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Pleiotropie Effects of Statins in Stroke Prevention
Cardiovascular disease is the leading cause of death and death and disability, and contributes substantially to healthcare budgets. The lipid-lowering drugs, 3-hydroxy-3-methylgulutaryl –coenzyme A (HMG-CoA) reductase inhibitor or statins, reducing mortality and cardiovascular morbidity in patient with established cardiovascular disease. Stantins ttherefore have a place in the secondary prevention of cardiovascular disease. Recent experimental and clinical studies suggest that statins may exert vacular protective beyond cholesterol reduction. The cholesterol reduction. The cholesteral-independet or “pleiotropic” effect of statin include the upergulation and activation of endothelial nitric acid synthase (eNOS) that can increase nitric oxide (NU)production. Augmentation of NO production increases cerebral blood flow, whichcan lead to neuroprotection during brain ischemia. By inhibiting mevalonate synthesis, statins prevent the formation of several isoprenoids (Including farnesylpyrophosphate and gerany geranyl geranypyroc phosphate). Inhibiting geranylgeranylation of RhoA small G proteins increases the stability of eNOS mRNA through the remodeling of edonthelial actin microfilamens. Moreover, statins directly increase eNOS activity within minutes by activating the pathway involving phosphoinositide 3-kinase and protein kinase B. In the secondary prevantion of stroke, the ose of strains reduces the incidence of either recurent stroke or other major vascular events and treatment should be initiated soon the event. The use of statins does not increase hemorrhagic stroke or cancer and may also favor atherosclerotic plaque regression.
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