Fluvastatin is an
HMG-CoA reductase inhibitor used to treat patients with hypercholesterolaemia. Since
fluvastatin was last reviewed in Drugs, trials have shown its efficacy in the
secondary prevention of
coronary heart disease (CHD) events and death and have expanded knowledge of its effects in primary CHD prevention and its mechanisms of activity. In addition to reducing total (TC) and
low density lipoprotein (
LDL-C)
cholesterol,
fluvastatin has antiatherogenic, antithrombotic and
antioxidant effects, can improve vascular function, and may have immunomodulatory effects. Although
fluvastatin interacts with
bile acid sequestrants (requiring separation 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 hypercholesterolaemia 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) by 12 to 18% and
apolipoprotein B by 19 to 28% and increasing
high density lipoprotein cholesterol by 3.3 to 5.6%. Attempts to find
fluvastatin dosages with efficacy equivalent to that of other
HMG-CoA reductase inhibitors produce 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 produce additive effects. Small noncomparative studies suggest
fluvastatin reduces
LDL-C in patients with hypercholesterolaemia secondary to kidney disorders by < or = 40.5% and with
type 2 diabetes mellitus by < or = 32%. Three large randomised, double-blind trials show
fluvastatin can help prevent CHD events or death and slow
disease progression in patients with CHD with or without hypercholesterolaemia. In the
Fluvastatin Angiographic Restenosis trial in patients undergoing balloon angioplasty,
fluvastatin 80 mg/day for 40 weeks reduced the postangioplasty rate of deaths plus
myocardial infarctions (1.5% vs 4% with placebo, p < 0.025) without altering vessel
luminal diameters. In the
Lipoprotein and
Coronary Atherosclerosis Study in patients with
coronary artery stenosis,
luminal diameter reduced to a significantly lesser extent after
fluvastatin 20 mg 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: