after oral ingestion, lovastatin is hydrolyzed to its beta-hydroxyacid form, becoming a specific inhibitor of HMG-CoA reductase. This enzyme is responsible for the conversion of HMG-CoA to mevalonate, an early rate limiting step in the synthesis of cholesterol. In therapeutic concentrations, HMG-CoA reductase is not completely blocked, allowing biologically necessary amounts of mevalonate to be produced. Mevacor reduces both normal and elevated LDL (low density lipoprotein) concentrations and VLDL (very low density lipoprotein) concentrations. It is not known whether Mevacor's therapeutic effect is due to an increased LDL catabolism, a decrease in VLDL (a precursor to LDL), or a direct decrease in LDL production. In addition to LDL reduction, Mevacor increases HDL (high density lipoprotein) concentrations. High LDL and low HDL levels have been shown to be risk factors in coronary heart disease.