LDL-C Reductions: Switching Therapy
In this section, you can review LDL cholesterol reduction results and LDL cholesterol goal attainment results from comparative clinical trials in which CRESTOR® (rosuvastatin) was used as an adjunct to diet in patients who switched statin therapy.
See how CRESTOR performed in lowering LDL cholesterol compared to other statins.
For detailed comparative clinical trial data, select the appropriate tab below.
Click on the "+" and "—" signs to expand and collapse the clinical information.
LDL-C Goal Attainment
In Arm 1 of the trial, 83% of patients who were on a 20 mg dose of CRESTOR for weeks 1-16 reached the LDL-C goal of <100 mg/dL.
In Arm 2 of the trial: 66%[†] of patients who were on a 10 mg dose of atorvastatin for weeks 1-8 and on a 10 mg dose of CRESTOR for weeks 9-16 reached the LDL-C goal of <100 mg/dL. († ^ P value is less than .001 for atorvastatin 10 mg switched to CRESTOR 10 mg vs atorvastatin 10 mg; atorvastatin 20 mg switched to CRESTOR 20 mg vs atorvastatin 20 mg.) 42% of patients who were on a 10 mg dose of atorvastatin for weeks 1-16 reached the LDL-C goal of <100 mg/dL.
In Arm 3 of the trial: 79%[†] of patients who were on a 20 mg dose of atorvastatin for weeks 1-8 and on a 20 mg dose of CRESTOR for weeks 9-16 reached the LDL-C goal of <100 mg/dL. († ^ P value is less than .001 for atorvastatin 10 mg switched to CRESTOR 10 mg vs atorvastatin 10 mg; atorvastatin 20 mg switched to CRESTOR 20 mg vs atorvastatin 20 mg.) 64% of patients who were on a 20 mg dose of atorvastatin for weeks 1-16 reached the LDL-C goal of <100 mg/dL.
* ^ CHD, established atherosclerotic disease, diabetes, or 10-year CHD risk score >20%.
The mean baseline LDL-C in patients were: 167 mg/dL to 169 mg/dL.
The number of patients in the treatment group of Arm 1 (Weeks 1-16) was:
CRESTOR 20 mg 362 patients
The number of patients in the treatment groups of Arm 2 (Week 16) were:
- CRESTOR 10 mg 189 patients
- atorvastatin 10 mg 180 patients
The number of patients in the treatment groups of Arm 3 (Week 16) were:
- CRESTOR 20 mg 184 patients
- atorvastatin 20 mg 182 patients
TRIAL DESCRIPTION:
Adapted from the MERCURY II trial.[2b] MERCURY II was a 16-week, randomized, open-label, 2-period, parallel-group, multicenter study. Following a 6-week dietary lead-in period, hypercholesterolemic were randomized to 1 of 5 arms: CRESTOR 20 mg, atorvastatin 10 mg, atorvastatin 20 mg, simvastatin 20 mg, or simvastatin 40 mg once daily (period 1: 8 weeks). Patients then remained on these treatments or were switched as follows: half from atorvastatin 10 mg and simvastatin 20 mg to CRESTOR 10 mg once daily; half from atorvastatin 20 mg and simvastatin 40 mg to CRESTOR 20 mg once daily (period 2: 8 weeks). Patients had either been treated with CRESTOR, atorvastatin, or simvastatin for 16 weeks or with CRESTOR for 8 weeks following 8 weeks of comparator treatment. The primary end point was percentage of patients achieving NCEP ATP III LDL-C goal <100 mg/dL at week 16. Changes in LDL-C at weeks 8 and 16 were secondary end points.
REFERENCE
In Arm 1 of the trial, 83% of patients who were on a 20 mg dose of CRESTOR for weeks 1-16 reached the LDL-C goal of <100 mg/dL.
In Arm 4 of the trial: 73%[†] of patients who were on a 20 mg dose of simvastatin for weeks 1-8 and on a 10 mg dose of CRESTOR for weeks 9-16 reached the LDL-C goal of <100 mg/dL. († ^ P value is less than .001 simvastatin 20 mg switched to CRESTOR 10 mg vs simvastatin 20 mg; simvastatin 40 mg switched to CRESTOR 20 mg vs simvastatin 40 mg.) 32% of patients who were on a 20 mg dose of simvastatin for weeks 1-16 reached the LDL-C goal of <100 mg/dL.
In Arm 5 of the trial: 84%[†] of patients who were on a 40 mg dose of simvastatin for weeks 1-8 and on a 20 mg dose of CRESTOR for weeks 9-16 reached the LDL-C goal of <100 mg/dL. († ^ P value is less than .001 simvastatin 20 mg switched to CRESTOR 10 mg vs simvastatin 20 mg; simvastatin 40 mg switched to CRESTOR 20 mg vs simvastatin 40 mg.) 56% of patients who were on a 40 mg dose of simvastatin for weeks 1-16 reached the LDL-C goal of <100 mg/dL.
* ^ CHD, established atherosclerotic disease, diabetes, or 10-year CHD risk score >20%.
The mean baseline LDL-C in patients were : 167 mg/dL to 169 mg/dL.
The number of patients in the treatment group of Arm 1 (Weeks 1-16) was:
CRESTOR 20 mg 362 patients
The number of patients in the treatment groups of Arm 4 (Week 16) were:
- CRESTOR 10 mg 179 patients
- simvastatin 20 mg 185 patients
The number of patients in the treatment groups of Arm 5 (Week 16) were:
- CRESTOR 20 mg 183 patients
- simvastatin 40 mg 183 patients
TRIAL DESCRIPTION:
Adapted from the MERCURY II trial.[2b] MERCURY II was a 16-week, randomized, open-label, 2-period, parallel-group, multicenter study. Following a 6-week dietary lead-in period, hypercholesterolemic patients with CHD, established atherosclerotic disease, diabetes, or 10-year CHD risk score >20% were randomized to 1 of 5 arms: CRESTOR 20 mg, atorvastatin 10 mg, atorvastatin 20 mg, simvastatin 20 mg, or simvastatin 40 mg once daily (period 1: 8 weeks). Patients then remained on these treatments or were switched as follows: half from atorvastatin 10 mg and simvastatin 20 mg to CRESTOR 10 mg once daily; half from atorvastatin 20 mg and simvastatin 40 mg to CRESTOR 20 mg once daily (period 2: 8 weeks). Patients had either been treated with CRESTOR, atorvastatin, or simvastatin for 16 weeks or with CRESTOR for 8 weeks following 8 weeks of comparator treatment. The primary end point was percentage of patients achieving NCEP ATP III LDL-C goal <100 mg/dL at week 16. Changes in LDL-C at weeks 8 and 16 were secondary end points.
REFERENCE:
LDL Reductions & Additional Results
LDL-C reductions in patients with CHD, established atherosclerotic disease, diabetes, or 10-year CHD risk score >20% switching to CRESTOR vs remaining on atorvastatin[2a]. Adapted from the MERCURY II Trial.
In Arm 1 of the trial patients who were on a 20 mg dose of CRESTOR for weeks 1-16 achieved a mean percentage change of -52% from baseline LDL-C at 16 weeks.
In Arm 2 of the trial: Patients who were on a 10 mg dose of atorvastatin for weeks 1-8 and on a 10 mg dose of CRESTOR for weeks 9-16 achieved a mean percentage change of -47%[*] from baseline LDL-C at 16 weeks. (* ^ P value is less than .001 for atorvastatin 10 mg switched to CRESTOR 10 mg vs atorvastatin 10 mg; atorvastatin 20 mg switched to CRESTOR 20 mg vs atorvastatin 20 mg.) Patients who were on a 10 mg dose of atorvastatin for weeks 1-16 achieved a mean percentage change of -36% from baseline LDL-C at 16 weeks.
In Arm 3 of the trial: Patients who were on a 20 mg dose of atorvastatin for weeks 1-8 and on a 20 mg dose of CRESTOR for weeks 9-16 achieved a mean percentage change of -51%[*] from baseline LDL-C at 16 weeks. (* ^ P value is less than .001 for atorvastatin 10 mg switched to CRESTOR 10 mg vs atorvastatin 10 mg; atorvastatin 20 mg switched to CRESTOR 20 mg vs atorvastatin 20 mg.) Patients who were on a 20 mg dose of atorvastatin for weeks 1-16 achieved a mean percentage change of -43% from baseline LDL-C at 16 weeks.
The mean baseline LDL-C in patients were : 167 mg/dL to 169 mg/dL.
The number of patients in the treatment group of Arm 1 (Weeks 1-16) was:
CRESTOR 20 mg 362 patients
The number of patients in the treatment groups of Arm 2 (Week 16) were:
- CRESTOR 10 mg 189 patients
- atorvastatin 10 mg 180 patients
The number of patients in the treatment groups of Arm 3 (Week 16) were:
- CRESTOR 20 mg 184 patients
- atorvastatin 20 mg 182 patients
TRIAL DESCRIPTION:
Adapted from the MERCURY II trial.[2b] MERCURY II was a 16-week, randomized, open-label, 2-period, parallel-group, multicenter study. Following a 6-week dietary lead-in period, hypercholesterolemic were randomized to 1 of 5 arms: CRESTOR 20 mg, atorvastatin 10 mg, atorvastatin 20 mg, simvastatin 20 mg, or simvastatin 40 mg once daily (period 1: 8 weeks). Patients then remained on these treatments or were switched as follows: half from atorvastatin 10 mg and simvastatin 20 mg to CRESTOR 10 mg once daily; half from atorvastatin 20 mg and simvastatin 40 mg to CRESTOR 20 mg once daily (period 2: 8 weeks). Patients had either been treated with CRESTOR, atorvastatin, or simvastatin for 16 weeks or with CRESTOR for 8 weeks following 8 weeks of comparator treatment. The primary end point was percentage of patients achieving NCEP ATP III LDL-C goal <100 mg/dL at week 16. Changes in LDL-C at weeks 8 and 16 were secondary end points.
REFERENCE:
LDL-C reductions in patients with CHD, established atherosclerotic disease, diabetes, or 10-year CHD risk score >20%, switching to CRESTOR vs remaining on simvastatin[2a]. Adapted from the MERCURY II Trial.
In Arm 1 of the trial, patients who were on a 20 mg dose of CRESTOR for weeks 1-16 achieved a mean percentage change of -52% from baseline LDL-C at 16 weeks.
In Arm 4 of the trial: Patients who were on a 20 mg dose of simvastatin for weeks 1-8 and on a 10 mg dose of CRESTOR for weeks 9-16 achieved a mean percentage change of -46%[*] from baseline LDL-C at 16 weeks. (* ^ P value is less than .001 for simvastatin 20 mg switched to CRESTOR 10 mg vs simvastatin 20 mg; simvastatin 40 mg switched to CRESTOR 20 mg vs simvastatin 40 mg.) Patients who were on a 20 mg dose of simvastatin for weeks 1-16 achieved a mean percentage change of -32% from baseline LDL-C at 16 weeks.
In Arm 5 of the trial: Patients who were on a 40 mg dose of simvastatin for weeks 1-8 and on a 20 mg dose of CRESTOR for weeks 9-16 achieved a mean percentage change of -54%[*] from baseline LDL-C at 16 weeks. (* ^ P value is less than .001 for simvastatin 20 mg switched to CRESTOR 10 mg vs simvastatin 20 mg; simvastatin 40 mg switched to CRESTOR 20 mg vs simvastatin 40 mg.) Patients who were on a 40 mg dose of simvastatin for weeks 1-16 achieved a mean percentage change of -40% from baseline LDL-C at 16 weeks.
The mean baseline LDL-C in patients were : 167 mg/dL to 169 mg/dL.
The number of patients in the treatment group of Arm 1 (Weeks 1-16) was:
CRESTOR 20 mg 362 patients
The number of patients in the treatment groups of Arm 4 (Week 16) were:
- CRESTOR 10 mg 179 patients
- simvastatin 20 mg 185 patients
The number of patients in the treatment groups of Arm 5 (Week 16) were:
- CRESTOR 20 mg 183 patients
- simvastatin 40 mg 183 patients
TRIAL DESCRIPTION:
Adapted from the MERCURY II trial.[2b] MERCURY II was a 16-week, randomized, open-label, 2-period, parallel-group, multicenter study. Following a 6-week dietary lead-in period, hypercholesterolemic were randomized to 1 of 5 arms: CRESTOR 20 mg, atorvastatin 10 mg, atorvastatin 20 mg, simvastatin 20 mg, or simvastatin 40 mg once daily (period 1: 8 weeks).Patients then remained on these treatments or were switched as follows: half from atorvastatin 10 mg and simvastatin 20 mg to CRESTOR 10 mg once daily; half from atorvastatin 20 mg and simvastatin 40 mg to CRESTOR 20 mg once daily (period 2: 8 weeks). Patients had either been treated with CRESTOR, atorvastatin, or simvastatin for 16 weeks or with CRESTOR for 8 weeks following 8 weeks of comparator treatment. The primary end point was percentage of patients achieving NCEP ATP III LDL-C goal <100 mg/dL at week 16. Changes in LDL-C at weeks 8 and 16 were secondary end points.
REFERENCE:
Raising HDL-C
Here you can review HDL cholesterol increase results from comparative clinical trials in which CRESTOR® (rosuvastatin) was used as an adjunct to diet in patients who started statin therapy and in patients who switched statin therapy.
See how CRESTOR compares to other statins in raising HDL-cholesterol.
Click on the "+" and "—" signs to expand and collapse the clinical information.
HDL-C increases vs atorvastatin in hypercholesterolemic patients with CHD, 10-year CHD risk score >20% (CHD risk equivalent), or clinical evidence of atherosclerosis[1a]
The following data details HDL-C increases vs atorvastatin in hypercholesterolemic patients with CHD, 10-year CHD risk score >20% (CHD risk equivalent), or clinical evidence of atherosclerosis[1b]
At week 6: Patients who were on a 10 mg dose of CRESTOR achieved a mean 7.7%[*] change in baseline HDL-C. (* ^ P value is less than .01 for CRESTOR 10 mg vs atorvastatin 10 mg.) Patients who were on a 10 mg dose of atorvastatin achieved a mean 5.3% change in baseline HDL-C.
At week 12: Patients who were on a 20 mg dose of CRESTOR achieved a mean 8.4%[†] change in baseline HDL-C. († ^ P value is less than .001 for CRESTOR 20 mg vs atorvastatin 20 mg; CRESTOR 40 mg vs atorvastatin 40 mg; CRESTOR 40 mg vs atorvastatin 80 mg.)
Patients who were on a 20 mg dose of atorvastatin achieved a mean 4.2% change in baseline HDL-C.
At week 18: Patients who were on a 40 mg dose of CRESTOR achieved a mean 7.8%[†] change in baseline HDL-C. († ^ P value is less than .001 for CRESTOR 20 mg vs atorvastatin 20 mg; CRESTOR 40 mg vs atorvastatin 40 mg; CRESTOR 40 mg vs atorvastatin 80 mg.) Patients who were on a 40 mg dose of atorvastatin achieved a mean 2.5% change in baseline HDL-C.
At week 24: Patients who were on a 40 mg dose of CRESTOR achieved a mean 8.4%[†] change in baseline HDL-C. († ^ P value is less than .001 for CRESTOR 20 mg vs atorvastatin 20 mg; CRESTOR 40 mg vs atorvastatin 40 mg; CRESTOR 40 mg vs atorvastatin 80 mg.) Patients who were on an 80 mg dose of atorvastatin achieved a mean 1.8% change in baseline HDL-C.
The mean baseline HDL-C were: 51 mg/dL to 52 mg/dL.
The number of patients in the treatment groups of Week 6 were:
- CRESTOR 10 mg 498 patients
- atorvastatin 10 mg 510 patients
The number of patients in the treatment groups of Week 12 were:
- CRESTOR 20 mg 492 patients
- atorvastatin 20 mg 494 patients
The number of patients in the treatment groups of Week 18 were:
- CRESTOR 40 mg 480 patients
- atorvastatin 40 mg 483 patients
The number of patients in the treatment groups of Week 24 were:
- CRESTOR 40 mg 464 patients
- atorvastatin 80 mg 476 patients
TRIAL DESCRIPTION:
Adapted from the ECLIPSE trial.[1c] ECLIPSE was a 24-week, open-label, randomized, multicenter, forced-titration, parallel-group trial comparing the efficacy and safety of CRESTOR and atorvastatin in 1036 patients with hypercholesterolemia and CHD, 10-year CHD risk score >20% (CHD risk equivalent), or clinical evidence of atherosclerosis. Following a 6-week dietary lead-in period, patients were randomized to receive CRESTOR 10 mg or atorvastatin 10 mg for 6 weeks. Doses were force-titrated at 6-week intervals until maximum doses were achieved. Statistical comparisons were not made across the dose range, only across the same time period. The primary end point was percentage of patients achieving NCEP ATP III LDL-C goal of <100 mg/dL at week 24. Percentage change from baseline in HDL-C was a secondary end point.
REFERENCE:
Changes in HDL-C in patients who switched to CRESTOR vs remaining on simvastatin or atorvastatin[2a]
In Arm 1 of the trial, patients who were on a 10 mg dose of CRESTOR for weeks 1-16 achieved a mean percentage change of 10.3% from baseline HDL-C at 16 weeks.
In Arm 2 of the trial: Patients who were on a 10 mg dose of atorvastatin for weeks 1-8 and on a 10 mg dose of CRESTOR for weeks 9-16 achieved a mean percentage change of 10.8%[*] from baseline HDL-C at 16 weeks. (* ^ P value is less than .05 for atorvastatin 10 mg switched to CRESTOR 10 mg vs atorvastatin 10 mg.) Patients who were on a 10 mg dose of atorvastatin for weeks 1-16 achieved a mean percentage change of 8.0% from baseline HDL-C at 16 weeks.
In Arm 3 of the trial: Patients who were on a 20 mg dose of atorvastatin for weeks 1-8 and on a 10 mg dose of CRESTOR for weeks 9-16 achieved a mean percentage change of 9.1%[†] from baseline HDL-C at 16 weeks. († ^ P value is less than .025 for atorvastatin 20 mg switched to CRESTOR 10 mg vs atorvastatin 20 mg.) Patients who were on a 20 mg dose of atorvastatin for weeks 1-8 and on a 10 mg dose of CRESTOR for weeks 9-16 achieved a mean percentage change of 8.2%[†] from baseline HDL-C at 16 weeks. Patients who were on a 20 mg dose of atorvastatin for weeks 1-16 achieved a mean percentage change of 5.7% from baseline HDL-C at 16 weeks. († ^ P value is less than .025 for atorvastatin 20 mg switched to CRESTOR 10 mg vs atorvastatin 20 mg.)
In Arm 4 of the trial: Patients who were on a 20 mg dose of simvastatin for weeks 1-8 and on a 10 mg dose of CRESTOR for weeks 9-16 achieved a mean percentage change of 10.0%* from baseline HDL-C at 16 weeks. Patients who were on a 20 mg dose of simvastatin for weeks 1-16 achieved a mean percentage change of 8.4% from baseline HDL-C at 16 weeks.
The number of patients in the treatment group of Arm 1 (Weeks 1-16) was:
CRESTOR 10 mg 521 patients
The number of patients in the treatment groups of Arm 2 (Week 16) were:
- CRESTOR 10 mg 276 patients
- atorvastatin 10 mg 240 patients
The number of patients in the treatment groups of Arm 3 (Week 16) were:
- CRESTOR 10 mg 293 patients
- CRESTOR 20 mg 305 patients
- atorvastatin 20 mg 299 patients
The number of patients in the treatment groups of Arm 4 (Week 16) were:
- CRESTOR 10 mg 277 patients
- simvastatin 20 mg 250 patients
TRIAL DESCRIPTION:
Adapted from the MERCURY I trial.[2b] MERCURY I was a 16-week, randomized, open-label, 2-period, multicenter, parallel-group study. Following a 6-week dietary lead-in period, hypercholesterolemic patients with CHD, established atherosclerotic disease, type 2 diabetes or a 10-year CHD risk score >20% (as defined by the Joint European Society, 1998) were randomized to 1 of 5 treatment arms: CRESTOR 10 mg, atorvastatin 10 mg, atorvastatin 20 mg, simvastatin 20 mg, or pravastatin 40 mg once daily (period 1: 8 weeks). Patients then remained on these treatments or were switched as follows: half from atorvastatin 10 mg, simvastatin 20 mg, and pravastatin 40 mg to CRESTOR 10 mg once daily; one third of each from atorvastatin 20 mg to CRESTOR 10 mg and 20 mg once daily (period 2: 8 weeks). Primary end point was percentage of patients reaching Joint European Societies’ LDL-C goal <116 mg/dL at week 16. Percentage change in HDL-C was a secondary end point.
REFERENCE:
At 6 weeks in the STELLAR Trial:
Patients who were on a 10 mg dose of CRESTOR achieved a mean 7.7%[*] change from baseline HDL-C. (* ^ P value is less than .002 for CRESTOR 10 mg vs pravastatin 10 mg. P value is non-significant in CRESTOR 10 mg vs atorvastatin 10 mg, 20 mg, 40 mg; simvastatin 10 mg, 20 mg, 40 mg; pravastatin 20 mg, 40 mg.)
Patients who were on a 20 mg dose of CRESTOR achieved a mean 9.5%[†] change from baseline HDL-C. († ^ P value is less than .002 for CRESTOR 20 mg vs atorvastatin 20 mg, 40 mg, 80 mg; simvastatin 40 mg; pravastatin 20 mg, 40 mg. P value is non-significant in CRESTOR 20 mg vs simvastatin 20 mg, 80 mg.)
Patients who were on a 40 mg dose of CRESTOR achieved a mean 9.6%[‡] change from baseline HDL-C. (‡ ^ P value is less than .002 for CRESTOR 40 mg vs atorvastatin 40 mg, 80 mg; simvastatin 40 mg; pravastatin 40 mg. P value is non-significant in CRESTOR 40 mg vs simvastatin 80 mg.)
Patients who were on a 10 mg dose of atorvastatin achieved a mean 5.7% change from baseline HDL-C.
Patients who were on a 20 mg dose of atorvastatin achieved a mean 4.8% change from baseline HDL-C.
Patients who were on a 40 mg dose of atorvastatin achieved a mean 4.4% change from baseline HDL-C.
Patients who were on an 80 mg dose of atorvastatin achieved a mean 2.1% change from baseline HDL-C.
Patients who were on a 10 mg dose of simvastatin achieved a mean 5.3% change from baseline HDL-C.
Patients who were on a 20 mg dose of simvastatin achieved a mean 6.0% change from baseline HDL-C.
Patients who were on a 40 mg dose of simvastatin achieved a mean 5.2% change from baseline HDL-C.
Patients who were on an 80 mg dose of simvastatin achieved a mean 6.8% change from baseline HDL-C.
Patients who were on a 10 mg dose of pravastatin achieved a mean 3.2% change from baseline HDL-C.
Patients who were on a 20 mg dose of pravastatin achieved a mean 4.4% change from baseline HDL-C.
Patients who were on a 40 mg dose of pravastatin achieved a mean 5.6% change from baseline HDL-C.
In the STELLAR trial, CRESTOR increased HDL-C at each dose.
At 6 weeks, CRESTOR demonstrated significant HDL-C increases.
+7.7% with CRESTOR 10 mg (P value is less than .002 vs pravastatin 10 mg).
+9.5% with CRESTOR 20 mg (P value is less than .002 vs atorvastatin 20 mg, 40 mg, 80 mg; simvastatin 40 mg; and pravastatin 20 mg, 40 mg).
The mean baseline HDL-C were : 50 mg/dL to 51 mg/dL.
The number of patients in the treatment groups were
- CRESTOR 473 patients
- atorvastatin 634 patients
- simvastatin 648 patients
- pravastatin 485 patients
TRIAL DESCRIPTION:
Adapted from the STELLAR trial.[3b], [4b] 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. Percentage change from baseline in HDL-C was a secondary end point. 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.
REFERENCES:
3. 3a 3b Jones PH, Davidson MH, Stein EA, et al; STELLAR Study Group. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR Trial). Am J Cardiol. 2003;92(2):152-160.
4. 4a 4b CRESTOR® (rosuvastatin) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2024.
HDL-C increases after switching to CRESTOR vs remaining on simvastatin in hypercholesterolemic patients with CHD, established atherosclerotic disease, diabetes, or a 10-year CHD risk >20%[5a]. Adapted from the MERCURY II Trial.
In Arm 1 of the trial, patients who were on a 20 mg dose of CRESTOR for weeks 1-16 achieved a mean percentage change of 7.2% from baseline HDL-C at 16 weeks.
In Arm 4 of the trial: Patients who were on a 20 mg dose of simvastatin for weeks 1-8 and on a 10 mg dose of CRESTOR for weeks 9-16 achieved a mean percentage change of 6.3% from baseline HDL-C at 16 weeks. Patients who were on a 20 mg dose of simvastatin for weeks 1-16 achieved a mean percentage change of 4.3% from baseline HDL-C at 16 weeks.
In Arm 5 of the trial: Patients who were on a 40 mg dose of simvastatin for weeks 1-8 and on a 20 mg dose of CRESTOR for weeks 9-16 achieved a mean percentage change of 7.6% from baseline HDL-C at 16 weeks. Patients who were on a 40 mg dose of simvastatin for weeks 1-16 achieved a mean percentage change of 6.9% from baseline HDL-C at 16 weeks. P value is non-significant in patients on simvastatin 20 mg switched to CRESTOR 10 mg vs simvastatin 20 mg, simvastatin 40 mg switched to CRESTOR 20 mg vs simvastatin 40 mg.
The mean baseline HDL-C was : 47 mg/dL.
The number of patients in the treatment group were Arm 1 (Weeks 1-16) was:
CRESTOR 20 mg 362 patients
The number of patients in the treatment groups Arm 4 (Week 16) were:
- CRESTOR 10 mg 179 patients
- simvastatin 20 mg 185 patients
The number of patients in the treatment groups Arm 5 (Week 16) were:
- CRESTOR 20 mg 183 patients
- simvastatin 40 mg 183 patients
TRIAL DESCRIPTION:
Adapted from the MERCURY II trial.[5b] MERCURY II was a 16-week, randomized, open-label, 2-period, parallel-group, multicenter study. Following a 6-week dietary lead-in period, hypercholesterolemic were randomized to 1 of 5 arms: CRESTOR 20 mg, atorvastatin 10 mg, atorvastatin 20 mg, simvastatin 20 mg, or simvastatin 40 mg once daily (period 1: 8 weeks). Patients then remained on these treatments or were switched as follows: half from atorvastatin 10 mg and simvastatin 20 mg to CRESTOR 10 mg once daily; half from atorvastatin 20 mg and simvastatin 40 mg to CRESTOR 20 mg once daily (period 2: 8 weeks). Patients had either been treated with CRESTOR, atorvastatin, or simvastatin for 16 weeks or with CRESTOR for 8 weeks following 8 weeks of comparator treatment. The primary end point was percentage of patients achieving NCEP ATP III LDL-C goal <100 mg/dL at week 16. Percentage change in HDL-C was a secondary end point.
REFERENCE:
Use in Patients with Diabetes
Hyperlipidemic patients with comorbid conditions are at increased risk and some patients may need aggressive treatment to reach LDL-C goals.[12]-[14]
In this section you can review results from clinical trials on LDL cholesterol in which CRESTOR® (rosuvastatin) was used as an adjunct to diet in patients with type 2 diabetes and dyslipidemia.
Click on the "+" and "—" signs to expand and collapse the clinical information.
In patients with type 2 diabetes, up to 94%[*] achieved LDL-C goal of <100 mg/dL with a starting dose of CRESTOR 10 mg. (* ^ In 2 titration trials of patients treated with a starting dose of CRESTOR 10 mg.)
In the ANDROMEDA trial of 240), 94% reached LDL-C goal of <96.5 mg/dL at 8 weeks. There was a mean LDL-C reduction of 51% from baseline of 131 mg/dL. The primary end point was the percentage change from baseline in LDL-C after 16 weeks[4b].
In the URANUS trial of 232), 65% reached LDL-C goal of <100 mg/dL at 4 weeks. There was a mean LDL-C reduction of 48% from baseline of 178 mg/dL. The primary end point was the percentage change from baseline in LDL-C after 16 weeks[5b].
TRIAL DESCRIPTION:
Adapted from the ANDROMEDA trial.[4c] ANDROMEDA was a randomized, double-blind, multicenter, parallel-group, forced-titration trial comparing the efficacy and safety of CRESTOR (10 mg and 20 mg) and atorvastatin (10 mg and 20 mg) in patients with type 2 diabetes mellitus and dyslipidemia. The primary end point was the percentage change from baseline in LDL-C after 16 weeks.
Adapted from the URANUS trial.[5c] URANUS was a 16-week, randomized, double-blind, forced-titration trial comparing CRESTOR and atorvastatin in 465 type 2 diabetics with dyslipidemia. Patients were randomized to CRESTOR 10 mg or atorvastatin 10 mg for 4 weeks and then titrated up if goal was not met. The primary end point, percentage change from baseline in LDL-C at 16 weeks, was significantly better in the rosuvastatin group (10 to 40 mg) when compared with the atorvastatin group (10 to 80 mg).
REFERENCES:
- 4. 4a 4b 4c Betteridge DJ, Gibson JM; ANDROMEDA Study Investigators. Effects of rosuvastatin on lipids, lipoproteins, and apolipoproteins in the dyslipidaemia of diabetes. Diabet Med. 2007;24(5):541-549.
- 5. 5a 5b 5c Berne C, Siewert-Delle A; URANUS Study Investigators. Comparison of rosuvastatin and atorvastatin for lipid lowering in patients with type 2 diabetes mellitus: results from the URANUS study. Cardiovasc Diabetol. 2005;4:7.
LDL-C reductions vs atorvastatin in patients with type 2 diabetes and dyslipidemia[4a]. Adapted from the ANDROMEDA Trial. URANUS study for LDL-C Reductions.
At 8 weeks: Patients who were on a 10 mg dose of CRESTOR achieved a mean -51%[*] change from baseline LDL-C. (* ^ P value is less than .001 for CRESTOR 10 mg vs atorvastatin 10 mg; CRESTOR 20 mg vs atorvastatin 20 mg.) Patients who were on a 10 mg dose of atorvastatin achieved a mean -39% change from baseline LDL-C.
At 16 weeks: Patients who were on a 20 mg dose of CRESTOR achieved a mean -57%[*] change from baseline LDL-C. (* ^ P value is less than .001 for CRESTOR 10 mg vs atorvastatin 10 mg; CRESTOR 20 mg vs atorvastatin 20 mg.) Patients who were on a 20 mg dose of atorvastatin achieved a mean -46% change from baseline LDL-C.
The mean baseline LDL-C in patients was: 131 mg/dL.
The number of patients in the treatment groups at Week 8 were:
- CRESTOR 10 mg 240 patients
- atorvastatin 10 mg 240 patients
The number of patients in the treatment groups Week 16 were:
- CRESTOR 20 mg 227 patients
- atorvastatin 20 mg 229 patients
TRIAL DESCRIPTION:
Adapted from the ANDROMEDA trial.[4b] ANDROMEDA was a randomized, double-blind, multicenter, parallel-group, forced-titration trial comparing the efficacy and safety of CRESTOR (10 mg and 20 mg) and atorvastatin (10 mg and 20 mg) in patients with type 2 diabetes mellitus and dyslipidemia. The primary end point was the percentage change from baseline in LDL-C after 16 weeks.
REFERENCE:
Use in Specific Populations
CRESTOR® (rosuvastatin) may be an effective cholesterol management option for a variety of hyperlipidemic patients.
In this section, you can review results from comparative clinical trials in which CRESTOR was used as an adjunct to diet in African-American and Hispanic-American patients.
Initiation of CRESTOR therapy with 5 mg once daily should be considered for Asian patients.
For detailed clinical trial data, select the appropriate tab below.
Click on the "+" and "—" signs to expand and collapse the clinical information.
Use in African-American Populations
LDL-C reductions vs atorvastatin in African-American adults with hypercholesterolemia[2a]. Adapted from the ARIES Trial.
At 6 weeks:
African-American adults who were on a 10 mg dose of CRESTOR achieved a mean -37%[*] change from baseline LDL-C.
African-American adults who were on a 10 mg dose of atorvastatin achieved a mean -32% change from baseline LDL-C. (* ^ P value is less than .01 for CRESTOR 10 mg vs atorvastatin 10 mg. P value is non-significant in CRESTOR 10 mg vs atorvastatin 20 mg.)
African-American adults who were on a 20 mg dose of CRESTOR achieved a mean -46%† change from baseline LDL-C. († ^ P value is less than .0001 for CRESTOR 20 mg vs atorvastatin 20 mg.)
African-American adults with hypercholesterolemia who were on a 20 mg dose of atorvastatin achieved a mean -39% change from baseline LDL-C.
The mean baseline LDL-C was: 189 mg/dL to 192 mg/dL.
The number of patients in the treatment groups were
- CRESTOR 10 mg 186 patients
- atorvastatin 10 mg 179 patients
- CRESTOR 20 mg 189 patients
- atorvastatin 20 mg 178 patients
TRIAL DESCRIPTION:
Adapted from the ARIES trial.[2b] ARIES was a 6-week, randomized, open-label, comparative, multicenter study. Following a 6-week dietary lead-in period, 774 self-described African-American adults with hypercholesterolemia were randomized to receive either CRESTOR 10 mg or 20 mg or atorvastatin 10 mg or 20 mg for 6 weeks. The primary end point was the percentage change from baseline in LDL-C at week 6.
REFERENCE:
HDL-C increases vs atorvastatin in African-American adults with hypercholesterolemia[2a]. Adapted from the ARIES Trial.
At 6 weeks:
African-American adults on a 10 mg dose of CRESTOR achieved a least squares mean change of -7.0%[*] from baseline in HDL-C. (* ^ P value is less than .01 for CRESTOR 10 mg vs atorvastatin 20 mg. P value is non-significant in CRESTOR 10 mg vs atorvastatin 10 mg. P value is non-significant in CRESTOR 20 mg vs atorvastatin 20 mg.)
African-American adults on a 10 mg dose of atorvastatin achieved a least squares mean change of -5.6% from baseline in HDL-C.
At 6 weeks, African-American adults on a 20 mg dose of CRESTOR achieved a least squares mean change of -6.5% from baseline in HDL-C.
At 6 weeks, African-American adults on a 20 mg dose of atorvastatin achieved a least squares mean change of -3.7% from baseline in HDL-C.
The mean baseline HDL-C was: 50 mg/dL to 53 mg/dL.
The number of patients in the treatment groups were
- CRESTOR 10 mg 186 patients
- atorvastatin 10 mg 179 patients
- CRESTOR 20 mg 189 patients
- atorvastatin 20 mg 178 patients
TRIAL DESCRIPTION:
Adapted from the ARIES trial.[2b] ARIES was a 6-week, randomized, open-label, comparative, multicenter study. Following a 6-week dietary lead-in period, 774 self-described African-American adults with hypercholesterolemia were randomized to receive either CRESTOR 10 mg or 20 mg or atorvastatin 10 mg or 20 mg for 6 weeks. The primary end point was the percentage change from baseline in LDL-C at week 6. Percentage change from baseline in HDL-C was a secondary end point.
REFERENCE:
Use in Hispanic-American Patients
LDL-C reductions vs atorvastatin in Hispanic-American adults with CHD, CHD risk equivalent, or a 10-year CHD risk score ≥10% and hypercholesterolemia[2a]. Adapted from the STARSHIP Trial.
At 6 weeks:
Hispanic-American adults who were on a 10 mg dose of CRESTOR achieved a mean -45%[*] change from baseline LDL-C. (* ^ P value is less than .0001 vs atorvastatin 10 mg, P value is non-significant in CRESTOR 10 mg vs atorvastatin 20 mg.)
Hispanic-American adults who were on a 10 mg dose of atorvastatin achieved a mean -36% change from baseline LDL-C.
Hispanic-American adults who were on a 20 mg dose of CRESTOR achieved a mean -50%[†] change from baseline LDL-C. († ^ P value is less than .0001 vs atorvastatin 20 mg.)
Hispanic-American adults who were on a 20 mg dose of atorvastatin achieved a mean -42% change from baseline LDL-C.
The mean baseline LDL-C in patients was: 159 mg/dL to 165 mg/dL.
The number of patients in the treatment groups were
- CRESTOR 10 mg 174 patients
- atorvastatin 10 mg 161 patients
- CRESTOR 20 mg 167 patients
- atorvastatin 20 mg 161 patients
TRIAL DESCRIPTION:
Adapted from the STARSHIP trial.[2b] STARSHIP was a 6-week, randomized, open-label, comparative, multicenter study. Following a 6-week dietary lead-in period, 696 Hispanic-American adults with CHD, CHD risk equivalent, or a 10-year CHD risk score ≥10% and hypercholesterolemia were randomized to 1 of 4 arms: CRESTOR 10 mg or 20 mg or atorvastatin 10 mg or 20 mg once daily for 6 weeks. The primary end point was the percentage change in LDL-C from baseline at 6 weeks.
REFERENCE:
At 6 weeks
74%[†] of Hispanic-American adults who were on a 10 mg dose of CRESTOR achieved NCEP ATP III LDL-C Goal Attainment <100 mg/dL. († ^ P value is equal to=.001 vs atorvastatin 10 mg; P value is non-significant in CRESTOR 10 mg vs atorvastatin 20 mg.)
52% of Hispanic-American adults who were on a 10 mg dose of atorvastatin achieved NCEP ATP III LDL-C Goal Attainment <100 mg/dL.
91%[‡] of Hispanic-American adults who were on a 20 mg dose of CRESTOR achieved NCEP ATP III LDL-C Goal Attainment <100 mg/dL. (‡ ^ P value is less than .0001 vs atorvastatin 20 mg.)
62% of Hispanic-American adults who were on a 20 mg dose of atorvastatin achieved NCEP ATP III LDL-C Goal Attainment <100 mg/dL.
The mean baseline LDL-C in patients was: 156 mg/dL to 166 mg/dL.
The number of patients in the treatment groups were
- CRESTOR 10 mg 116 patients
- atorvastatin 10 mg 106 patients
- CRESTOR 20 mg 106 patients
- atorvastatin 20 mg n=106 patients
The statistical comparison of rosuvastatin versus atorvastatin in goal attainment was a post-hoc analysis from the STARSHIP trial.
TRIAL DESCRIPTION:
Adapted from the STARSHIP trial.[2b] STARSHIP was a 6-week, randomized, open-label, comparative, multicenter study. Following a 6-week dietary lead-in period, 696 Hispanic-American adults with CHD, CHD risk equivalent, or a 10-year CHD risk score ≥10% and hypercholesterolemia were randomized to 1 of 4 arms: CRESTOR 10 mg or 20 mg or atorvastatin 10 mg or 20 mg once daily for 6 weeks. The primary end point was the change in LDL-C at 6 weeks. The percentage of patients achieving NCEP ATP III LDL-C goal of <100 mg/dL was a secondary end point.
REFERENCES:
Primary Prevention of CVD Indications
Based on the impressive results of the JUPITER trial, CRESTOR® (rosuvastatin) has a primary prevention of cardiovascular disease (CVD) indication.
CRESTOR is indicated in patients without clinically evident coronary heart disease (CHD), to reduce the risk of myocardial infarction, stroke, and arterial revascularization in men≥50 years and women ≥60 years with hsCRP ≥2 mg/L and at least one additional cardiovascular disease risk factor.[5a], [11a]
In the JUPITER trial, CRESTOR 20 mg vs placebo demonstrated[5b], [11b]
- 54% relative risk reduction in myocardial infarction (P value is less than .001)
0.4% absolute risk reduction - 48% relative risk reduction in stroke (P value is equal to .002)
0.3% absolute risk reduction - 46% relative risk reduction in arterial revascularization (P value is less than .001)
0.7% absolute risk reduction
Click on the "+" and "—" signs to expand and collapse the clinical information.
In the trial, patients who were on a 20 mg dose of CRESTOR had a 54% percent relative risk reduction [With a hazard ratio of .46 and 95 percent confidence interval of .30 to .70 and a P value of less than .001] and a 0.4% absolute risk reduction[*] over patients who were on a placebo. (* ^ Absolute risk reduction %=(events in placebo arm/total number of subjects in placebo arm - events in CRESTOR arm/total number of subjects in CRESTOR arm) x 100.)
HR equals =hazard ratio.
CI equals =confidence interval.
In the trial, patients who were on a 20 mg dose of CRESTOR had 31 events, patients who were on a placebo had 68 events.
Number at risk
CRESTOR
Placebo
8901
8901
8449
8411
3929
3939
1374
1373
546
549
TRIAL DESCRIPTION:
Adapted from the JUPITER trial.[1b], [2b] JUPITER was a long-term, randomized, double-blind, placebo-controlled study in 17,802 patients (CRESTOR=8901, placebo=8901) 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. Patients were followed for a mean duration of 2 years. 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. The study population had 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.
In a post-hoc subgroup analysis of JUPITER subjects of 1405; CRESTOR=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 CRESTOR treatment.
REFERENCES:
In the trial, patients who were on a 20 mg dose of CRESTOR had a 48% percent relative risk reduction [with a hazard ratio of .52 and 95 percentage confidence interval of .34 to .79 and P value less than .002] and a 0.3% absolute risk reduction[*] over patients who were on a placebo. (* ^ Absolute risk reduction %=(events in placebo arm/total number of subjects in placebo arm - events in CRESTOR arm/total number of subjects in CRESTOR arm) x 100.)
HR equals =hazard ratio.
CI equals =confidence interval.
In the trial, patients who were on a 20 mg dose of CRESTOR had 33 events, patients who were on a placebo had 64 events.
Number at risk
CRESTOR
Placebo
8901
8901
8448
8403
3931
3943
1375
1387
547
561
TRIAL DESCRIPTION:
Adapted from the JUPITER trial.[1b], [2b] JUPITER was a long-term, randomized, double-blind, placebo-controlled study in 17,802 patients (CRESTOR=8901, placebo=8901) 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. Patients were followed for a mean duration of 2 years. 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.
The study population had 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.
In a post-hoc subgroup analysis of JUPITER subjects (n=1405; CRESTOR=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 CRESTOR treatment.
REFERENCES:
In the trial, patients who were on a 20 mg dose of CRESTOR had a 46% percent relative risk reduction [with a hazard ratio of .54 and 95 percentage confidence interval of .41 to .72 and a P value of less than .001] and a 0.7% absolute risk reduction[†] over patients who were on a placebo. († ^ Absolute risk reduction %=(events in placebo arm/total number of subjects in placebo arm - events in CRESTOR arm/total number of subjects in CRESTOR arm) x 100.)
HR equals =hazard ratio.
CI equals =confidence interval.
* ^ Including coronary artery bypass graft, or bypass grafting of a peripheral artery or carotid artery, or angioplasty or stent placement.
In the trial, patients who were on a 20 mg dose of CRESTOR had 71 events, patients who were on a placebo had 131 events.
Number at risk
CRESTOR
Placebo
8901
8901
8430
8398
3909
3903
1359
1351
541
539
TRIAL DESCRIPTION:
Adapted from the JUPITER trial.[1b], [2b] JUPITER was a long-term, randomized, double-blind, placebo-controlled study in 17,802 patients (CRESTOR=8901, placebo=8901) 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. Patients were followed for a mean duration of 2 years. 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.
The study population had 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.
In a post-hoc subgroup analysis of JUPITER subjects (n=1405; CRESTOR=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 CRESTOR treatment.
REFERENCES:
Next: Patient Savings
SAVINGS ELIGIBILITY
Important Safety Information for CRESTOR® (rosuvastatin) Tablets
- CRESTOR is contraindicated in patients with active liver disease, which may include unexplained persistent elevations of hepatic transaminase levels or a known hypersensitivity to any component of this product
- Cases of myopathy and rhabdomyolysis with acute renal failure secondary to myoglobinuria have been reported with statins, including CRESTOR. These risks can occur at any dose level, but are increased at the highest dose (40 mg)
- CRESTOR should be prescribed with caution in patients with predisposing factors for myopathy (eg, age ≥65 years, inadequately treated hypothyroidism, renal impairment). The risk of myopathy during treatment with CRESTOR may be increased in Asian patients and with concurrent administration of some other lipid-lowering therapies (fibrates or niacin), cyclosporine, teriflunomide, enasidenib, capmatinib, fostamatinib, febuxostat, gemfibrozil, tafamidis, darolutamide, regorafenib, atazanavir/ritonavir, lopinavir/ritonavir, simeprevir or combination of sofosbuvir/velpatasvir/voxilaprevir, dasabuvir/ombitasvir/paritaprevir/ritonavir, elbasvir/grazoprevir, sofosbuvir/velpatasvir, glecaprevir/pibrentasvir, all combinations with ledipasvir (including ledipasvir/sofosbuvir), colchicine or ticagrelor
- Therapy with CRESTOR should be discontinued if markedly elevated CK levels occur or myopathy is diagnosed or suspected. All patients should be advised to promptly report unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever, and if muscle signs and symptoms persist after discontinuing CRESTOR
- There have been rare reports of immune-mediated necrotizing myopathy (IMNM), an autoimmune myopathy, associated with statin use. IMNM is characterized by proximal muscle weakness and elevated serum creatine kinase, which persist despite discontinuation of statin treatment; positive anti-HMG CoA reductase antibody; muscle biopsy showing necrotizing myopathy; and improvement with immunosuppressive agents. Treatment with immunosuppressive agents may be required. Discontinue CRESTOR if IMNM is suspected
- Increases in serum transaminases have occurred, some persistent. Rare reports of fatal and non-fatal hepatic failure have occurred. Consider testing liver enzymes before initiating therapy and as clinically indicated thereafter. If serious hepatic injury with clinical symptoms and/or hyperbilirubinemia or jaundice occurs, promptly discontinue CRESTOR
- CRESTOR should be used with caution in patients who consume substantial quantities of alcohol and/or have a history of chronic liver disease
- CRESTOR significantly increased INR in patients receiving coumarin anticoagulants (eg, warfarin). In patients taking coumarin anticoagulants and CRESTOR concomitantly, INR should be determined before starting CRESTOR and frequently enough during early therapy to ensure that no significant alteration of INR occurs
- Dipstick-positive proteinuria and microscopic hematuria were observed among patients treated with CRESTOR. These findings were more frequent in patients taking CRESTOR 40 mg, though it was generally transient and was not associated with worsening renal function. Although the clinical significance of this finding is unknown, dose reduction should be considered for patients on CRESTOR therapy with unexplained persistent proteinuria and/or hematuria during routine urinalysis testing
- Increases in HbA1c and fasting serum glucose levels have been reported with statins, including CRESTOR. Based on clinical trial data with CRESTOR, in some instances these increases may exceed the threshold for the diagnosis of diabetes mellitus
- In the controlled clinical trials database, the most common adverse reactions were headache (3.7%), myalgia (3.1%), abdominal pain (2.6%), asthenia (2.5%), and nausea (2.2%)
- Rare post-marketing reports of cognitive impairment (eg, memory loss, forgetfulness, amnesia, memory impairment, confusion) have been associated with statin use, including CRESTOR. These reports are generally nonserious and reversible upon statin discontinuation
- Discontinue CRESTOR when pregnancy is recognized. Alternatively, consider the ongoing therapeutic needs of the individual patient
- CRESTOR 40 mg should be used only for those patients not achieving their LDL-C goal with 20 mg
- Administer CRESTOR at least 2 hours before aluminum and magnesium hydroxide combination antacids
INDICATIONS
- To reduce the risk of major adverse cardiovascular (CV) events (CV death, nonfatal myocardial infarction, nonfatal stroke, or an arterial revascularization procedure) in adults without established coronary heart disease who are at increased risk of CV disease based on age, high-sensitivity C-reactive protein (hsCRP) ≥2 mg/L, and at least one additional CV risk factor
- Adjunct to diet to:
- reduce low-density lipoprotein cholesterol (LDL-C) in adults with primary hyperlipidemia
- reduce LDL-C and slow the progression of atherosclerosis in adults
- reduce LDL-C in patients aged 8 years and older with heterozygous familial hypercholesterolemia (HeFH)
- Adjunct to other LDL-C lowering therapies, or alone if such treatments are unavailable, to reduce LDL-C in patients aged 7 years and older with homozygous familial hypercholesterolemia (HoFH)
- Adjunct to diet for the treatment of adults with primary dysbetalipoproteinemia or hypertriglyceridemia
Read full Prescribing Information.
You may report side effects related to AstraZeneca products
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References:
1a 1b 1c 1d 1e 1f 1g 1h 1i CRESTOR® (rosuvastatin) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2024.
- 1a 1b 1c 1c 1d CRESTOR® (rosuvastatin) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2024.
- ^ Falk, E; Aarhus University Hospital (Skejby). Pathogenesis of atherosclerosis. Am J Cardiol. 2006;47(8):C7-12.
- ^ Nissen, S; Cleveland Clinic Foundation. Rationale for a postintervention continuum of care; insights from intravascular ultrasound. Am J Cardiol. 2000;86(4):H12-17.
- ^ Lexcol® (fluvastatin sodium) [package insert]. East Hanover, New Jersey: Novartis; 2020
- ^ Mevacor® (lovastatin) [package insert]. Whitehouse Station, New Jersey: Merck & Company, Inc. 2012
- ^ Pravachol® (pravastatin) [package insert]. Princeton, New Jersey: Bristol-Myers Squibb Company, 2020.
- ^ Lipitor® (atorvastatin) [package insert]. New York, New York: Pfizer, 2021
- ^ Livalo® (pitavastatin) [package insert]. Montgomery, AL: Kowa group of companies, 2020.
- ^ Zocor® (simvastatin) [package insert]. Jersey City, NJ: Organon & Company, 2022
- ^ Vytorin® (ezetimibe/simvastatin) [package insert]. Jersey City, NJ: Organon & Company, 2022.
- ^ Lexcol® (fluvastatin sodium) [package insert]. East Hanover, New Jersey: Novartis; 2020
- ^ Mevacor® (lovastatin) [package insert]. Whitehouse Station, New Jersey: Merck & Company, Inc. 2012
- ^ Pravachol® (pravastatin) [package insert]. Princeton, New Jersey: Bristol-Myers Squibb Company, 2020.
- ^ Lipitor® (atorvastatin) [package insert]. New York, New York: Pfizer, 2021
- ^ Livalo® (pitavastatin) [package insert]. Montgomery, AL: Kowa group of companies, 2020.
- ^ Zocor® (simvastatin) [package insert]. Jersey City, NJ: Organon & Company, 2022
- ^ Vytorin® (ezetimibe/simvastatin) [package insert]. Jersey City, NJ: Organon & Company, 2022.
- ^ Faergeman O, Hill L, Windler E, et al; on behalf of the ECLIPSE Study Investigators. Efficacy and tolerability of rosuvastatin and atorvastatin when force-titrated in patients with primary hypercholesterolemia. Cardiology. 2008;111(4):219-228.
- ^ Ballantyne CM, Bertolami M, Hernandez Garcia HR, et al. Achieving LDL cholesterol, non-HDL cholesterol, and apolipoprotein B target levels in high-risk patients: Measuring Effective Reductions in Cholesterol Using Rosuvastatin therapY (MERCURY) II. Am Heart J. 2006;151(5):975.e1-975.e9.
- ^ Schuster H, Barter PJ, Stender S, et al. Effects of switching statins on achievement of lipid goals: Measuring Effective Reductions in Cholesterol Using Rosuvastatin therapY (MERCURY I) study. Am Heart J. 2004;147(4):705-713.
- ^ Jones PH, Davidson MH, Stein EA, et al; STELLAR Study Group. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR Trial). Am J Cardiol. 2003;92(2):152-160.
- ^ CRESTOR® (rosuvastatin) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2024.
- ^ Betteridge DJ, Gibson JM; ANDROMEDA Study Investigators. Effects of rosuvastatin on lipids, lipoproteins, and apolipoproteins in the dyslipidaemia of diabetes. Diabet Med. 2007;24(5):541-549.
- ^ Berne C, Siewert-Delle A; URANUS Study Investigators. Comparison of rosuvastatin and atorvastatin for lipid lowering in patients with type 2 diabetes mellitus: results from the URANUS study. Cardiovasc Diabetol. 2005;4:7.
- ^ Ferdinand KC, Clark LT, Watson KE, et al; ARIES Study Group. Comparison of efficacy and safety of rosuvastatin versus atorvastatin in African-American patients in a six-week trial. Am J Cardiol. 2006;97(2):229-235.
- ^ Lloret R, Yčas J, Stein M, Haffner S; STARSHIP Study Group. Comparison of rosuvastatin versus atorvastatin in Hispanic-Americans with hypercholesterolemia (from the STARSHIP trial). Am J Cardiol. 2006;98(6):768-773.
- ^ Data on File, REF-148952, AstraZeneca Pharmaceuticals LP.
- 11a 11b Data on File, REF-148935, AstraZeneca Pharmaceuticals LP.
- ^ Guyton AC, Hall JE. Textbook of Medical Physiology. 11th ed. Philadelphia, PA: Elsevier Inc; 2006.
- ^ Lusis AJ. Atherosclerosis. Nature. 2000;407:233-241.
- ^ National Heart, Lung, and Blood Institute. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III): Final Report. Bethesda, MD: National Institutes of Health; 2002. NIH Publication 02-5215
- 1a 1b CRESTOR® (rosuvastatin) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2024.
- ^ Lusis AJ. Atherosclerosis. Nature. 2000;407:233-241.
- ^ Naghavi M, Falk E, Hecht HS, et al; for the SHAPE Task Force. From vulnerable plaque to vulnerable patient—part III: executive summary of the Screening for Heart Attack Prevention and Education (SHAPE) Task Force report. Am J Cardiol. 2006;98(suppl):2H-15H.
- ^ Falk E. Pathogenesis of atherosclerosis. J Am Coll Cardiol. 2006;47(suppl):C7-C12.
- ^ Crouse JR 3rd, Raichlen JS, Riley WA, et al; METEOR Study Group. Effect of rosuvastatin on progression of carotid intima-media thickness in low-risk individuals with subclinical atherosclerosis: the METEOR Trial. JAMA. 2007;297(12):1344-1353.
- ^ Data on File, REF-148945, AstraZeneca Pharmaceuticals LP.
- 1a 1b 1c CRESTOR® (rosuvastatin) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2024.
- ^ Faergeman O, Hill L, Windler E, et al; ECLIPSE Study Investigators. Efficacy and tolerability of rosuvastatin and atorvastatin when force-titrated in patients with primary hypercholesterolemia: results from the ECLIPSE study. Cardiology. 2008;111(4):219-228.
- 3a 3b Faergeman O, Sosef F, Duffield E; on behalf of the ECLIPSE study investigators. Efficacy and tolerability of rosuvastatin and atorvastatin when force titrated in high-risk patients: results from the ECLIPSE study. Poster presented at: 14th International Symposium on Atherosclerosis; June 18-22, 2006; Rome, Italy.
- Grundy SM, Cleeman JI, Merz CNB, et al; for the Coordinating Committee of the National Cholesterol Education Program. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation. 2004;110:227-239.
- ^ Jones PH, Davidson MH, Stein EA, et al; for the STELLAR Study Group. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR Trial). Am J Cardiol. 2003;92:152-160.
- 6a 6b 6c McKenney JM, Jones PH, Adamczyk MA, Cain VA, Bryzinski BS, Blasetto JW; STELLAR Study Group. Comparison of the efficacy of rosuvastatin versus atorvastatin, simvastatin, and pravastatin in achieving lipid goals: results from the STELLAR trial. Curr Med Res Opin. 2003;19(8):689-698.
- ^ Data on File, REF-148955, AstraZeneca Pharmaceuticals LP
- ^ Nicholls SJ, Brandrup-Wognsen G, Palmer N, et al. Meta-analysis of comparative efficacy of increasing dose of atorvastatin versus rosuvastatin versus simvastatin on lowering levels of atherogenic lipids (from VOYAGER). Am J Cardiol. 2010;105:69-76.
1a 1b 1c 1d 1e 1f 1g 1h 1i 1j 1k 1l 1m 1n 1o 1p 1q 1r CRESTOR® (rosuvastatin) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2024.
1a 1b 1c 1d1d CRESTOR® (rosuvastatin) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2024.
- 1a CRESTOR® (rosuvastatin) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2024.
- 2a Lipitor® (atorvastatin calcium) [prescribing information]. Morgantown, WV: Viatris Specialty LLC, 2024.
- 3a Faergeman O, Hill L, Windler E, et al; on behalf of the ECLIPSE Study Investigators. Efficacy and tolerability of rosuvastatin and atorvastatin when force-titrated in patients with primary hypercholesterolemia. Cardiology. 2008;111(4):219-228.
- 4a Jones PH, Davidson MH, Stein EA, et al; for the STELLAR Study Group. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR Trial). Am J Cardiol. 2003;92:152-160.
- 5a Crouse JR 3rd, Raichlen JS, Riley WA, et al; METEOR Study Group. Effect of rosuvastatin on progression of carotid intima-media thickness in low-risk individuals with subclinical atherosclerosis: the METEOR Trial. JAMA. 2007;297(12):1344-1353.
Lipitor is a registered trademark of Upjohn Manufacturing Ireland Unlimited Company, a Viatris Company.
1a 1b 1c 1d CRESTOR® (rosuvastatin) [prescribing information]. Wilmington, DE: AstraZeneca Pharmaceuticals LP; 2024.
This product information is intended for US Health Care Professionals only.
IMPORTANT SAFETY INFORMATION FOR CRESTOR® (ROSUVASTATIN) TABLETS
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