期刊
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
卷 31, 期 9, 页码 2007-2014出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.111.226167
关键词
acute coronary syndromes; arterial thrombosis; atherosclerosis; pathology; positron emission tomography
资金
- Merck-Schering/Plough
- Michigan State University
- Edward Sparrow Hospital, Lansing, MI
- Novartis
- General Electric, Lantheus Medical Imaging, Pfizer
- Janssen
Objective-This study evaluated effects of lipid lowering with ezetimibe on plaque burden and associated cholesterol crystallization and inflammation in a rabbit model of plaque disruption and thrombosis. Methods and Results-Atherosclerotic rabbits (Group I, n = 10 without; Group II, n = 12 with ezetimibe, 1 mg/kg per day) were pharmacologically triggered for plaque disruption. Fluorodeoxyglucose positron emission tomography, RAM 11 macrophage staining, and serum inflammatory markers detected arterial inflammation. Serum and aortic wall cholesterol levels were measured, and thrombus area was planimetered. Cholesterol crystal density on aortic surface was scored (0 to + 3) by scanning electron microscopy. Serum and aortic wall cholesterol, plaque area, and thrombosis area were significantly lower in Group II versus Group I (83.4 +/- 106.4 versus 608 +/- 386 mg/dL, P = 0.002; 3.12 +/- 1.40 versus 9.39 +/- 5.60 mg/g, P = 0.003; 10.84 +/- 1.6 versus 17.48 +/- 1.8 mm(2), P < 0.001; and 0.05 +/- 0.15 versus 0.72 +/- 0.58 mm(2), P = 0.01, respectively). There were significant correlations between crystal density and plaque area (r = 0.75, P < 0.003) and between crystal density and RAM 11 (r = 0.82, P < 0.001). Scanning electron microscopy demonstrated that there were fewer crystals in Group II versus Group I (+ 1.2 +/- 0.61 versus + 2.4 +/- 0.63, P < 0.001) and less inflammation detected by fluorodeoxyglucose positron emission tomography and RAM 11 (P < 0.004 and P < 0.04, respectively). Conclusion-Lowering cholesterol levels with ezetimibe reduced plaque burden, crystallization, and inflammation, preventing plaque disruption and thrombosis. (Arterioscler Thromb Vasc Biol. 2011;31:2007-2014.)
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