title: In vivo coronary plaque histology in patients with stable and acute coronary syndromes: relationships with hyperlipidemic status and statin treatment.
abstract: OBJECTIVE
  Aim of the study was to investigate whether maintained moderate statin treatment influence atheroma, macrophage content, neoangiogenesis and/or haemorrhage in coronary plaques from patients with non-fatal coronary syndromes.
  
  
  METHODS
  A total of 48 patients underwent elective directional coronary atherectomy on "de novo" culprit lesions; 16 patients had non-treated hypercholesterolemia, 16 patients received maintained moderate statin treatment for hypercholesterolemia and 16 had no lipoprotein abnormalities. These three patients groups were matched for age and clinical diagnosis of stable angina (SA) or unstable angina/non-ST-elevation myocardial infarction (UA/NSTEMI). Atherectomy specimens were stained with antibodies against macrophages, endothelial cells and glycophorin A. Results of histology and immunohistochemistry were morphometrically analyzed by using computer-assisted image analysis.
  
  
  RESULTS
  Atheroma and fibrous tissue, neoangiogenesis, macrophage and haemorrhage (i.e., glycophorin A) differed between the three groups (P<0.05). Statin-treated group showed significantly decreased atheroma (P=0.016), fibrous tissue (P=0.42), macrophage content (P=0.012), neoangiogenesis (P=0.00048) and haemorrhage (P=0.0092) as compared with the non-treated hyperlipidemic group.
  
  
  CONCLUSIONS
  The present findings show that maintained moderate statin treatment may contribute to plaque stabilization in non-fatal coronary syndromes by decreasing intraplaque neoangiogenesis and haemorrhage, lipid burden and macrophage content, and, on the other hand, by increasing plaque collagenization.
authors.affiliation: Pathology Department, Regina Margherita Hospital, Turin, Italy. angelapucci@libero.it
authors.forename: Angela
authors.initials: A
authors.lastname: Pucci
authors.forename: Imad
authors.initials: I
authors.lastname: Sheiban
authors.forename: Luisa
authors.initials: L
authors.lastname: Formato
authors.forename: Angela
authors.initials: A
authors.lastname: Celeste
authors.forename: Elvis
authors.initials: E
authors.lastname: Brscic
authors.forename: Claudio
authors.initials: C
authors.lastname: Moretti
authors.forename: Alberto
authors.initials: A
authors.lastname: De Bernardi
authors.forename: Alessandro
authors.initials: A
authors.lastname: Alberti
authors.forename: Laura
authors.initials: L
authors.lastname: Bergamasco
authors.forename: Gianpaolo
authors.initials: G
authors.lastname: Trevi
authors.forename: Valentin
authors.initials: V
authors.lastname: Fuster
mesh_terms: D000208:Acute Disease; D000368:Aged; D000789:Angina, Unstable / Q000188:drug therapy* / Q000473:pathology; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D017225:Atherectomy, Coronary; D000069059:Atorvastatin; D003324:Coronary Artery Disease / Q000188:drug therapy* / Q000473:pathology; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006021:Glycophorins / Q000378:metabolism; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006949:Hyperlipidemias / Q000188:drug therapy* / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000627:therapeutic use*; D011758:Pyrroles / Q000627:therapeutic use; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000069059:Atorvastatin; D006021:Glycophorins; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D017035:Pravastatin; D011758:Pyrroles; C067980:CD68 antigen, human; D000097382:CD68 Molecule