LOVASTATIN, is a cholesterol-lowering agent isolated from a strain of Aspergillus terreus. After oral ingestion, lovastatin, which is an inactive lactone, is hydrolyzed to the corresponding ß-hydroxy acid form. This principal metabolite is a specific inhibitor of 3-hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, which is an early and rate-limiting step in the biosynthesis of cholesterol. Lovastatin reduces cholesterol production by the liver and induces some changes in cholesterol transport and disposition in the blood and tissues. The mechanism(s) of this effect is believed to involve both reduction of the synthesis of Low Density Lipoprotein (LDL), and an increase in LDL catabolism as a result of induction of the hepatic LDL receptors.
As with all statin like drugs the major side effect is myalgia or myalgia like symptoms. Please ask you pharmacist for more details.
LOVASTATIN is indicated as an adjunct to diet, at least equivalent to the American Heart Association (AHA) Step 1 diet, for the reduction of elevated total and Low Density Lipoprotein Cholesterol (LDL-C) levels in patients with primary hypercholesterolemia (Types IIa and IIb),12 (a disorder of lipid metabolism characterized by elevated serum cholesterol levels in association with normal triglyceride levels (Type IIa) or with increased triglyceride levels [Type IIb]) when the response to diet and other nonpharmacological measures alone has been inadequate. After establishing that the elevation in plasma lipids represents a primary disorder not due to secondary conditions such as poorly-controlled diabetes mellitus, hypothyroidism, the nephrotic syndrome, liver disease, or dysproteinemias, prospective patient should have an elevated LDL-C level as the cause for an elevated total serum cholesterol. This may be particularly relevant for patients with total triglycerides (TG) over 4.52 mmol/L (400 mg/dL) or with markedly elevated High Density Lipoprotein Cholesterol (HDL-C) values, where non-LDL lipoprotein fractions may contribute significantly to total cholesterol levels without apparent increase in cardiovascular risk. In general, LDL-C may be estimated according to the following equations [reference 8]: LDL-C (mmol/L) = Total cholesterol - [(0.37 x triglycerides) + HDL-C] LDL-C (mg/dL) = Total cholesterol - [(0.16 x triglycerides) + HDL-C] When total triglycerides are greater than 4.52 mmol/L (400 mg/dL) this equation is not applicable. In such patients, LDL-C may be obtained by ultracentrifugation. Coronary Heart Disease LOVASTATIN® was also found to slow the progression of coronary atherosclerosis in patients with coronary heart disease as part of a treatment strategy to lower total and LDL-C to target levels. In two trials including this type of patient 4, 7, 51, i.e. in a secondary prevention intervention, LOVASTATIN® mono-therapy was shown to slow the progression of coronary atherosclerosis as evaluated by computerized quantitative coronary angiography (QCA). This effect, however, was not accompanied by an improvement in the clinical endpoints (death, fatal/nonfatal myocardial infarction, hospitalization for unstable angina, and coronary revascularization procedure [PTCA and CABG]) within the 2-21/2 years' trial period. These trials, however, were not designed to demonstrate a reduction in the risk of coronary morbidity and mortality. The effect of lovastatin on the progression of atherosclerosis in the coronary arteries has been corroborated by similar findings in carotid vasculature. In the Asymptomatic Carotid Artery Progression Study (ACAPS) which included hyperlipidemic patients with early asymptomatic carotid lesions and without known coronary artery disease, the effect of therapy with lovastatin on carotid atherosclerosis was assessed by B-mode ultrasonography. There was a significant regression of carotid lesions in patients receiving lovastatin alone compared to those receiving placebo alone. The predictive value of changes in the carotid vasculature for stroke has not yet been established. In the lovastatin group there was a significant reduction in the number of patients with major cardiovascular events relative to the placebo group (5 vs 14) and a significant reduction in all-cause mortality (1 vs 8) however, it was not powered to demonstrate a reduction in the risk of coronary morbidity and mortality. This trial should be viewed as supportive and complementary to the others mentioned above.