EFFICACY AND SAFETY OF A NEW HMG-COA REDUCTASE INHIBITOR, ATORVASTATIN, IN PATIENTS WITH HYPERTRIGLYCERIDEMIA

Objective.-To assess the lipid-lowering effect of atorvastatin (a new 3-hydroxy-3-methylglutaryl coenzyme A [HMG-CoA] reductase inhibitor) o n levels of serum triglycerides and other lipoprotein fractions in pat ients with primary hypertriglyceridemia, determine if atorvastatin cau ses a redistribution of triglycerides in various lipoprotein fractions , and assess its safety by reporting adverse events and clinical labor atory measurements. Design.-Randomized double-blind, placebo-controlle d, parallel-group, multicenter trial. Setting.-Community- and universi ty-based research centers. Patients.-A total of 56 patients (aged 26 t o 74 years) with a mean baseline triglyceride level of 6.80 mmol/L (60 3.3 mg/dL) and a mean baseline low-density lipoprotein cholesterol (LD L-C) level of 3.07 mmol/L (118.7 mg/dL). Interventions.-Cholesterol-lo wering diet (National Institutes of Health National Cholesterol Educat ion Program Step I Diet) and either 5 mg, 20 mg, or 80 mg of atorvasta tin, or placebo. Main Outcome Measures.-Percent change from baseline i n total triglycerides for three dose levels of atorvastatin compared w ith placebo. Results.-Mean reductions in total triglycerides between 5 mg, 20 mg, and 80 mg of atorvastatin and placebo after 4 weeks of tre atment were -26.5%, -32.4%, -45.8%, and -8.9%, respectively. Mean redu ctions in LDL-C were -16.7%, -33.2%, -41.4%, and -1.4%, respectively, and very low-density lipoprotein cholesterol (VLDL-C) were -34.3%, -45 .9%, -57.7%, and -5.5%, respectively. Similar mean changes in total ap olipoprotein B (apo B) (-16.9%, -32.8%, -41.7%, and +1.0%), apo B in L DL (-14.8%, -29.8%, -42.0%, and -3.1%), and apo B in VLDL (-23.8%, -35 .8%, -34.4%, and +11.7%) were observed. In addition, comparable mean c hanges in LDL triglycerides (-22.5%, -30.7%, -39.9%, and +3.9%) and VL DL triglycerides (-28.1%, -34.0%, -47.3%, and -10.8%) were seen. Concl usions.-In atorvastatin treatment groups, total serum triglyceride lev els decreased in a dose-dependent manner; reductions in the 20-mg and 80-mg groups were statistically significant (P<.05) compared with plac ebo. Atorvastatin did not cause a redistribution of triglycerides but consistently lowered triglycerides in all lipoprotein fractions. Atorv astatin was well tolerated.