title: Beneficial changes of serum calcification markers and contralateral carotid plaques echogenicity after combined carotid artery stenting plus intensive lipid-lowering therapy in patients with bilateral carotid stenosis.
abstract: OBJECTIVE
  In symptomatic patients treated with ipsilateral carotid artery stenting (CAS) plus intensive lipid lowering, we assessed the changes of osteopontin (OPN), osteoprotegerin (OPG) and the Gray-Scale Median (GSM) score contralateral to symptomatic carotid stenosis.
  
  
  METHODS
  Forty-six symptomatic patients (group A) with significant carotid stenosis (North American Symptomatic Carotid Endarterectomy Trial (NASCET): >70%) underwent ipsilateral CAS. Those patients had simultaneously contralateral low-grade carotid stenosis (NASCET: 30-69%). Group B included 67 symptomatic patients with low-grade bilateral carotid stenosis (NASCET: 30-69%), but without indications for revascularisation. All patients were treated with atorvastatin (10-80mg) to target low-density lipoprotein (LDL)<100mgdl(-1). Blood samples and plaques' GSM score contralateral to brain infarct were assayed at baseline and after 6 months.
  
  
  RESULTS
  At baseline, there were no significant differences between groups (p>0.05). Six-month atorvastatin treatment equivalently improved lipid profile in both groups (p<0.05). The parameters hsCRP, OPN and OPG were significantly down-regulated within both groups, but to a greater extent in group A (p<0.05). Besides this, contralateral GSM score was significantly improved from baseline in both groups (p<0.01), but that increment was more pronounced in group A (vs. group B; p=0.041). These changes were inversely correlated with changes in OPN (p=0.014), OPG (p=0.011) and LDL (p=0.041).
  
  
  CONCLUSIONS
  Ipsilateral CAS plus intensive lipid-lowering therapy was associated with enhanced contralateral carotid plaque stability and attenuated inflammatory burden and calcification inhibitors to a greater extent than atorvastatin therapy alone in patients with bilateral carotid stenosis.
authors.affiliation: First Department of Internal Medicine, Hippokratio General Hospital of Thessaloniki, Thessaloniki, Greece. nikoskad@yahoo.com
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: Kapelouzou
authors.forename: A
authors.initials: A
authors.lastname: Moumtzouoglou
authors.forename: E D
authors.initials: ED
authors.lastname: Avgerinos
authors.forename: J D
authors.initials: JD
authors.lastname: Kakisis
authors.forename: P E
authors.initials: PE
authors.lastname: Karayannacos
authors.forename: C D
authors.initials: CD
authors.lastname: Liapis
mesh_terms: D000368:Aged; D017130:Angioplasty / Q000295:instrumentation*; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002114:Calcinosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000628:therapy*; D016893:Carotid Stenosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000628:therapy*; D003131:Combined Modality Therapy; D015536:Down-Regulation; D005260:Female; D006115:Greece; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; 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; D015607:Stents; D013997:Time Factors; D016896:Treatment Outcome; D018608:Ultrasonography, Doppler
chemical_list: D015415:Biomarkers; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D053244:Osteoprotegerin; D011758:Pyrroles; C506895:SPP1 protein, human; C506030:TNFRSF11B protein, human; D053495:Osteopontin; D002097:C-Reactive Protein; D000069059:Atorvastatin