Background Rosuvastatin (Crestor), a new, highly efficacious statin,
has demonstrated dose-dependent low-density lipoprotein cholesterol (LDL-C)
reductions of up to 65% in a dose-ranging programme with doses of 1
to 80 mg.
Design A randomized, double-blind multicentre trial compared
rosuvastatin with commonly used starting doses of pravastatin and simvastatin to
determine relative efficacy in LDL-C reduction and impact on other lipid
parameters in primary hypercholesterolaemia.
Methods and results A total of 502 patients (≥ 18 years;
LDL-C ≥ 4.14 mmol/l [160mg/dl] and <6.50mmol/l [250mg/dl]
and triglycerides <4.52 mmol/l [400mg/dl]) were randomized to 12
weeks of rosuvastatin 5 mg (n=120) or 10mg
(n=115), pravastatin 20 mg
(n=137) or simvastatin 20 mg
(n=130). Rosuvastatin 5 and 10mg reduced LDL-C by 42
and 49%, respectively, compared with 28% for pravastatin
(P< 0.001 versus both rosuvastatin doses) and
37% for simvastatin (P<0.01 versus
rosuvastatin 5mg; P < 0.001 versus 10mg). National
Cholesterol Education Program Adult Treatment Panel II (NCEP ATP II) goals were
achieved by 87% of rosuvastatin 10mg patients, 71% of
rosuvastatin 5 mg patients, 53% of pravastatin patients, and
64% of simvastatin patients; similar proportions of patients achieved
NCEP ATP III goals. European Atherosclerosis Society (EAS) goals were achieved
by 83, 63, 20 and 50% of patients, respectively. All study treatments
were well tolerated.
Conclusions Both doses of rosuvastatin were more effective than
pravastatin and simvastatin in meeting NCEP ATP II and EAS LDL-C targets.
Rosuvastatin 10mg was more effective than pravastatin and simvastatin in meeting
NCEP ATP III targets.
METHODS AND RESULTS: A total of 305 subjects with primary hypercholesterolemia were randomized in a 3:1 ratio to receive either atorvastatin 10 mg daily or pravastatin 20 mg daily according to a 16-week double-blind comparative study of the effect on apolipoprotein and lipoprotein particle levels. All patients had low-density lipoprotein (LDL)-cholesterol levels between 4.2 and 6.6 mM and triglyceride concentrations below 4.5 mM at baseline. After 16 weeks of treatment, apoB (-27% and -16%; P <.001), apoE (-13.3% and -5.6%; P <.05) and the triglyceride-rich LpC-III:B particle (-33% and -26%; P <.05) levels were reduced to a significantly greater extent in the atorvastatin than in the pravastatin treatment group. Both atorvastatin and pravastatin increased apoA-I levels, an effect that was more pronounced in the pravastatin group (+7% and +11%; P <.002). The increased apoA-I levels predominated on LpA-I in the atorvastatin group (+11%) and on LpA-I:A-II in the pravastatin group (+13%). ApoA-II levels were decreased with atorvastatin to a greater extent than with pravastatin (-1% and +2.8%; P <.05). CONCLUSIONS: Although atorvastatin and pravastatin belong to the same therapeutic family, they produce different effects in apoliprotein concentrations in hypercholesterolemic patients. Atorvastatin, an agent of the new generation, appears to efficiently reduce apoB-containing lipoprotein particles containing apoC-III.
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