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HMG-CoA reductase inhibition: anti-inflammatory effects beyond lipid lowering?
J Cardiovasc Risk. 2003 Jun; 10(3):169-79.JC

Abstract

Atherosclerosis has many features of a chronic inflammatory disease. Atherosclerotic lesions contain inflammatory cells. 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. 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. High-density lipoproteins (HDL) oppose these effects by inhibiting the oxidation of LDL, and by down-regulating the expression of adhesion molecules and selectins. Treatment with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) has proven the most successful strategy to reduce the concentration of LDL in the circulation. These compounds lower LDL cholesterol by inhibiting the mevalonate pathway in the liver. 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 statins may not entirely be due to their effect on the levels of circulating lipoproteins. In vitro observations of anti-inflammatory actions of statins on vascular cells may contribute 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 on the net clinical benefit of statin treatment.

Authors+Show Affiliations

Clinical Institute of Medical and Chemical Laboratory Diagnostics, Karl Franzens-University, Graz, Austria. winfried.maerz@klinikum-graz.atNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

12775949

Citation

März, Winfried, and Wolfgang Köenig. "HMG-CoA Reductase Inhibition: Anti-inflammatory Effects Beyond Lipid Lowering?" Journal of Cardiovascular Risk, vol. 10, no. 3, 2003, pp. 169-79.
März W, Köenig W. HMG-CoA reductase inhibition: anti-inflammatory effects beyond lipid lowering? J Cardiovasc Risk. 2003;10(3):169-79.
März, W., & Köenig, W. (2003). HMG-CoA reductase inhibition: anti-inflammatory effects beyond lipid lowering? Journal of Cardiovascular Risk, 10(3), 169-79.
März W, Köenig W. HMG-CoA Reductase Inhibition: Anti-inflammatory Effects Beyond Lipid Lowering. J Cardiovasc Risk. 2003;10(3):169-79. PubMed PMID: 12775949.
* 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,Winfried, AU - Köenig,Wolfgang, PY - 2003/5/31/pubmed PY - 2003/11/28/medline PY - 2003/5/31/entrez SP - 169 EP - 79 JF - Journal of cardiovascular risk JO - J Cardiovasc Risk VL - 10 IS - 3 N2 - Atherosclerosis has many features of a chronic inflammatory disease. Atherosclerotic lesions contain inflammatory cells. 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. 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. High-density lipoproteins (HDL) oppose these effects by inhibiting the oxidation of LDL, and by down-regulating the expression of adhesion molecules and selectins. Treatment with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) has proven the most successful strategy to reduce the concentration of LDL in the circulation. These compounds lower LDL cholesterol by inhibiting the mevalonate pathway in the liver. 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 statins may not entirely be due to their effect on the levels of circulating lipoproteins. In vitro observations of anti-inflammatory actions of statins on vascular cells may contribute 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 on the net clinical benefit of statin treatment. SN - 1350-6277 UR - https://www.unboundmedicine.com/medline/citation/12775949/HMG_CoA_reductase_inhibition:_anti_inflammatory_effects_beyond_lipid_lowering L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=12775949.ui DB - PRIME DP - Unbound Medicine ER -