***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Many patients at high risk of cardiovascular disease do not achieve recommended low-density lipoprotein cholesterol ( LDL-C ) goals . This study compared the efficacy and safety of low doses of rosuvastatin ( 10 mg ) and atorvastatin ( 20 mg ) in high-risk patients with hypercholesterolemia . Methods A total of 996 patients with hypercholesterolemia ( LDL-C ≥ 3.4 and < 5.7 mmol/L [ 130 and 220 mg/dL ] ) and coronary heart disease ( CHD ) , atherosclerosis , or a CHD-risk equivalent were r and omized to once-daily  rosuvastatin 10 mg or atorvastatin 20 mg  . The primary endpoint was the percentage change from baseline in LDL-C levels at 6 weeks . Secondary endpoints included LDL-C goal achievement ( National Cholesterol Education Program Adult Treatment Panel III [ NCEP ATP III ] goal < 100 mg/dL ; 2003 European goal < 2.5 mmol/L for patients with atherosclerotic disease , type 2 diabetes , or at high risk of cardiovascular events , as assessed by a Systematic COronary Risk Evaluation ( SCORE ) risk ≥ 5 % or 3.0 mmol/L for all other patients ) , changes in other lipids and lipoproteins , cost-effectiveness , and safety . Results Rosuvastatin 10 mg reduced LDL-C levels significantly more than atorvastatin 20 mg at week 6 ( 44.6 % vs. 42.7 % , p < 0.05 ) . Significantly more patients achieved NCEP ATP III and 2003 European LDL-C goals  with rosuvastatin 10 mg compared with atorvastatin 20 mg ( 68.8 % vs. 62.5 % , p < 0.05 ; 68.0 % vs. 63.3 % , p < 0.05 , respectively ) . High-density lipoprotein cholesterol was increased significantly with rosuvastatin 10 mg versus atorvastatin 20 mg ( 6.4 % vs. 3.1 % , p < 0.001 ) . Lipid ratios and levels of apolipoprotein A-I also improved more with rosuvastatin 10 mg than with atorvastatin 20 mg . The use of rosuvastatin 10 mg was also cost-effective compared with atorvastatin 20 mg in both a US and a UK setting . Both treatments were well tolerated , with a similar incidence of adverse  events ( rosuvastatin 10 mg , 27.5 % ; atorvastatin 20 mg , 26.1 % ) . No cases of rhabdomyolysis , liver , or renal insufficiency were recorded . Conclusion In high-risk patients with hypercholesterolemia , rosuvastatin 10 mg was more efficacious than atorvastatin 20 mg at reducing LDL-C , enabling LDL-C goal achievement and improving other lipid parameters . Both treatments were well tolerated BACKGROUND In a multinational trial ( 4522IL/0081 ) , we assessed the effects of switching to low doses of rosuvastatin from commonly used doses of atorvastatin , simvastatin , and pravastatin on low-density lipoprotein cholesterol ( LDL-C ) goal achievement in high-risk patients . METHODS Hypercholesterolemic patients ( n = 3140 ) with coronary heart disease , atherosclerosis , or type 2 diabetes were r and omized to open-label rosuvastatin 10 mg , atorvastatin 10 or 20 mg , simvastatin 20 mg , or pravastatin 40 mg for 8 weeks . Patients either remained on these treatments for another 8 weeks or switched treatments from atorvastatin 10 mg , simvastatin 20 mg , and pravastatin 40 mg to rosuvastatin 10 mg or from atorvastatin 20 mg to rosuvastatin 10 or 20 mg . The primary efficacy measure was the proportion of patients reaching the Joint European Societies ' LDL-C goal ( < 116 mg/dL ) at week 16 . For measures of cholesterol goal achievement , treatment arms were compared using logistic-regression analysis . RESULTS Significant improvement in LDL-C goal achievement was found for patients who switched to rosuvastatin 10 mg , compared with patients who remained on atorvastatin 10 mg ( 86 % vs 80 % , P < .05 ) , simvastatin 20 mg ( 86 % vs 72 % , P < .0001 ) , and pravastatin 40 mg ( 88 % vs 66 % , P < .0001 ) , and between patients switched to rosuvastatin 20 mg and those who remained on atorvastatin 20 mg ( 90 % vs 84 % , P < .01 ) . Similar results were found for achievement of the European combined LDL-C and total cholesterol goals and National Cholesterol Education Program Adult Treatment Panel III LDL-C goals . All statins were well tolerated over 16 weeks . CONCLUSIONS We demonstrated that switching to a more efficacious statin is an effective strategy to improve lipid goal achievement in patients requiring lipid-lowering therapy Reduction of serum cholesterol levels with statin therapy decreases the risk of coronary heart disease . Inhibition of HMG-CoA reductase by statin results in decreased synthesis of cholesterol and other products downstream of mevalonate , which may produce adverse effects in statin therapy . We studied the reductions of serum ubiquinol-10 and ubiquinone-10 levels in hypercholesterolemic patients treated with atorvastatin . Fourteen patients were treated with 10 mg/day of atorvastatin  , and serum lipid , ubiquinol-10 and ubiquinone-10 levels were measured before and after 8 weeks of treatment . Serum total cholesterol and LDL-cholesterol levels decreased significantly . All patients showed definite reductions of serum ubiquinol-10 and ubiquinone-10 levels , and mean levels of serum ubiquinol-10 and ubiquinone-10 levels decreased significantly from 0.81 + /- 0.21 to 0.46 + /- 0.10 microg/ml ( p < 0.0001 ) , and from 0.10 + /- 0.06 to 0.06 + /- 0.02 microg/ml ( p = 0.0008 ) , respectively . Percent reductions of ubiquinol-10 and those of total cholesterol showed a positive correlation ( r = 0.627 , p = 0.0165 ) . As atorvastatin reduces serum ubiquinol-10 as well as serum cholesterol levels in all patients , it is imperative that physicians are forewarned about the risks associated with ubiquinol-10 depletion ABSTRACT Objective : Paraoxonase-1 ( PON-1 ) is a high-density lipoprotein ( HDL ) associated enzyme involved in the protective mechanisms of HDL . Our aim was to compare the effect of treatment with rosuvastatin and atorvastatin on serum PON-1 activity . Methods : We performed a prespecified prospect i ve study in 68 patients , part of a larger , multicentre r and omized study – RADAR  ( Rosuvastatin and Atorvastatin in different Dosages And Reverse cholesterol transport ) . Patients aged 40–80 years , all men , with established cardiovascular disease and high-density lipoprotein cholesterol ( HDL‑C ) < 1.0 mmol/L ( < 40 mg/dL ) entered a 6-week dietary run-in period before receiving treatment with rosuvastatin 10 mg or atorvastatin 20 mg daily for 6 weeks . Doses were increased after 6 weeks to rosuvastatin 20 mg or atorvastatin 40 mg and after 12 weeks to rosuvastatin 40 mg or atorvastatin 80 mg daily . Serum PON-1 activity and lipid profile were determined at baseline , 6 and 18 weeks . Results : After 18 weeks , the rosuvastatin arm showed a significant increase of PON-1 activity ( 6.39 U/L , p = 0.02 ) whereas this was not observed in the atorvastatin arm ( 1.84 U/L , p = 0.77 ) . The difference between groups did not reach significance ( p = 0.11 ) . Both rosuvastatin and atorvastatin result ed in significant ( p = 0.0001 ) and similar increases in HDL‑C after 6 weeks [ 0.06 mmol/L ( 2.32 mg/dL ) vs. 0.05 mmol/L ( 1.93 mg/dL ) ] and after 18 weeks [ 0.10 mmol/L ( 3.87 mg/dL ) vs. 0.10 mmol/L ( 3.87 mg/dL ) ] . Conclusions : Rosuvastatin treatment result ed in a significant increment of serum PON-1 activity with increasing dose while this was not observed with atorvastatin BACKGROUND Epidemiologic studies have shown that serum uric acid is a risk factor of coronary artery disease . In addition to fenofibrate , there is some evidence that atorvastatin may have a hypouricemic action , but the underlying mechanisms remain speculative . METHODS This r and omized trial was conducted to investigate the effects of atorvastatin and simvastatin on uric acid homeostasis in patients treated for primary hyperlipidemia . A total of 180 patients were enrolled ; patients were r and omly assigned to 40 mg/d of either atorvastatin or simvastatin .  Serum lipid and metabolic parameters were measured at baseline and at 6 and 12 weeks of treatment ; r and om urine sample s were simultaneously obtained for creatinine , sodium , and uric acid determinations . RESULTS Baseline serum uric acid levels correlated positively with the body mass index , serum insulin , creatinine , and triglyceride levels and inversely with serum HDL cholesterol levels . Both statins caused a favorable effect on lipids and a significant decrease in fibrinogen and high-sensitivity CRP levels . However , only atorvastatin reduced serum uric acid levels ( from 5.6 + /- 1.7 to 4.9 + /- 1.5 mg/dL , P < .0001 ) by augmenting its urinary fractional excretion ( from 10.4 % + /- 7.9 % to 12.0 % + /- 7.4 % , P < .01 ) . In a multivariate logistic regression analysis , the reduction of uric acid levels was independently associated with baseline serum uric acid concentration but not to other variables , including lipid parameters ( OR , 1.65 ; 95 % CI , 1.14 to 2.40 ; P = .008 ) . CONCLUSIONS Atorvastatin ( but not simvastatin ) significantly lowered serum uric acid levels . This result may be in favor of a preferable choice of atorvastatin for the treatment of hyperlipidemic patients presenting with hyperuricemia This 6-week , double-blind clinical trial evaluated lipid parameter responses to different dosages of atorvastatin in patients with primary hypercholesterolemia .  Atorvastatin is a new 3-hydroxy-3-methylglutaryl coenzyme A ( HMG-CoA ) reductase inhibitor under development . After completing an 8-week placebo-baseline dietary phase , 81 patients were r and omly assigned to receive either placebo or 2.5 , 5 , 10 , 20 , 40 , or 80 mg atorvastatin once daily for 6 weeks . Plasma LDL cholesterol reductions from baseline were dose related , with 25 % to 61 % reduction from the minimum dose to the maximum dose of 80 mg atorvastatin once a day . Plasma total cholesterol and apo B reductions were also dose related . Previously , reductions in LDL cholesterol of the magnitude observed in this study have been seen only with combination drug therapy . In this study , atorvastatin was well tolerated by hyperlipidemic patients , had an acceptable safety profile , and provided greater reduction in cholesterol than other previously reported HMG-CoA reductase inhibitors ABSTRACT Background : The ratio of low-density lipoprotein cholesterol and high-density lipoprotein cholesterol ( LDL‐C/HDL‐C ) is a reliable predictor of cardiovascular risk . Low HDL‐C levels in patients with coronary artery disease are associated with a high risk for cardiovascular events . Objectives : This study compared the effects of rosuvastatin and atorvastatin on the LDL‐C/HDL‐C ratio in patients with cardiovascular disease and low HDL‐C. Methods : Patients aged 40–80 years with established cardiovascular disease and HDL‐C < 1.0 mmol/L ( < 40 mg/dL ) entered a 6‐week di 
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Subgroup analyses suggested that the atorvastatin effect was greater in females than in males and was greater in non-familial than in familial hypercholesterolaemia .
Studies show that atorvastatin decreases blood total cholesterol and LDL-cholesterol in a linear dose-related manner over the commonly prescribed dose range .
New findings include that atorvastatin is more than three-fold less potent than rosuvastatin , and that the cholesterol-lowering effects of atorvastatin are greater in females than in males and greater in non-familial than in familial hypercholesterolaemia .