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TRIAL: STELLAR
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HDL-C increases by dose in patients with hyperlipidemia or mixed dyslipidemia5

HDL Graph

Adapted from the STELLAR trial. STELLAR was a 6-week, multicenter, open-label, randomized, 15-arm trial comparing the efficacy and safety of CRESTOR with atorvastatin, simvastatin, and pravastatin in 2240 patients with hyperlipidemia or mixed dyslipidemia. The primary end point was percentage change from baseline in LDL-C at week 6. The study performed the following dose comparisons: CRESTOR 10 mg vs atorvastatin 10 mg, 20 mg, and 40 mg, simvastatin 10 mg, 20 mg, and 40 mg, and pravastatin 10 mg, 20 mg, and 40 mg; CRESTOR 20 mg vs atorvastatin 20 mg, 40 mg, and 80 mg, simvastatin 20 mg, 40 mg and 80 mg, and pravastatin 20 mg and 40 mg; and CRESTOR 40 mg vs atorvastatin 40 mg and 80 mg, simvastatin 40 mg and 80 mg, and pravastatin 40 mg.5

*P<.002 CRESTOR 10 mg vs pravastatin 10 mg
†P<.002 CRESTOR 20 mg vs atorvastatin 20 mg, 40 mg, 80 mg; simvastatin 40 mg; pravastatin 20 mg, 40 mg
‡P<.002 CRESTOR 40 mg vs atorvastatin 40 mg, 80 mg; simvastatin 40 mg; pravastatin 40 mg

Mean baseline HDL-C: 49 mg/dL to 51 mg/dL

CRESTOR n=473
atorvastatin n=634
simvastatin n=648
pravastatin n=485

At 6 weeks, CRESTOR demonstrated HDL-C increases

  • +7.7% with CRESTOR 10 mg*
  • +9.5% with CRESTOR 20 mg†

TRIAL: STELLAR
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In STELLAR, a separate comparative trial, CRESTOR showed

LDL-C reductions at each dose in patients with hyperlipidemia or mixed dyslipidemia1,5,6

LDL Graph

Adapted from the STELLAR trial. STELLAR was a 6-week, multicenter, open-label, randomized, 15-arm trial comparing the efficacy and safety of CRESTOR with atorvastatin, simvastatin, and pravastatin in 2240 patients with hyperlipidemia or mixed dyslipidemia. The primary end point was percentage change from baseline in LDL-C at week 6. The study performed the following dose comparisons: CRESTOR 10 mg vs atorvastatin 10 mg, 20 mg, and 40 mg, simvastatin 10 mg, 20 mg, and 40 mg, and pravastatin 10 mg, 20 mg, and 40 mg; CRESTOR 20 mg vs atorvastatin 20 mg, 40 mg, and 80 mg, simvastatin 20 mg, 40 mg and 80 mg, and pravastatin 20 mg and 40 mg; and CRESTOR 40 mg vs atorvastatin 40 mg and 80 mg, simvastatin 40 mg and 80 mg, and pravastatin 40 mg.5

*P<.002 CRESTOR 10 mg vs atorvastatin 10 mg; simvastatin 10 mg, 20 mg, 40 mg; pravastatin 10 mg, 20 mg, 40 mg
†P<.002 CRESTOR 20 mg vs atorvastatin 20 mg, 40 mg; simvastatin 20 mg, 40 mg, 80 mg; pravastatin 20 mg, 40 mg
‡P<.002 CRESTOR 40 mg vs atorvastatin 40 mg; simvastatin 40 mg, 80 mg; pravastatin 40 mg

Mean baseline LDL-C: 187 mg/dL to 194 mg/dL

CRESTOR n=473
atorvastatin n=634
simvastatin n=648
pravastatin n=485

At 6 weeks, CRESTOR demonstrated LDL-C reductions

  • –46% with CRESTOR 10 mg
  • –52% with CRESTOR 20 mg

TRIAL: METEOR
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In the METEOR trial, in patients with hyperlipidemia,

Annualized rate of change in maximum CIMT1,7

Athero Graph

Adapted from the METEOR trial, a randomized, double-blind, placebo-controlled trial comparing the effect of CRESTOR 40 mg with placebo on the progression of atherosclerosis over 2 years in 984 low-risk patients (defined as Framingham risk score of <10% over 10 years) with hypercholesterolemia (mean LDL-C of 155 mg/dL) and subclinical atherosclerosis as detected by CIMT for 12 carotid artery sites and assessed via B-mode ultrasound. The primary end point was the annualized rate of change in maximum CIMT for 12 carotid artery sites.7

In the METEOR trial, carotid intima-media thickness (CIMT) increased in the placebo group but did not change in the CRESTOR group

  • The most common adverse reactions (%) in the METEOR trial for CRESTOR vs placebo, respectively, were myalgia (12.7 vs 12.1), arthralgia (10.1 vs 7.1), headache (6.4 vs 5.3), dizziness (4.0 vs 2.8), increased CPK (2.6 vs 0.7), abdominal pain (2.4 vs 1.8), and ALT >3x ULN (2.2 vs 0.7)
  • CRESTOR 40 mg should only be used for those patients not achieving their LDL-C goal with 20 mg. Patients initiating CRESTOR therapy or switching from another statin should begin treatment with CRESTOR at the appropriate starting dose
     

Adapted from the JUPITER trial. JUPITER was a long-term, randomized, double-blind, placebo-controlled study designed to assess the effects of CRESTOR 20 mg in the primary prevention of CVD events in men (≥50 years) and women (≥60 years) who had no clinically evident CVD, LDL-C levels <130 mg/dL, and hsCRP levels ≥2 mg/L.2 The primary end point was a composite end point consisting of the time-to-first occurrence of any of the following major cardiovascular (CV) events: CV death, nonfatal myocardial infarction, nonfatal stroke, hospitalization for unstable angina, or an arterial revascularization procedure.2

The study population has an estimated baseline CHD risk of 11.6% over 10 years based on the Framingham risk criteria and included a high percentage of patients with additional risk factors such as hypertension (58%), low HDL-C levels (23%), cigarette smoking (16%), or a family history of premature CHD (12%). Study participants had a median baseline LDL-C of 108 mg/dL and hsCRP of 4.3 mg/L.1

In a post-hoc subgroup analysis of JUPITER subjects (n=1405; rosuvastatin=725, placebo=680) with an hsCRP ≥2 mg/L and no other traditional risk factors (smoking, BP ≥140/90 mm Hg or taking antihypertensives, low HDL-C) other than age, after adjustment for high HDL-C, there was no significant treatment benefit with rosuvastatin treatment.1

 

Important Safety Information from the JUPITER Study

  • A higher percentage of rosuvastatin-treated patients vs placebo-treated patients (6.6% and 6.2%, respectively) discontinued study medication due to an adverse event, irrespective of treatment causality. Myalgia was the most common adverse reaction that led to treatment discontinuation1
  • In JUPITER, there was a significantly higher frequency of diabetes mellitus reported in patients taking rosuvastatin (2.8%) vs patients taking placebo (2.3%). Mean HbA1c was significantly increased by 0.1% in rosuvastatin-treated patients compared to placebo-treated patients1
  • The most common adverse reactions reported were myalgia (7.6% vs 6.6%), arthralgia (3.8% vs 3.2%), constipation (3.3% vs 3.0%), and nausea (2.4% vs 2.3%) for CRESTOR vs placebo, respectively1
 

JUPITER trial design

Adapted from the JUPITER trial. JUPITER was a long-term, randomized, double-blind, placebo-controlled study designed to assess the effects of CRESTOR 20 mg in the primary prevention of CVD events in men (≥50 years) and women (≥60 years) who had no clinically evident CVD, LDL-C levels <130 mg/dL, and hsCRP levels ≥2 mg/L.2 The primary end point was a composite end point consisting of the time-to-first occurrence of any of the following major cardiovascular (CV) events: CV death, nonfatal myocardial infarction, nonfatal stroke, hospitalization for unstable angina, or an arterial revascularization procedure.2

The study population has an estimated baseline CHD risk of 11.6% over 10 years based on the Framingham risk criteria and included a high percentage of patients with additional risk factors such as hypertension (58%), low HDL-C levels (23%), cigarette smoking (16%), or a family history of premature CHD (12%). Study participants had a median baseline LDL-C of 108 mg/dL and hsCRP of 4.3 mg/L.1

In a post-hoc subgroup analysis of JUPITER subjects (n=1405; rosuvastatin=725, placebo=680) with an hsCRP ≥2 mg/L and no other traditional risk factors (smoking, BP ≥140/90 mm Hg or taking antihypertensives, low HDL-C) other than age, after adjustment for high HDL-C, there was no significant treatment benefit with rosuvastatin treatment.1

Journal Resources

This Web site and reprint link are provided as a service by AstraZeneca.

This link will take you to the following:

Effect of Rosuvastatin on Progression of Carotid Intima-Media Thickness in Low-Risk Individuals With Subclinical Atherosclerosis: The METEOR Trial

John R. Crouse III; Joel S. Raichlen; Ward A. Riley; Gregory W. Evans; Mike K. Palmer; Daniel H. O'Leary; Diederick E. Grobbee; Michiel L. Bots; for the METEOR Study Group. JAMA. 2007;297:1344-1353. Published online March 25, 2007 (doi:10.1001/jama.297.12.1344).

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CRESTOR® (rosuvastatin calcium)



 

Slowing Atherosclerosis Progression

In this section, you can review results from the METEOR trial, demonstrating the effects of CRESTOR® (rosuvastatin calcium) treatment as an adjunct to diet on the progression of atherosclerosis. You can also download the publication.

METEOR Trial

  • The METEOR trial evaluated changes in carotid intima-media thickness (CIMT) in low-risk patients with hypercholesterolemia treated with either CRESTOR or placebo.1,2 Adapted from the METEOR Trial
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TRIAL: METEOR
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The METEOR trial evaluated changes in carotid intima-media thickness (CIMT) in low-risk patients with hypercholesterolemia treated with either CRESTOR or placebo.1,2

METEOR Trial: CIMT Increase with CRESTOR vs. placebo group 1 2

In the METEOR trial, compared to baseline, overall, no significant progression of atherosclerosis was observed with CRESTOR,* while significant disease progression was observed with placebo.†

*P=.32 with CRESTOR.
†P<.0001 with placebo.

In the METEOR trial, CRESTOR was well tolerated over the 2-year study period2 — further supporting its proven safety profile as demonstrated in other clinical studies.3

The most common adverse reactions (%) in the METEOR trial for CRESTOR vs placebo, respectively, were myalgia (12.7 vs 12.1), arthralgia (10.1 vs 7.1), headache (6.4 vs 5.3), dizziness (4.0 vs 2.8), increased CPK (2.6 vs 0.7), abdominal pain (2.4 vs 1.8), ALT>3x ULN (2.2 vs 0.7).1

Enlarge Chart 1 2
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Adapted from the METEOR trial, a randomized, double-blind, placebo-controlled trial comparing the effect of CRESTOR 40 mg with placebo on the progression of atherosclerosis over 2 years in 984 low-risk patients (defined as Framingham risk score of <10% over 10 years) with hypercholesterolemia (mean LDL-C of 155 mg/dL) and subclinical atherosclerosis as detected by CIMT for 12 carotid artery sites and assessed via B-mode ultrasound. The primary end point was the annualized rate of change in maximum CIMT for 12 carotid artery sites.2