Title of article
In vivo coronary plaque histology in patients with stable and acute coronary syndromes: Relationships with hyperlipidemic status and statin treatment
Author/Authors
Angela Pucci، نويسنده , , Imad Sheiban، نويسنده , , Luisa Formato، نويسنده , , Angela Celeste، نويسنده , , Elvis Brscic، نويسنده , , Claudio Moretti، نويسنده , , Alberto De Bernardi، نويسنده , , Alessandro Alberti، نويسنده , , Laura Bergamasco، نويسنده , , GianPaolo Trevi، نويسنده , , Valentin Fuster، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2007
Pages
7
From page
189
To page
195
Abstract
Objectives
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.
Keywords
inflammation , coronary disease , lipoproteins , angiogenesis , immunohistochemistry
Journal title
Atherosclerosis
Serial Year
2007
Journal title
Atherosclerosis
Record number
632496
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