Fluvastatin - A review of its use in lipid disorders

Fluvastatin is an HMG-CoA reductase inhibitor used to treat patients with h ypercholesterolaemia, Since fluvastatin was last reviewed in Drugs, trials have shown its efficacy in the secondary prevention of coronary heart disea se (CHD) events and death and have expanded knowledge of its effects in pri mary CHD prevention and its mechanisms of activity. In addition to reducing total (TC) and low density lipoprotein (LDL-C) chol esterol, fluvastatin has antiatherogenic, antithrombotic and antioxidant ef fects, can improve vascular function, and may have immunomodulatory effects , Although fluvastatin interacts with bile acid sequestrants (requiring sep aration of doses), its pharmacokinetics permit oral administration to most patient groups. Fluvastatin is well tolerated, with adverse effects usually mild and transient. Use of fluvastatin to reduce lipids in patients with primary hypercholester olaemia is well established, Its effects are similar in most patient groups . with 20 to 80 mg/day reducing LDL-C by 22 to 36%, triglycerides (TG) bq 1 2 to 18% and apolipoprotein B by 19 to 28% and increasing high density lipo protein cholesterol by 3.3 to 5.6%. Attempts to find fluvastatin dosages wi th efficacy equivalent to that of other HMG-CoA reductase inhibitors produc e variable results, but larger per-milligram fluvastatin dosages are needed when patients switch from other HMG-CoA reductase inhibitors. Combinations of fluvastatin with fibric acid derivatives and bile acid sequestrants pro duce additive effects, Small noncomparative studies suggest fluvastatin red uces LDL-C in patients with hypercholesterolaemia secondary to kidney disor ders by less than or equal to 40.5% and with type 2 diabetes mellitus by le ss than or equal to 32%. Three large randomised, double-blind trials show fluvastatin can help preve nt CHD events or death and slow disease progression in patients with CHD wi th or without hypercholesterolaemia, In the Fluvastatin Angiographic Resten osis trial in patients undergoing balloon angioplasty. fluvastatin SO mg/da y for 40 weeks reduced the postangioplasty rate of deaths plus myocardial i nfarctions (1.5% vs 4% with placebo. p < 0.025) without altering vessel lum inal diameters, In the Lipoprotein and Coronary Atherosclerosis Study in pa tients with coronary artery stenosis, luminal diameter reduced to a signifi cantly lesser extent after fluvastatin 20mg twice daily than placebo after 2.5 years (-0.028 vs -0.01 mm, p < 0.005). The Lescol in Symptomatic Angina study found reductions in all cardiac events or cardiac death in patients after 1 year of fluvastatin 40 mg/day (1.6% vs 5.6% for placebo, p < 0.05). Conclusions: An evolving pattern of data suggests that, in addition to its well established efficacy and cost effectiveness in reducing hypercholester olaemia, fluvastatin may now also be considered for use in the secondary pr evention of CHD.