
  RESULTS
  Systolic blood pressure, hsCRP, fibrinogen, OPN and OPG levels differed significantly between patients with carotid stenosis and healthy controls at baseline (p<0.05). Atorvastatin treatment improved lipid profile and significantly reduced hsCRP (p=0.002), WBC count (p=0.041), OPN (p<0.001) and OPG levels (p<0.001). GSM score increased considerably after atorvastatin therapy (from 58.33+/-24.38 to 79.33+/-22.3; p<0.001) and that effect appeared related to OPN (p=0.001), OPG (p=0.013) and LDL (p=0.01) reduction.
  
  
  CONCLUSIONS
  In patients with carotid stenosis, intensive lipid-lowering therapy with statins attenuates serum OPN and OPG levels and enhances carotid plaque echogenicity, outlining their beneficial effects on plaque stability.
authors.affiliation: Department of Vascular Surgery, Medical School, University of Athens, Greece.
authors.forename: N P E
authors.initials: NP
authors.lastname: Kadoglou
authors.forename: T
authors.initials: T
authors.lastname: Gerasimidis
authors.forename: A
authors.initials: A
authors.lastname: Moumtzouoglou
authors.forename: A
authors.initials: A
authors.lastname: Kapelouzou
authors.forename: N
authors.initials: N
authors.lastname: Sailer
authors.forename: G
authors.initials: G
authors.lastname: Fotiadis
authors.forename: I
authors.initials: I
authors.lastname: Vitta
authors.forename: A
authors.initials: A
authors.lastname: Katinios
authors.forename: P
authors.initials: P
authors.lastname: Kougias
authors.forename: S
authors.initials: S
authors.lastname: Bandios
authors.forename: K
authors.initials: K
authors.lastname: Voliotis
authors.forename: P E
authors.initials: PE
authors.lastname: Karayannacos
authors.forename: C D
authors.initials: CD
authors.lastname: Liapis
mesh_terms: D000368:Aged; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D002097:C-Reactive Protein / Q000378:metabolism; D002114:Calcinosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy*; D016893:Carotid Stenosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy*; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D053495:Osteopontin / Q000097:blood*; D053244:Osteoprotegerin / Q000097:blood*; D011446:Prospective Studies; D011758:Pyrroles / Q000627:therapeutic use*; D012720:Severity of Illness Index; D016896:Treatment Outcome; D014463:Ultrasonography
chemical_list: D015415:Biomarkers; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D053244:Osteoprotegerin; D011758:Pyrroles; C506030:TNFRSF11B protein, human; D053495:Osteopontin; D005340:Fibrinogen; D002097:C-Reactive Protein; D000069059:Atorvastatin