Rosuvastatin: A New Pharmacotherapy
for LDL-Cholesterol Reduction

Volume VI, Number 6 | November/December 2003
Katie E. Meister, Pharm.D.

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The cornerstone of cholesterol-lowering therapy consists of agents that inhibit the hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase enzyme. The primary goal of HMG-CoA reductase inhibitors (HMG-CoA RIs), commonly referred to as "statins," is to decrease the risk of coronary heart disease (CHD) events, which is most effectively achieved through the reduction of low-density-lipoprotein (LDL) cholesterol.1 Elevated LDL-cholesterol is the most significant risk factor for the development of atherosclerosis and, in fact, a significant correlation has been established between elevated LDL-cholesterol and the risk for CHD.2 The literature has demonstrated a direct correlation between lower total cholesterol and CHD risk reduction, with a meta-analysis suggesting that for every 10% reduction in cholesterol level, there was a subsequent decrease in CHD mortality risk and total mortality by 15% and 11%, respectively.3

The current recommended goals for cholesterol reduction in the United States are provided by the National Cholesterol Education Program (NCEP) — Adult Treatment Panel III (ATP-III).1 This panel identifies LDL-cholesterol as the primary target for antihyperlipidemic therapy, with goal LDL-cholesterol levels based on risk classifications shown in Table 1. The most rigorous target of <100 mg/dl of LDL-cholesterol is the goal in patients with CHD or CHD-risk equivalents, such as diabetes, other clinical forms of atherosclerotic disease such as peripheral arterial disease, or a combination of risk factors that equal a 10-year risk for CHD of greater than 20%.

Table 1. LDL-Cholesterol Risk Categories and Therapeutic Goals
Risk Category LDL Goals (mg/dl)
CHD or CHD-Risk Equivalent* <100
Multiple (2+) Risk Factors** <130
0-1 Risk Factors** <160

* Risk Equivalents: diabetes, peripheral arterial disease, abdominal aortic aneurysms, or symptomatic carotid artery disease, multiple risk factors that confer >20% 10-year CHD risk
**Risk Factors: cigarette smoking, hypertension, use of antihypertensive drugs, low HDL-cholesterol, family history of premature CHD, male >/= 45 years old, female >/=55 years old.
Adapted from NCEP ATP-III. JAMA 2001;285:2490.

Recent data have suggested that a possible benefit may be gained with aggressive LDL-cholesterol lowering beyond the current recommendation of 100 mg/dl in patients with CHD or CHD-risk equivalents to further decrease the risk of CHD complications.4,5 Additionally, the literature has demonstrated that there may not be a threshold for low LDL-cholesterol levels resulting in CHD-risk reduction. The results of the Heart Protection Study indicated that the addition of a HMG-CoA RI produced mortality benefits, regardless of a patient's initial LDL-cholesterol concentration.6 The risk reduction in patients in this study with a pre-investigation LDL-cholesterol of 97 mg/dl that was reduced to 65 mg/dl was equal to patients who presented with higher LDL-cholesterol.

A survey of patients in 2000 revealed that only 18% of CHD patients who receive any type of antihyperlipidemic therapy achieve the recommended LDL-cholesterol level of <100 mg/dl.7 The primary reasons for non-achievement of LDL goals included 1) use of low dosages or inappropriate choice of medications by prescribers, 2) poor tolerability and non-compliance by patients, and 3) limited drug effectiveness at achieving lower LDL-cholesterol goals, suggesting a possible benefit from a therapy that is more potent at reducing LDL-cholesterol. The ability of a medication to further reduce LDL-cholesterol and protect against CHD would also be beneficial in achieving the current ATP-III goals.

The other HMG-CoA RIs include atorvastatin [Lipitor®], simvastatin [Zocor®], lovastatin [Mevacor®], pravastatin [Pravachol®], and fluvastatin [Lescol®]. In an across-the-dose comparison of these HMG-CoA RIs, atorvastatin produced the greatest reduction in LDL-cholesterol in milligram equivalent doses of 10-, 20-, and 40-mg. The atorvastatin 80 mg dosage caused the greatest decrease in LDL-cholesterol by 54% from baseline values.8 The equipotent doses of the other HMG-CoA RIs are shown in Table 2, demonstrating that 1) the lipid-lowering effects of atorvastatin 40 mg can only be achieved by the simvastatin 80 mg dose and 2) there is no therapy equal to the lipid-lowering effects of the atorvastatin 80 mg dose. Clinical utilization of an agent that can even more effectively inhibit cholesterol production would further determine the CHD-risk reduction from lower LDL-cholesterol targets. Rosuvastatin [Crestor®; AstraZeneca], a new HMG-CoA RI, was approved by the Food and Drug Administration (FDA) on August 12, 2003, with the aim of achieving this goal.

Table 2. Comparative Equipotent Dosages of the HMG-CoA RI
Atorvastatin Simvastatin Lovastatin or Pravastatin Fluvastatin
5 mg 10 mg 20 mg 40 mg
10 mg 20 mg 40 mg 80 mg
20 mg 40 mg 80 mg ---
40 mg 80 mg --- ---
80 mg --- --- ---

Adapted from: Roberts WC et al. Baylor University Medical Center Proceedings 2000;13:139-43.


Rosuvastatin was designed to optimize the pharmacologic properties beyond those of the currently available HMG-CoA RIs, in terms of potency, hepatic specificity, pharmacokinetics, and safety.10 FDA-approved indications for rosuvastatin include 1) reduction of cholesterol levels as an adjunct to diet in patients with primary hypercholesterolemia and mixed dyslipidemia, 2) reduction of elevated serum triglyceride levels, and 3) as an adjunct to other lipid-lowering therapies in homozygous familial hypercholesterolemia.11

With the availability of this new cholesterol-lowering agent, it must be determined whether it is a unique and clinically beneficial option compared to the current treatment choices or if it only increases prescribing options with no clinical difference in efficacy or safety.


Rosuvastatin, similar to all other HMG-CoA RIs, reduces cholesterol by blocking the actions of HMG-CoA reductase, which is an early and rate-limiting step in the cholesterol synthesis process. By blocking the action of this enzyme, the conversion of HMG-CoA to mevalonic acid is inhibited and the subsequent result is a decrease in cholesterol production in the hepatocytes.12 Compared to other HMG-CoA RIs, rosuvastatin possesses the highest bonding interactions with HMG-CoA reductase, resulting in the most potent inhibition of cholesterol synthesis.

Rosuvastatin is a hydrophilic molecule that is selective for hepatic cells. Hydrophilicity results in reduced diffusion into non-hepatic cells, thereby decreasing the potential for adverse effects.10,13 Pravastatin is the only other HMG-CoA RI with similar properties.


The bioavailability of rosuvastatin (20%) is comparable to other HMG-CoA RI agents. Concurrent administration with food does not affect the bioavailability of rosuvastatin, but can decrease its rate of absorption.11 The half-life of rosuvastatin is approximately 20 hours, which is longer than the other HMG-CoA RIs. An advantage with rosuvastatin is that it is not significantly metabolized by the liver. Rosuvastatin is primarily eliminated through biliary excretion (90%) and found unchanged in the feces, with the remainder of elimination occurring in the urine.2 The small percentage that is hepatically metabolized occurs via the cytochrome P-450 (CYP) enzymes 2C9 and 2C19, with almost no metabolism by CYP 3A4.10

Select Clinical Trials

The majority of rosuvastatin's clinical trials are comparator-controlled studies between rosuvastatin and pravastatin, simvastatin, or atorvastatin.14-18 Patients who participated in these studies had baseline LDL-cholesterol levels that ranged from 160-250 mg/dl. The primary endpoints of these investigations were the difference in the percent change of LDL-cholesterol from baseline and the percentage of patients who achieved LDL-cholesterol goals according to the NCEP ATP-II or -III (depending on publishing date). Since LDL-cholesterol reduction has the strongest correlation with decreasing CHD morbidity and mortality, it was the primary outcome of the studies.4 A description of these studies is shown in Table 3. These study results were similar in demonstrating that rosuvastatin produced a greater LDL-cholesterol reduction and target achievement in comparison with the other agents.

Table 3. Rosuvastatin Camparator-Controlled Trials in Patients with Primary Hypercholesterolemia
Study N Treatments (dose/day) Results
      % of LDL-Cholesterol Reduction from Baseline % of Patients
Achieving ATP-II
or -III Targets
Olsson et al. 200114
Randomized, open-label, comparator- and placebo-controlled trial
6 weeks
142 Rosuvastatin 1-40 mg 34-65 N/A
Atorvastatin 10 mg 44
Atorvastatin 80 mg 59
Placebo -3.6
Paoletti et al. 200115
Randomized, double-blind, multi-center, comparatory-controlled trial
12 weeks
502 Rosuvastatin 5 mg 42 71
Rosuvastatin 10 mg 49 87
Pravastatin 20 mg 28 53
Simvastatin 20 mg 37 64
Brown et al. 200216
Randomized, double-blind, multi-center, comparator-controlled trial
Fixed Dose Period
12 wks

Rosuvastatin 5 mg 39 80
Rosuvastatin 10 mg 47 90
Pravastatin 20 mg 27 53
Simvastatin 20 mg 35 69
Dose Titration Period
52 wks

Rosuvastatin 5-80 mg 42 88
Rosuvastatin 10-80 mg 48 88
Pravastatin 40 mg 32 60
Simvastatin 80 mg 38 73
Olsson et al. 200217
Randomized, double-blind, multi-center, comparator-controlled trial
Fixed Dose Period
12 wks

Rosuvastatin 5 mg 46 86
Rosuvastatin 10 mg 50 73
Atorvastatin 10 mg 39 86
Dose Titration Period
52 wks

Rosuvastatin 5-80 mg 47 88
Rosuvastatin 10-80 mg 53 98
Atorvastatin 80 mg 44 87
Davidson et al. 200218
Randomized, double-blind, multi-center, comparator- and placebo-controlled trial
12 weeks
516 Rosuvastatin 5 mg 40 84
Rosuvastatin 10 mg 43 82
Atorvastatin 10 mg 35 72
Placebo 0 12

Adapted from Olsson AG et al. Am J Cardiol 2001; 88:504-8, Paoletti R et al. J Cardiovasc Risk 2001:8:383-90, Brown WV et al. Am Heart J 2002; 144: 1036-43, Olsson AG et al. Am Heart J 2002;144:1044-51, Davidson M et al. Am J Cardiol 2002;89:268-75.

The study by Olsson and colleagues in 2001 was a placebo-controlled, dose-ranging study investigating rosuvastatin and atorvastatin. The study demonstrated that when compared with placebo, rosuvastatin resulted in significant reductions in LDL-cholesterol. However, there were no statistical comparisons between rosuvastatin and atorvastatin in terms of efficacy.14

Paoletti and colleagues compared rosuvastatin to pravastatin and simvastatin over a 12-week period. They concluded that rosuvastatin was more effective than pravastatin and simvastatin at reaching the primary endpoints. The 20 mg/day pravastatin dose was comparatively lower than pravastatin doses used in other investigations, and therefore a study limitation.15

The trials by Brown and Olsson in 2002 were designed similarly and investigated LDL-cholesterol reduction and target achievement after 12 weeks, and then instituted dosage increases until the LDL-target goals were achieved. The maximum dosage was 80 mg for rosuvastatin, atorvastatin, and simvastatin and 40 mg for pravastatin. Both studies concluded that rosuvastatin offered the greatest reduction in LDL-cholesterol levels and attainment of target goals.16,17

Davidson and colleagues compared rosuvastatin to atorvastatin in a placebo-controlled environment. This trial found significant differences in efficacy with rosuvastatin use, but the differences were relatively small with rosuvastatin 10 mg decreasing LDL-cholesterol by 43% and atorvastatin 10 mg decreasing it by 35%. The target goal of LDL-cholesterol was achieved in 11% more patients taking rosuvastatin versus atorvastatin.18

The last two trials that investigated rosuvastatin were across-the-dose comparison trials. Schneck and colleagues compared the dose ranges of rosuvastatin and atorvastatin (n=374) and demonstrated an 8.4% decrease in LDL-cholesterol with rosuvastatin in contrast to atorvastatin across equivalent dosages.19 A larger across-the-dose comparison by Jones and colleagues compared the dosage range of rosuvastatin and the most commonly used HMG-CoA RIs: atorvastatin, simvastatin, and pravastatin. This trial (n=2,431) had the primary endpoint of reduction in LDL-cholesterol. The percentages of LDL-cholesterol reduction after 6 weeks of treatment in this study are shown in Table 4, along with the changes in the additional lipid measurements of high-density lipoprotein (HDL) cholesterol, triglycerides, and total cholesterol. Analysis of the cholesterol reductions revealed that the largest decrease in LDL-cholesterol occurred with rosuvastatin treatment at equivalent doses. The reduction by rosuvastatin across-the-doses was 8.2% more than atorvastatin, 12 to 18% more than simvastatin, and 26% more than pravastatin. Additionally, rosuvastatin was more effective at increasing HDL-cholesterol levels and was significantly different across-the-dose range than pravastatin and simvastatin, and significant in comparison to atorvastatin at all doses except 10 mg. There was no difference in the reduction of triglycerides between rosuvastatin or atorvastatin usage, but significant reductions were found with rosuvastatin in comparison to pravastatin and simvastatin. Rosuvastatin also reduced total cholesterol 4.7% more than atorvastatin, 9 to 12.5% more than simvastatin, and 18.7% more than pravastatin across-the-doses. The actual clinical significance of these smaller lipid differences observed with rosuvastatin over the other therapies is not known, such as rosuvastatin increasing HDL-cholesterol by 1.3% versus atorvastatin and 3% versus simvastatin at equivalent doses.20 Additionally, evidence supporting rosuvastatin's ability to reduce the risk for CHD is not yet supported in the literature.1

Table 4. Results of Across-the-Dose Comparison Trial of Rosuvastatin, Atorvastatin, Simvastatin, and Pravastatin
Rosuvastatin Atorvastatin Simvastatin Pravastatin
LDL-Cholesterol (mg/dl)
10 mg -45.8 -36.8 -28.3 -20.1
20 mg -52.4 -42.6 -35.0 -24.4
40 mg -55.0 -47.8 -38.8 -29.7
80 mg N/A -51.1 -45.8 N/A
HDL-Cholesterol (mg/dl)
10 mg +7.7 +5.7 +5.3 +3.2
20 mg +9.5 +4.8 +6.0 +4.4
40 mg +9.6 +4.4 +5.2 +5.6
80 mg N/A +2.1 +6.8 N/A
Triglycerides (mg/dl)  
10 mg -19.8 -20.0 -11.9 -8.2
20 mg -23.7 -22.6 -17.6 -7.7
40 mg -26.1 -26.8 -14.8 -13.2
80 mg N/A -28.2 -18.2 N/A
Total Cholesterol (mg/dl)  
10 mg -32.9 -27.1 -20.3 -14.7
20 mg -37.6 -31.8 -25.7 -17.2
40 mg -40.2 -35.8 -27.9 -21.5
80 mg N/A -38.9 -32.9 N/A

Adapted from Jones P et al. Am J Cardiol 2003:92:152-60.

Drug-Drug Interactions

Since there is minimal metabolism via the CYP isoenzyme system, the potential for drug-drug interactions with rosuvastatin is minimal. The potential is much less than with the other medications in this class, except for pravastatin, which is metabolized through sulfation.

Drug-drug interactions have been investigated with rosuvastatin use among many of the common CYP-inhibiting and -inducing medications. According to product labeling, clinically significant interactions were identified with coadministration of cyclosporine [Neoral®] or gemfibrozil [Lopid®], which both increased concentrations of rosuvastatin, thereby requiring a decrease in rosuvastatin dose when administered concomitantly. In patients previously stabilized on warfarin [Coumadin®], the concurrent use of rosuvastatin increased patients' INRs. There are no current recommendations for empiric management of this drug-drug interaction; however, INR measurements should be obtained more frequently when rosuvastatin is added to warfarin therapy.

Concurrent use of warfarin with the other HMG-CoA RIs also has been documented to have the potential to increase the effects of warfarin, with the least documented interactions occurring with pravastatin and atorvastatin.21 Antacid use with aluminum and magnesium hydroxide combinations was also found to affect the concentration of rosuvastatin by decreasing levels; therefore, it is recommended to take these antacids at least 2 hours after rosuvastatin administration.11

Adverse Effects

Proteinuria has been observed in clinical trials evaluating rosuvastatin use. Physicians, nurses, and pharmacists need to be aware of this unique adverse effect. Evidence of proteinuria was most frequent in patients taking greater than or equal to 40 mg of rosuvastatin. Product labeling recommends that patients who experience unexplained persistent proteinuria have a dosage reduction, but currently there are no specific recommendations for monitoring proteinuria with rosuvastatin use. It would be reasonable to obtain a baseline urine dipstick test before initiating rosuvastatin and then periodically monitor patients for proteinuria along with the additional required HMG-CoA RI laboratory measurements of safety and efficacy. Monitoring should be done more frequently in patients who are at an increased risk for proteinuria, such as in those with diabetes, hypertension, or receiving an increased rosuvastatin dose.11

Rosuvastatin's other adverse drug reactions are similar to those associated with other HMG-CoA RIs. Adverse effects that occurred most commonly in patients receiving rosuvastatin therapy in comparison to placebo were myalgia, constipation, asthenia, abdominal pain, and nausea.11

Liver function tests should be performed with rosuvastatin at baseline, after 12 weeks of therapy, and periodically thereafter. Rosuvastatin should be discontinued if liver enzymes increase to three times the upper limit of normal (ULN), which occurred in clinical trials between the range of 0 to 0.4%.11 The current incidence of this liver enzyme elevation occurring with HMG-CoA RIs as a class is 1.5%.22

Elevated creatinine kinase (CK) levels, myopathy, and in rare cases, rhabdomyolysis have also been reported with rosuvastatin. Elevated CK of greater than ten times the ULN has been found to occur with 40 mg doses of rosuvastatin in 0.2 to 0.4% of patients. Additionally, myopathy, defined as increased levels of CK in addition to muscle aches, was reported in 0.1% of patients. The occurrence of rhabdomyolysis was only noted with 80 mg doses (not currently FDA-approved) of rosuvastatin in rare cases. The recommendation for management is discontinuation of rosuvastatin with any report of myopathy or elevated CK.11 It is also important to educate patients on the adverse effects of HMG-CoA RIs, which should increase the percentage of patients who self-report toxicities.11

Dosage and Administration

The FDA-approved dosage range of rosuvastatin is 5 to 40 mg daily, however the 40 mg dose should only be used in patients who do not reach their LDL-cholesterol goal with the 20 mg dosage. The recommended starting dose of rosuvastatin should be individualized to each patient, with an initial dose of 10 mg daily in most patients, administered with or without food. A 5 mg daily dose is recommended in patients 1) requiring less aggressive cholesterol reduction, 2) with renal impairment, 3) with concurrent use of cyclosporine, or 4) with predisposing risk factors for myopathy. In patients with higher LDL-cholesterol (>190 mg/dl) and in patients with homozygous familial hypercholesterolemia, the recommended starting dose of rosuvastatin is 20 mg.11

Pregnancy and Lactation

Rosuvastatin, in addition to all of the other HMG-CoA RIs, is classified as a pregnancy-risk category X. Category X is defined as studies in animals or human beings have demonstrated fetal abnormalities or there is evidence of fetal risk based on human experience or both, and the risk of the use of the drug in pregnant women clearly outweighs any possible benefit. Therefore, rosuvastatin is contraindicated in women who are or may become pregnant, and should only be administered to women of childbearing age if their ability to conceive is highly unlikely and they have been informed of the potential hazards.11

Additionally, it is unknown if rosuvastatin is excreted in human milk. Studies in lactating rats indicated that the levels of rosuvastatin in breast milk are three times higher than plasma levels, therefore, it is recommended for lactating women that either nursing or administration of rosuvastatin be discontinued.11


Select average costs of rosuvastatin 10 mg and other HMG-CoA RIs starting doses are listed in Table 5. The cost of rosuvastatin is comparable to the other agents; however, lovastatin and fluvastatin are the least expensive.

Table 5. Cost Comparison of the Recommended Starting Doses of the HMG-CoA RIs23-25
  Cost Per Tablet Cost Per 30 Tablets
Crestor® Rosuvastatin 10 mg $2.67 $80.00
Lipitor® Atorvastatin 10 mg $2.33 $70.00
Zocor® Simvastatin 20 mg $4.00 $120.00
Mevacor®/ Lovastatin* 20 mg $2.50/$1.50 $75.00/$45.00
Pravachol® Pravastatin 40 mg $4.16 $125.00
Lescol® Fluvastatin 40 mg $2.00 $60.00
Lescol XL® Fluvastatin 80 mg $2.33 $70.00

*Available generically


Rosuvastatin appears to be more efficacious at lowering LDL-cholesterol levels than atorvastatin and the other available HMG-CoA RIs. However, it has not been investigated if this difference decreases CHD events and mortality. The currently available HMG-CoA RIs, most specifically simvastatin6, pravastatin26, and lovastatin27 offer experience and literature to support CHD benefit with their use. Also, it is currently unknown if the further decrease in LDL-cholesterol of 8.2 to 8.4% by rosuvastatin will provide significantly better primary and secondary prevention of CHD. Rosuvastatin has potentially desirable pharmacologic and pharmacokinetic properties, making it a beneficial selection for cholesterol treatment in terms of hepatic selectivity, hydrophilicity, half-life, and biliary excretion. These properties potentially lead to increased efficacy as well as decreased adverse effects and drug interactions with rosuvastatin. The current place in therapy for rosuvastatin remains to be decided. Important issues which must be taken into consideration include the potential development of proteinuria and a significant drug interaction with warfarin, both of which may limit the use of rosuvastatin. It is clear, however, that rosuvastatin will be an option for the hyperlipidemic patient who requires aggressive reduction of LDL-cholesterol and cannot reach the recommended target goal with the current lipid-lowering therapies.


Rosuvastatin is currently a non-formulary medication that has not yet been requested for review by the Cleveland Clinic Foundation's Pharmacy and Therapeutics Committee.

The article's author and the CCF Drug Information Center would like to thank Michael A. Militello, Pharm.D., BCPS, for his input and review of this article.

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Copyright © 2000-2017 The Cleveland Clinic Foundation. All Rights Reserved.
Center for Continuing Education | 1950 Richmond Road, TR204, Lyndhurst, OH 44124