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März W, Winkelmann BR
HMG-CoA Reductase Inhibition in the Treatment of Atherosclerosis: Effects Beyond Lipid Lowering
Journal für Kardiologie - Austrian Journal of Cardiology 2002; 9 (7-8): 284-294

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Abb. 1: Simvastatin - Schlaganfall Abb. 2: Pravastatin - C-reaktives Protein Aktuelles Bild - Abb. 3: Pravastatin - Plaque
Abbildung 3: Pravastatin - Plaque
Effect of statin treatment on the composition of atherosclerotic plaques. Consecutive patients with symptomatic carotid artery stenoses received 40 mg daily pravastatin (n = 11) or no lipid-lowering therapy (n = 13) for 3 months before elective carotid endarterectomy. Carotid plaque composition was assessed with special stains and immunocytochemistry with quantitative image analysis. Compared to controls, pravastatin decreased the contents lipids, oxidized LDL, macrophages, T cells, matrix metalloproteinase 2 (MMP-2) and apoptotic cells, but increased the tissue inhibitor of metalloproteinase 1 (TIMP-1) and collagen. A slight increase in smooth muscle cells was also observed. Modified according to [147].
 
Pravastatin - Plaque
Vorheriges Bild Nächstes Bild  


Abbildung 3: Pravastatin - Plaque
Effect of statin treatment on the composition of atherosclerotic plaques. Consecutive patients with symptomatic carotid artery stenoses received 40 mg daily pravastatin (n = 11) or no lipid-lowering therapy (n = 13) for 3 months before elective carotid endarterectomy. Carotid plaque composition was assessed with special stains and immunocytochemistry with quantitative image analysis. Compared to controls, pravastatin decreased the contents lipids, oxidized LDL, macrophages, T cells, matrix metalloproteinase 2 (MMP-2) and apoptotic cells, but increased the tissue inhibitor of metalloproteinase 1 (TIMP-1) and collagen. A slight increase in smooth muscle cells was also observed. Modified according to [147].
 
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