Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2563523 | Pharmacology & Therapeutics | 2009 | 14 Pages |
Abstract
Lipid-lowering using HMG-CoA reductase inhibitors or statin therapy forms the cornerstone of medical therapy in the primary and secondary prevention of cardiovascular disease. In addition, to the improvements in lipid profile, the beneficial effects elicited by this class of drugs may be attributed to their diverse variety of non-lipid lowering pleiotropic effects, including improved endothelial function, reduced oxidative stress, less platelet adhesion, and increased atherosclerotic plaque stability. A less appreciated effect of statin therapy that has been reported in experimental studies is its cardioprotective effect with respect to its ability to directly protect the myocardium from the detrimental effects of acute ischaemia-reperfusion injury. In the current article we review the cardioprotective effects of statin therapy beyond serum lipid lowering, the underlying mechanisms involved and the potential implications for patients with coronary heart disease.
Keywords
PCIIPCGGPPMPTPeNOS8-OHdGiNOSPMN8-SPTAARULNCK-MBMACEPI3K8-hydroxydeoxyguanosineMPOI/RIRIl-NAMEReperfusion injuryStatinmitochondrial permeability transition poreIschaemiareperfusion injury salvage kinaseUpper limit of normalCardioprotectionmajor adverse cardiac eventsRiskReperfusioninducible nitric oxide synthaseendothelial nitric oxide synthasePMIphosphatase and tensin homolog deleted on chromosome tenphosphoinositide-3 kinasepolymorphonuclear leukocytepercutaneous coronary interventionarea at riskHMG-CoA reductase inhibitormyeloperoxidaseknock outWild type.nitro-l-arginine methyl esterNitric oxidePtenCreatine kinaseAdenosine receptor
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Authors
Andrew Ludman, Vinod Venugopal, Derek M. Yellon, Derek J. Hausenloy,