Abstract
Current theory holds that atherosclerotic plaque formation results from injuries which damage the histological and functional integrity of the endothelium (for review see e.g. Miller 1984). As causative factors low density lipoproteins (LDL), hemodynamic shearing at bifurcations of the arterial system, nicotine, and others have been identified in endothelial damage. Once the endothelial lining is disrupted, plasma components, especially LDL, are deposited in the denuded area followed by migration of smooth muscle cells into the subendothelial space.
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References
Krüger B, Lang E (1984) Effects of two different doses of etofibrate on platelet aggregation and lipoproteins. Eur J Clin Invest 14(2), pt II, Abstr 46
Miller NE (1984) Atherosclerosis: mechanisms and approaches to therapy. Raven, New York
Puglisi L, Maggi F, Accomazzo MR, Schatton W (1984) The antiatherosclerotic property of etofibrate. Eur J Clin Invest 14(2), pt II, Abstr 44
Wagner HA, Cremer P, Creutzfeldt C, Seidel D (1984) Influence of etofibrate on prostaglandins and lipoproteins in 11 hyperlipoproteinemics. Eur J Clin Invest 14(2), pt II, Abstract 45
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© 1987 Springer-Verlag Berlin Heidelberg
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Noseda, G., Fragiacomo, C., Radelli, A., Bosisio, E., De Fabiani, E., Galli, G. (1987). Effect of Etofibrate on Platelet Function in Hyperlipidemic Patients. In: Paoletti, R., Kritchevsky, D., Holmes, W.L. (eds) Drugs Affecting Lipid Metabolism. Proceedings in Life Sciences. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71702-4_74
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DOI: https://doi.org/10.1007/978-3-642-71702-4_74
Publisher Name: Springer, Berlin, Heidelberg
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