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HMG-CoA reductase inhibition: anti-inflammatory effects beyond lipid lowering?
Herz 2000; 25(2):117-25HERZ

Abstract

Atherosclerosis has many features of a chronic inflammatory disease. Atherosclerotic lesions contain inflammatory cells like activated T-lymphocytes and macrophages. Systemic markers of inflammation such as white blood cells, C-reactive protein, serum amyloid A, interleukin 6 and soluble adhesion molecules are predictive of future cardiovascular events, even after adjustment for the contribution of established cardiovascular risk factors. Atherogenic lipoprotein particles, in particular modified low-density lipoproteins (LDL), elicit pro-inflammatory responses of cellular elements of the vessel wall, including endothelial dysfunction and activation of monocyte-derived macrophages. Treatment, with HMG-CoA reductase inhibitors has proven the most successful strategy to reduce the concentration of LDL in the circulatory system. These compounds lower LDL cholesterol by inhibiting the mevalonate pathway in the liver, which in turn depletes the regulatory pool of cholesterol and enhances the activity of LDL receptors. Five prospective clinical trials have convincingly demonstrated that HMG-CoA reductase inhibitors can effectively lower the incidence of cardiovascular events in primary and secondary prevention. Post hoc analyses of these trials suggest that the clinical benefit brought about by HMG-CoA reductase inhibitors may not entirely be due to their effect on the levels of circulating lipoproteins. In-vitro observations of anti-inflammatory actions of HMG-CoA reductase inhibitors on vascular cells have been suggested to explain effects beyond lipid-lowering. It is, however, not clear whether these findings are relevant to the in-vivo situation. Further investigation is now necessary in order to determine the relative significance of cholesterol lowering and of ancillary effects to the overall clinical benefit of statin treatment.

Authors+Show Affiliations

Department of Medicine, Albert Ludwigs-University, Freiburg im Breisgau, Germany. maerz@med1.ukl.uni-freiburg.deNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Review

Language

eng

PubMed ID

10829251

Citation

März, W, and H Wieland. "HMG-CoA Reductase Inhibition: Anti-inflammatory Effects Beyond Lipid Lowering?" Herz, vol. 25, no. 2, 2000, pp. 117-25.
März W, Wieland H. HMG-CoA reductase inhibition: anti-inflammatory effects beyond lipid lowering? Herz. 2000;25(2):117-25.
März, W., & Wieland, H. (2000). HMG-CoA reductase inhibition: anti-inflammatory effects beyond lipid lowering? Herz, 25(2), pp. 117-25.
März W, Wieland H. HMG-CoA Reductase Inhibition: Anti-inflammatory Effects Beyond Lipid Lowering. Herz. 2000;25(2):117-25. PubMed PMID: 10829251.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - HMG-CoA reductase inhibition: anti-inflammatory effects beyond lipid lowering? AU - März,W, AU - Wieland,H, PY - 2000/6/1/pubmed PY - 2000/7/6/medline PY - 2000/6/1/entrez SP - 117 EP - 25 JF - Herz JO - Herz VL - 25 IS - 2 N2 - Atherosclerosis has many features of a chronic inflammatory disease. Atherosclerotic lesions contain inflammatory cells like activated T-lymphocytes and macrophages. Systemic markers of inflammation such as white blood cells, C-reactive protein, serum amyloid A, interleukin 6 and soluble adhesion molecules are predictive of future cardiovascular events, even after adjustment for the contribution of established cardiovascular risk factors. Atherogenic lipoprotein particles, in particular modified low-density lipoproteins (LDL), elicit pro-inflammatory responses of cellular elements of the vessel wall, including endothelial dysfunction and activation of monocyte-derived macrophages. Treatment, with HMG-CoA reductase inhibitors has proven the most successful strategy to reduce the concentration of LDL in the circulatory system. These compounds lower LDL cholesterol by inhibiting the mevalonate pathway in the liver, which in turn depletes the regulatory pool of cholesterol and enhances the activity of LDL receptors. Five prospective clinical trials have convincingly demonstrated that HMG-CoA reductase inhibitors can effectively lower the incidence of cardiovascular events in primary and secondary prevention. Post hoc analyses of these trials suggest that the clinical benefit brought about by HMG-CoA reductase inhibitors may not entirely be due to their effect on the levels of circulating lipoproteins. In-vitro observations of anti-inflammatory actions of HMG-CoA reductase inhibitors on vascular cells have been suggested to explain effects beyond lipid-lowering. It is, however, not clear whether these findings are relevant to the in-vivo situation. Further investigation is now necessary in order to determine the relative significance of cholesterol lowering and of ancillary effects to the overall clinical benefit of statin treatment. SN - 0340-9937 UR - https://www.unboundmedicine.com/medline/citation/10829251/HMG_CoA_reductase_inhibition:_anti_inflammatory_effects_beyond_lipid_lowering L2 - https://medlineplus.gov/cholesterolmedicines.html DB - PRIME DP - Unbound Medicine ER -