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Mechanism Of Action
CRESTOR is a selective and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate, a precursor of cholesterol. In vivo studies in animals, and in vitro studies in cultured animal and human cells have shown rosuvastatin to have a high uptake into, and selectivity for, action in the liver, the target organ for cholesterol lowering. In in vivo and in vitro studies, rosuvastatin produces its lipid-modifying effects in two ways. First, it increases the number of hepatic LDL receptors on the cell-surface to enhance uptake and catabolism of LDL. Second, rosuvastatin inhibits hepatic synthesis of VLDL, which reduces the total number of VLDL and LDL particles.
- Absorption: In clinical pharmacology studies in
man, peak plasma concentrations of rosuvastatin were reached 3 to 5 hours
following oral dosing. Both C max and AUC increased in approximate proportion
to CRESTOR dose. The absolute bioavailability of rosuvastatin is approximately
Administration of CRESTOR with food did not affect the AUC of rosuvastatin.
The AUC of rosuvastatin does not differ following evening or morning drug administration.
- Distribution: Mean volume of distribution at steady-state of rosuvastatin is approximately 134 liters. Rosuvastatin is 88% bound to plasma proteins, mostly albumin. This binding is reversible and independent of plasma concentrations.
- Metabolism: Rosuvastatin is not extensively metabolized; approximately 10% of a radiolabeled dose is recovered as metabolite. The major metabolite is N-desmethyl rosuvastatin, which is formed principally by cytochrome P450 \ 2C9, and in vitro studies have demonstrated that N-desmethyl rosuvastatin has approximately one-sixth to one-half the HMG-CoA reductase inhibitory activity of the parent compound. Overall, greater than 90% of active plasma HMG-CoA reductase inhibitory activity is accounted for by the parent compound.
- Excretion: Following oral administration, rosuvastatin and its metabolites are primarily excreted in the feces (90%). The elimination half-life (t ½ ) of rosuvastatin is approximately 19 hours. After an intravenous dose, approximately 28% of total body clearance was via the renal route, and 72% by the hepatic route.
- Race: A population pharmacokinetic analysis revealed no clinically relevant differences in pharmacokinetics among Caucasian, Hispanic, and Black or Afro-Caribbean groups. However, pharmacokinetic studies, including one conducted in the US, have demonstrated an approximate 2-fold elevation in median exposure (AUC and C max ) in Asian subjects when compared with a Caucasian control group.
- Gender: There were no differences in plasma concentrations of rosuvastatin between men and women.
- Pediatric: In a population pharmacokinetic analysis of two pediatric trials involving patients with heterozygous familial hypercholesterolemia 10 to 17 years of age and 8 to 17 years of age, respectively, rosuvastatin exposure appeared comparable to or lower than rosuvastatin exposure in adult patients.
- Geriatric: There were no differences in plasma concentrations of rosuvastatin between the nonelderly and elderly populations (age ≥ 65 years).
- Renal Impairment: Mild to moderate renal impairment (CLcr ≥ 30 mL/min/1.73 m²) had no influence on plasma concentrations of rosuvastatin. However, plasma concentrations of rosuvastatin increased to a clinically significant extent (about 3-fold) in patients with severe renal impairment (CLcr < 30 mL/min/1.73 m²) not receiving hemodialysis compared with healthy subjects (CLcr > 80 mL/min/1.73 m²).
- Hemodialysis: Steady-state plasma concentrations of rosuvastatin in patients on chronic hemodialysis were approximately 50% greater compared with healthy volunteer subjects with normal renal function.
- Hepatic Impairment: In patients with chronic alcohol liver disease, plasma concentrations of rosuvastatin were modestly increased.
In patients with Child-Pugh A disease, C max and AUC were increased by 60% and 5%, respectively, as compared with patients with normal liver function. In patients with Child-Pugh B disease, C max and AUC were increased 100% and 21%, respectively, compared with patients with normal liver function.
Rosuvastatin clearance is not dependent on metabolism by cytochrome P450 3A4 to a clinically significant extent.
Rosuvastatin is a substrate for certain transporter proteins including the hepatic uptake transporter organic anion-transporting polyprotein 1B1 (OATP1B1) and efflux transporter breast cancer resistance protein (BCRP). Concomitant administration of CRESTOR with medications that are inhibitors of these transporter proteins (e.g. cyclosporine, certain HIV protease inhibitors) may result in increased rosuvastatin plasma concentrations and an increased risk of myopathy [see DOSAGE AND ADMINISTRATION]. It is recommended that prescribers consult the relevant product information when considering administration of such products together with CRESTOR.
Table 4: Effect of Coadministered Drugs on
Rosuvastatin Systemic Exposure
|Coadministered drug and dosing regimen||Rosuvastatin|
|Mean Ratio (ratio with/without coadministered drug) No Effect = 1.0|
|Change in AUC||Change in Cmax|
|Cyclosporine - stable dose required (75 mg - 200 mg BID)||10 mg QD for 10 days||7.12||112|
|Atazanavir/ritonavir combination 300 mg/100 mg QD for 8 days||10 mg||3.12||72|
|Simeprevir 150 mg QD, 7 days||10 mg, single dose||2.82
|Lopinavir/ritonavir combination 400 mg/100 mg BID for 17 days||20 mg QD for 7 days||2.12
|Gemfibrozil 600 mg BID for 7 days||80 mg||1.92
|Eltrombopag 75 mg QD, 5 days||10 mg||1.6
|Darunavir 600 mg/ritonavir 100 mg BID, 7 days||10 mg QD for 7 days||1.5
|Tipranavir/ritonavir combination 500 mg/200mg BID for 11 days||10 mg||1.4
|Dronedarone 400 mg BID||10 mg||1.4|
|Itraconazole 200 mg QD, 5 days||10 mg or 80 mg||1.4
|Ezetimibe 10 mg QD, 14 days||10 mg QD for 14 days||1.2
|Fosamprenavir/ritonavir 700 mg/100 mg BID for 7 days||10 mg||1.1||1.5|
|Fenofibrate 67 mg TID for 7 days||10 mg||1.2
|Rifampicin 450 mg QD, 7 days||20 mg|
|Aluminum & magnesium hydroxide combination antacid|
|Administered simultaneously||40 mg||0.52
|Administered 2 hours apart||40 mg||0.8
|Ketoconazole 200 mg BID for 7 days||80 mg||1.0
|Fluconazole 200 mg QD for 11 days||80 mg||1.1
|Erythromycin 500 mg QID for 7 days||80 mg||0.8
|1Single dose unless otherwise noted.
2Clinically significant [see DOSAGE AND ADMINISTRATION and WARNINGS AND PRECAUTIONS]
3Mean ratio with 90% CI
(with/without coadministered drug, e.g., 1= no change, 0.7 = 30% decrease, 11=11 fold increase in exposure)
Table 5: Effect of
Rosuvastatin Coadministration on Systemic Exposure To Other Drugs
|Rosuvastatin Dosage Regimen||Coadministered Drug|
|Name and Dose||Mean Ratio (ratio with/without coadministered drug) No Effect = 1.0|
|Change in AUC||Change in Cmax|
|40 mg QD for 10 days||Warfarin1 25 mg single dose||R- Warfarin 1.0
|40 mg QD for 12 days||Digoxin 0.5 mg single dose||1.0
|40 mg QD for 28 days||Oral Contraceptive (ethinyl estradiol 0.035 mg & norgestrel 0.180, 0.215 and 0.250 mg) QD for 21 Days||EE 1.3
|EE = ethinyl estradiol, NG =
1Clinically significant pharmacodynamic effects [see WARNINGS AND PRECAUTIONS]
2Mean ratio with 90% CI (with/without coadministered drug, e.g., 1= no change, 0.7=30% decrease, 11=11-fold increase in exposure)
Disposition of HMG-CoA reductase inhibitors, including rosuvastatin, involves OATP1B1 and other transporter proteins. Higher plasma concentrations of rosuvastatin have been reported in very small groups of patients (n=3 to 5) who have two reduced function alleles of the gene that encodes OATP1B1 (SLCO1B1 521T > C). The frequency of this genotype (i.e., SLCO1B1 521 C/C) is generally lower than 5% in most racial/ethnic groups. The impact of this polymorphism on efficacy and/or safety of rosuvastatin has not been clearly established. Doses should be titrated according to patient response and tolerability.
Animal Toxicology And/Or Pharmacology
Rosuvastatin crosses the placenta and is found in fetal tissue and amniotic fluid at 3% and 20%, respectively, of the maternal plasma concentration following a single 25 mg/kg oral gavage dose on gestation day 16 in rats. A higher fetal tissue distribution (25% maternal plasma concentration) was observed in rabbits after a single oral gavage dose of 1 mg/kg on gestation day 18.
In female rats given oral gavage doses of 5, 15, 50 mg/kg/day rosuvastatin before mating and continuing through day 7 postcoitus results in decreased fetal body weight (female pups) and delayed ossification at the high dose (systemic exposures 10 times the human exposure at 40 mg/day based on AUC).
In pregnant rats given oral gavage doses of 2, 10, 50 mg/kg/day from gestation day 7 through lactation day 21 (weaning), decreased pup survival occurred in groups given 50 mg/kg/day, systemic exposures ≥ 12 times the human exposure at 40 mg/day based on body surface area.
In pregnant rabbits given oral gavage doses of 0.3, 1, 3 mg/kg/day from gestation day 6 to lactation day 18 (weaning), exposures equivalent to the human exposure at 40 mg/day based on body surface area, decreased fetal viability and maternal mortality was observed.
Rosuvastatin was not teratogenic in rats at ≤ 25 mg/kg/day or in rabbits ≤ 3 mg/kg/day (systemic exposures equivalent to the human exposure at 40 mg/day based on AUC or body surface area, respectively).
Central Nervous System Toxicity
CNS vascular lesions, characterized by perivascular hemorrhages, edema, and mononuclear cell infiltration of perivascular spaces, have been observed in dogs treated with several other members of this drug class. A chemically similar drug in this class produced dose-dependent optic nerve degeneration (Wallerian degeneration of retinogeniculate fibers) in dogs, at a dose that produced plasma drug levels about 30 times higher than the mean drug level in humans taking the highest recommended dose. Edema, hemorrhage, and partial necrosis in the interstitium of the choroid plexus was observed in a female dog sacrificed moribund at day 24 at 90 mg/kg/day by oral gavage (systemic exposures 100 times the human exposure at 40 mg/day based on AUC). Corneal opacity was seen in dogs treated for 52 weeks at 6 mg/kg/day by oral gavage (systemic exposures 20 times the human exposure at 40 mg/day based on AUC). Cataracts were seen in dogs treated for 12 weeks by oral gavage at 30 mg/kg/day (systemic exposures 60 times the human exposure at 40 mg/day based on AUC). Retinal dysplasia and retinal loss were seen in dogs treated for 4 weeks by oral gavage at 90 mg/kg/day (systemic exposures 100 times the human exposure at 40 mg/day based on AUC). Doses ≤ 30 mg/kg/day (systemic exposures ≤ 60 times the human exposure at 40 mg/day based on AUC) did not reveal retinal findings during treatment for up to one year.
Hyperlipidemia And Mixed Dyslipidemia
CRESTOR reduces Total-C, LDL-C, ApoB, nonHDL-C, and TG, and increases HDL-C, in adult patients with hyperlipidemia and mixed dyslipidemia.
Dose-Ranging Study: In a multicenter, double-blind, placebo-controlled, dose-ranging study in patients with hyperlipidemia CRESTOR given as a single daily dose for 6 weeks significantly reduced Total-C, LDL-C, nonHDL-C, and ApoB, across the dose range (Table 6).
Table 6: Dose-Response in Patients With Hyperlipidemia
(Adjusted Mean % Change From Baseline at Week 6)
|CRESTOR 5 mg||17||-33||-45||-44||-38||-35||13|
|CRESTOR 10 mg||17||-36||-52||-48||-42||-10||14|
|CRESTOR 20 mg||17||-40||-55||-51||-46||-23||8|
|CRESTOR 40 mg||18||-46||-63||-60||-54||-28||10|
Active-Controlled Study: CRESTOR was compared with the HMG-CoA reductase inhibitors atorvastatin, simvastatin, and pravastatin in a multicenter, open-label, dose-ranging study of 2240 patients with hyperlipidemia or mixed dyslipidemia. After randomization, patients were treated for 6 weeks with a single daily dose of either CRESTOR, atorvastatin, simvastatin, or pravastatin (Figure 1 and Table 7).
Figure 1: Percent LDL-C
Change by Dose of CRESTOR, Atorvastatin, Simvastatin, and Pravastatin at Week 6
in Patients with Hyperlipidemia or Mixed Dyslipidemia
Box plots are a representation of the 25th, 50th, and 75th percentile values, with whiskers representing the 10th and 90th percentile values. Mean baseline LDL-C: 189 mg/dL.
Table 7: Percent Change in
LDL-C From Baseline to Week 6 (LS Mean1) by Treatment Group (sample
sizes ranging from 156–167 patients per group)
|Treatment||Treatment Daily Dose|
|10 mg||20 mg||40 mg||80 mg|
|1Corresponding standard errors are
2 CRESTOR 10 mg reduced LDL-C significantly more than atorvastatin 10 mg; pravastatin 10 mg, 20 mg, and 40 mg; simvastatin 10 mg, 20 mg, and 40 mg. (p < 0.002)
3 CRESTOR 20 mg reduced LDL-C significantly more than atorvastatin 20 mg and 40 mg; pravastatin 20 mg and 40 mg; simvastatin 20 mg, 40 mg, and 80 mg. (p < 0.002)
4 CRESTOR 40 mg reduced LDL-C significantly more than atorvastatin 40 mg; pravastatin 40 mg; simvastatin 40 mg, and 80 mg. (p < 0.002)
Heterozygous Familial Hypercholesterolemia
Active-Controlled Study: In a study of patients with heterozygous FH (baseline mean LDL of 291), patients were randomized to CRESTOR 20 mg or atorvastatin 20 mg. The dose was increased by 6-week intervals. Significant LDL-C reductions from baseline were seen at each dose in both treatment groups (Table 8).
Table 8: Mean LDL-C
Percentage Change from Baseline
(n=435) LS Mean1 (95% CI)
(n=187) LS Mean1 (95% CI)
|Week 6||20 mg||-47%
|Week 12||40 mg||-55%
|Week 18||80 mg||NA||-52%
|1 LS Means are least square means adjusted for baseline LDL-C|
Dose-Response Study: In a double-blind, placebo-controlled dose-response study in patients with baseline TG levels from 273 to 817 mg/dL, CRESTOR given as a single daily dose (5 to 40 mg) over 6 weeks significantly reduced serum TG levels (Table 9).
Table 9: Dose-Response in
Patients With Primary Hypertriglyceridemia Over 6 Weeks Dosing Median (Min,
Max) Percent Change From Baseline
|CRESTOR 5 mg
|CRESTOR 10 mg
|CRESTOR 20 mg
|CRESTOR 40 mg
|Triglycerides||1 (-40, 72)||-21 (-58, 38)||-37 (-65, 5)||-37 (-72, 11)||-43 (-80, -7)|
|nonHDL-C||2 (-13, 19)||-29 (-43, -8)||-49 (-59, -20)||-43 (-74, 12)||-51 (-62, -6)|
|VLDL-C||2 (-36, 53)||-25 (-62, 49)||-48 (-72, 14)||-49 (-83, 20)||-56 (-83, 10)|
|Total-C||1 (-13, 17)||-24 (-40, -4)||-40 (-51, -14)||-34 (-61, -11)||-40 (-51, -4)|
|LDL-C||5 (-30, 52)||-28 (-71, 2)||-45 (-59, 7)||-31 (-66, 34)||-43 (-61, -3)|
|HDL-C||-3 (-25, 18)||3 (-38, 33)||8 (-8, 24)||22 (-5, 50)||17 (-14, 63)|
Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia)
In a randomized, multicenter, double-blind crossover study, 32 patients (27 with ε2/ε2 and 4 with apo E mutation [Arg145Cys] with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia) entered a 6-week dietary lead-in period on the NCEP Therapeutic Lifestyle Change (TLC) diet. Following dietary lead-in, patients were randomized to a sequence of treatments in conjunction with the TLC diet for 6 weeks each: rosuvastatin 10 mg followed by rosuvastatin 20 mg or rosuvastatin 20 mg followed by rosuvastatin 10 mg. CRESTOR reduced non HDL-C (primary end point) and circulating remnant lipoprotein levels. Results are shown in the table below.
Table 10: Lipid-modifying Effects of Rosuvastatin 10
mg and 20 mg in Primary Dysbetalipoproteinemia(Type III hyperlipoproteinemia)
after Six weeks by Median Percent Change (95% CI) from Baseline (N=32)
|Median at Baseline (mg/dL)||Median percent change from baseline (95% CI) CRESTOR 10 mg||Median percent change from baseline (95% CI) CRESTOR 20 mg|
(-46.9, - 37.5)
Homozygous Familial Hypercholesterolemia
In an open-label, forced-titration study, homozygous FH patients (n=40, 8-63 years) were evaluated for their response to CRESTOR 20 to 40 mg titrated at a 6-week interval. In the overall population, the mean LDL-C reduction from baseline was 22%. About one-third of the patients benefited from increasing their dose from 20 mg to 40 mg with further LDL lowering of greater than 6%. In the 27 patients with at least a 15% reduction in LDL-C, the mean LDL-C reduction was 30% (median 28% reduction). Among 13 patients with an LDL-C reduction of < 15%, 3 had no change or an increase in LDL-C. Reductions in LDL-C of 15% or greater were observed in 3 of 5 patients with known receptor negative status.
Pediatric Patients With Heterozygous Familial Hypercholesterolemia
In a double-blind, randomized, multicenter, placebo-controlled, 12 week study, 176 (97 male and 79 female) children and adolescents with heterozygous familial hypercholesterolemia were randomized to rosuvastatin 5, 10 or 20 mg or placebo daily. Patients ranged in age from 10 to 17 years (median age of 14 years) with approximately 30% of the patients 10 to 13 years and approximately 17%, 18%, 40%, and 25% at Tanner stages II, III, IV, and V, respectively. Females were at least 1 year postmenarche. Mean LDL-C at baseline was 233 mg/dL (range of 129 to 399). The 12-week double blind phase was followed by a 40-week open label dose-titration phase, where all patients (n=173) received 5 mg, 10 mg or 20 mg rosuvastatin daily.
Rosuvastatin significantly reduced LDL-C (primary end point), total cholesterol and ApoB levels at each dose compared to placebo. Results are shown in Table 11 below.
Table 11: Lipid-Modifying Effects Of Rosuvastatin In
Pediatric Patients 10 to 17 Years Of Age With Heterozygous Familial
Hypercholesterolemia (Least-Squares Mean Percent Change From Baseline To Week
|1Median percent change
2Difference from placebo not statistically significant
At the end of the 12-week, double-blind treatment period, the percentage of patients achieving the LDL-C goal of less than 110 mg/dL (2.8 mmol/L) was 0% for placebo, 12% for rosuvastatin 5 mg, 41% for rosuvastatin 10 mg and 41% for rosuvastatin 20 mg. For the 40-week, open-label phase, 71% of the patients were titrated to the maximum dose of 20 mg and 41% of the patients achieved the LDL-C goal of 110 mg/dL.
Rosuvastatin was also studied in a two year open-label, uncontrolled, titration to goal trial that included 175 children and adolescents with heterozygous familial hypercholesterolemia who were 8 to 17 years old (79 boys and 96 girls). All patients had a documented genetic defect in the LDL receptor or in Apo B. Approximately 89% were Caucasian, 7% were Asian, 1% were Black, and fewer than 1% were Hispanic. Mean LDL-C at baseline was 236 mg/dL. Fifty-eight (33%) patients were prepubertal at baseline. The starting rosuvastatin dosage for all children and adolescents was 5 mg once daily. Children 8 to less than 10 years of age (n=41 at baseline) could titrate to a maximum dosage of 10 mg once daily, and children and adolescents 10 to 17 years of age could titrate to a maximum dosage of 20 mg once daily.
The reductions in LDL-C from baseline were generally consistent across age groups within the trial as well as with previous experience in both adult and pediatric controlled trials.
The long-term efficacy of rosuvastatin therapy initiated in childhood to reduce morbidity and mortality in adulthood has not been established.
Slowing Of The Progression Of Atherosclerosis
In the Measuring Effects on Intima Media Thickness: an Evaluation Of Rosuvastatin 40 mg (METEOR) study, the effect of therapy with CRESTOR on carotid atherosclerosis was assessed by B-mode ultrasonography in patients with elevated LDL-C, at low risk (Framingham risk < 10% over ten years) for symptomatic coronary artery disease and with subclinical atherosclerosis as evidenced by carotid intimal-medial thickness (cIMT). In this double-blind, placebo-controlled clinical study 984 patients were randomized (of whom 876 were analyzed) in a 5:2 ratio to CRESTOR 40 mg or placebo once daily. Ultrasonograms of the carotid walls were used to determine the annualized rate of change per patient from baseline to two years in mean maximum cIMT of 12 measured segments. The estimated difference in the rate of change in the maximum cIMT analyzed over all 12 carotid artery sites between patients treated with CRESTOR and placebo-treated patients was -0.0145 mm/year (95% CI –0.0196, –0.0093; p < 0.0001).
The annualized rate of change from baseline for the placebo group was +0.0131 mm/year (p < 0.0001). The annualized rate of change from baseline for the group treated with CRESTOR was -0.0014 mm/year (p=0.32).
At an individual patient level in the group treated with CRESTOR, 52.1% of patients demonstrated an absence of disease progression (defined as a negative annualized rate of change), compared to 37.7% of patients in the placebo group.
Primary Prevention of Cardiovascular Disease
In the Justification for the Use of Statins in Primary Prevention
An Intervention Trial Evaluating Rosuvastatin (JUPITER) study, the effect of CRESTOR (rosuvastatin calcium) on the occurrence of major cardiovascular (CV) disease events was assessed in 17,802 men ( ≥ 50 years) and women ( ≥ 60 years) who had no clinically evident cardiovascular disease, LDL-C levels < 130 mg/dL (3.3 mmol/l) and hs-CRP levels ≥ 2 mg/L. The study population had an estimated baseline coronary heart disease 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. Study participants were randomly assigned to placebo (n=8901) or rosuvastatin 20 mg once daily (n=8901) and were followed for a mean duration of 2 years. The JUPITER study was stopped early by the Data Safety Monitoring Board due to meeting predefined stopping rules for efficacy in rosuvastatin-treated subjects.
The primary end point was a composite end point consisting of the time-to-first occurrence of any of the following major CV events: CV death, nonfatal myocardial infarction, nonfatal stroke, hospitalization for unstable angina or an arterial revascularization procedure.
Rosuvastatin significantly reduced the risk of major CV events (252 events in the placebo group vs. 142 events in the rosuvastatin group) with a statistically significant (p < 0.001) relative risk reduction of 44% and absolute risk reduction of 1.2% (see Figure 2). The risk reduction for the primary end point was consistent across the following predefined subgroups: age, sex, race, smoking status, family history of premature CHD, body mass index, LDL-C, HDL-C, and hsCRP levels.
Figure 2: Time to first occurrence of major
cardiovascular events in JUPITER
The individual components of the primary end point are presented in Figure 3. Rosuvastatin significantly reduced the risk of nonfatal myocardial infarction, nonfatal stroke, and arterial revascularization procedures. There were no significant treatment differences between the rosuvastatin and placebo groups for death due to cardiovascular causes or hospitalizations for unstable angina.
Rosuvastatin significantly reduced the risk of myocardial infarction (6 fatal events and 62 nonfatal events in placebo-treated subjects vs. 9 fatal events and 22 nonfatal events in rosuvastatin-treated subjects) and the risk of stroke (6 fatal events and 58 nonfatal events in placebo-treated subjects vs. 3 fatal events and 30 nonfatal events in rosuvastatin-treated subjects).
In a post-hoc subgroup analysis of JUPITER subjects (n=1405; rosuvastatin=725, placebo=680) with a hsCRP ≥ 2 mg/L and no other traditional risk factors (smoking, BP ≥ 140/90 or taking antihypertensives, low HDL-C) other than age, after adjustment for high HDL-C, there was no significant treatment benefit with rosuvastatin treatment.
Figure 3: Major CV events by treatment group in
At one year, rosuvastatin increased HDL-C and reduced LDL-C, hsCRP, total cholesterol and serum triglyceride levels (p < 0.001 for all versus placebo).
Last reviewed on RxList: 1/5/2016
This monograph has been modified to include the generic and brand name in many instances.
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