title: Galectin-3, Carotid Plaque Vulnerability, and Potential Effects of Statin  Therapy.
abstract: OBJECTIVE
  Galectin-3, a member of galectines, a family of b-galactoside-specific lectins, has been reported to propagate vascular inflammation. The role of galectin-3 in carotid atherosclerosis is controversial. The aim of this study was to investigate the relationship of galectin-3 with plaque vulnerability in patients with high grade carotid stenosis.
  
  
  METHODS
  This was a cross sectional study of patients undergoing carotid endarterectomy (CEA). Carotid plaques obtained from 78 consecutive patients (40 symptomatic [SG], 38 asymptomatic [AG]) undergoing CEA were histologically analyzed for galectin-3, macrophages (CD68) and laminin. Pre-operatively the biochemical profile and plaque echogenicity (gray-scale median, GSM) score were determined.
  
  
  RESULTS
  There were no significant differences in clinical and demographic parameters between SG and AG(p > .05). The SG had a lower GSM score (44.21 ± 18.24 vs. 68.79 ± 28.79, p < .001) and a smaller positive stained area for galectin-3 (4.89 ± 1.60% vs. 12.01 ± 5.91%, p < .001) and laminin (0.88 ± 0.71% vs. 3.46 ± 2.12%, p < .001) than the AG. On the other hand, intra-plaque macrophage content was increased in SG (p < .001). For the whole cohort, symptomatic status was independently associated with intra-plaque contents of both galectin-3 (OR=0.634, p < .001), and GSM score (OR=0.750, p < .001). Notably, patients on long term statin treatment had elevated galectin-3 and lowered macrophage intra-plaque concentrations compared with those on short term treatment (p < .05).
  
  
  CONCLUSIONS
  A low galectin-3 intra-plaque concentration seems to correlate with clinically and ultrasonically defined unstable human carotid plaques. Long term statin treatment may induce increase of intra-plaque galectin-3 concentration mediating plaque stabilization.
authors.forename: N P E
authors.initials: NP
authors.lastname: Kadoglou
authors.forename: G S
authors.initials: GS
authors.lastname: Sfyroeras
authors.forename: A
authors.initials: A
authors.lastname: Spathis
authors.forename: C
authors.initials: C
authors.lastname: Gkekas
authors.forename: A
authors.initials: A
authors.lastname: Gastounioti
authors.forename: G
authors.initials: G
authors.lastname: Mantas
authors.forename: K S
authors.initials: KS
authors.lastname: Nikita
authors.forename: P
authors.initials: P
authors.lastname: Karakitsos
authors.forename: C D
authors.initials: CD
authors.lastname: Liapis
mesh_terms: D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D002097:C-Reactive Protein / Q000032:analysis; D002340:Carotid Artery Diseases / Q000150:complications / Q000000981:diagnostic imaging / Q000473:pathology* / Q000628:therapy*; D016893:Carotid Stenosis / Q000209:etiology; D003430:Cross-Sectional Studies; D016894:Endarterectomy, Carotid; D005260:Female; D037502:Galectin 3 / Q000032:analysis* / Q000097:blood; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D007150:Immunohistochemistry; D007797:Laminin / Q000032:analysis; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D008297:Male; D058226:Plaque, Atherosclerotic / Q000737:chemistry* / Q000000981:diagnostic imaging; D012044:Regression Analysis; D014463:Ultrasonography; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D002097:C-Reactive Protein; D037502:Galectin 3; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007797:Laminin; C067980:CD68 antigen, human; D000097382:CD68 Molecule