Abstract
Elevated plasma levels of low-density lipoprotein cholesterol (LDL-C) are associated with an increased cardiovascular (CV) risk; numerous clinical studies have shown that a reduction in plasma LDL-C levels results in a reduction in the incidence of CV events, and that a greater the reduction in LDL-C level, the greater the CV benefit. Statins are cornerstones in the treatment of hypercholesterolemia; by inhibiting the activity of the rate-limiting enzyme 3-hydroxy-3-methylglutaryl–coenzyme A reductase (HMG-CoAR), statins reduce the endogenous synthesis of cholesterol. As a consequence, the hepatic expression of LDL receptor (LDLR) increases, promoting the uptake of LDL from the circulation and the reduction of plasma LDL-C levels. These effects translate into a reduction in CV morbidity and mortality, and there are clear demonstrations that the effect is proportional to the absolute reduction of LDL-C, independent of the type of treatment.
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