title: Comparison of rosuvastatin versus atorvastatin in patients with heterozygous familial hypercholesterolemia.
abstract: Heterozygous familial hypercholesterolemia (HFH) is a common genetic disorder that confers a significantly increased risk of early coronary artery disease. This study compared atorvastatin and rosuvastatin in reducing low-density lipoprotein (LDL) cholesterol in HFH in a global, 18-week, weighted-randomization, double-blind, parallel-group, forced-titration study. Following a 6-week diet lead-in, 623 patients were randomized to 20 mg/day of atorvastatin (n = 187) or rosuvastatin (n = 436) with forced titration at 6-week intervals to 80 mg/day. The primary end point was percentage change in LDL cholesterol from baseline to week 18. At week 18, rosuvastatin therapy produced a significantly greater reduction in LDL cholesterol than atorvastatin (-57.9% vs -50.4%; p <0.001) and a significantly greater increase in high-density lipoprotein (HDL) cholesterol (12.4% vs 2.9%; p <0.001). Rosuvastatin also produced significantly greater reductions in apolipoprotein-B and all 4 major lipid ratios, as well as a significantly greater increases in apolipoprotein A-I (all p <0.001). More patients with HFH with coronary artery disease achieved the National Cholesterol Education Program Adult Treatment Panel III goal of LDL cholesterol <100 mg/dl (<2.6 mmol/L) on rosuvastatin 40 and 80 mg than atorvastatin 80 mg (17%, 24%, and 4.5%, respectively). High-sensitivity C-reactive protein median values were reduced by 33% to 34% in both the 80-mg rosuvastatin- and atorvastatin-treated groups. Both treatments were well tolerated. Thus, in HFH, rosuvastatin force titrated from 20 to 80 mg/day produced significantly greater reductions than atorvastatin 20 to 80 mg/day in LDL cholesterol and improvements in HDL cholesterol and other lipid parameters, and enabled more patients to achieve LDL cholesterol goals.
authors.affiliation: Metabolic and Atherosclerosis Research Center, Cincinnati, Ohio, USA. ESteinMRL@aol.com
authors.forename: Evan A
authors.initials: EA
authors.lastname: Stein
authors.forename: Kristina
authors.initials: K
authors.lastname: Strutt
authors.forename: Harry
authors.initials: H
authors.lastname: Southworth
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Diggle
authors.forename: Elinor
authors.initials: E
authors.lastname: Miller
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D000069059:Atorvastatin; D008078:Cholesterol, LDL / Q000187:drug effects*; D004311:Double-Blind Method; D005260:Female; D005464:Fluorobenzenes / Q000627:therapeutic use*; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006579:Heterozygote; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006938:Hyperlipoproteinemia Type II / Q000188:drug therapy*; D016018:Least-Squares Analysis; D008297:Male; D008875:Middle Aged; D011743:Pyrimidines / Q000627:therapeutic use*; D011758:Pyrroles / Q000627:therapeutic use*; D000068718:Rosuvastatin Calcium; D018709:Statistics, Nonparametric; D013449:Sulfonamides / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D008078:Cholesterol, LDL; D005464:Fluorobenzenes; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011743:Pyrimidines; D011758:Pyrroles; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium; D000069059:Atorvastatin