Composition of coronary plaques obtained by directional atherectomy in stable angina: its relation to serum lipids and statin treatment.
OBJECTIVE
The stability and inflammatory activity in atherosclerotic plaques may be modulated by lipids and lipoproteins as well as the pleiotropic effects of statins. The aim of this study was to analyse the effect of statin treatment as well as the relation of plasma lipids and lipoproteins to tissue composition in atherosclerotic plaques.


METHODS
Patients with stable angina and coronary plaques suitable for directional coronary atherectomy (DCA) were randomized to atorvastatin (80 mg once daily) or placebo (29 randomized, 22 underwent DCA, 11/group). After an average treatment of 10 weeks, patients underwent DCA, tissue specimens were obtained, and the tissue composition was determined by immunohistochemistry.


RESULTS
Atorvastatin reduced the T-cell content, but did not change lipid, collagen, smooth muscle cell, or macrophage content. Plasma levels of apolipoprotein AI (apoAI) correlated positively with tissue collagen and inversely with metalloproteinase-9 and macrophage content. About half the specimens contained neutrophil granulocytes.


CONCLUSIONS
Short-term atorvastatin treatment tended to reduce the T-cell content of atherosclerotic plaques, indicating modulation of cell-mediated immunity. High plasma levels of apoAI correlated with increased collagen content and reduced inflammation, supporting the notion that plasma apoAI stabilizes atherosclerotic plaques. The significance of neutrophils in the lesions merits further study.
Department of Cardiology and Wallenberg Laboratory, Sahlgrenska University Hospital, Göteborg, Sweden.
J
J
Solem
M
M
Levin
T
T
Karlsson
L
L
Grip
P
P
Albertsson
O
O
Wiklund
D000328:Adult; D000368:Aged; D000787:Angina Pectoris / Q000276:immunology / Q000378:metabolism / Q000628:therapy*; D016632:Apolipoprotein A-I / Q000097:blood; D017225:Atherectomy, Coronary; D000069059:Atorvastatin; D015415:Biomarkers / Q000032:analysis; D003094:Collagen / Q000032:analysis; D003131:Combined Modality Therapy; D003324:Coronary Artery Disease / Q000276:immunology / Q000378:metabolism / Q000628:therapy*; D004311:Double-Blind Method; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007091:Image Processing, Computer-Assisted / Q000379:methods; D007111:Immunity, Cellular / Q000187:drug effects; D018836:Inflammation Mediators / Q000097:blood; D008055:Lipids / Q000097:blood*; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000627:therapeutic use*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology
D016632:Apolipoprotein A-I; D015415:Biomarkers; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators; D008055:Lipids; D011758:Pyrroles; D003094:Collagen; D000069059:Atorvastatin