In vivo coronary plaque histology in patients with stable and acute coronary syndromes: relationships with hyperlipidemic status and statin treatment.
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.
Pucci
Angela
A
Pathology Department, Regina Margherita Hospital, Turin, Italy. angelapucci@libero.it
Sheiban
Imad
I
Formato
Luisa
L
Celeste
Angela
A
Brscic
Elvis
E
Moretti
Claudio
C
De Bernardi
Alberto
A
Alberti
Alessandro
A
Bergamasco
Laura
L
Trevi
Gianpaolo
G
Fuster
Valentin
V
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
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