***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 — Statins reduce the rate of major cardiovascular events in high-risk patients , but their potential benefit as treatment for heart failure ( HF ) is less clear . Methods and Results — Patients ( n=10 001 ) with stable coronary disease were r and omized to treatment with atorvastatin 80 or 10 mg/d and followed up for a median of 4.9 years . A history of HF was present in 7.8 % of patients . A known ejection fraction < 30 % and advanced HF were exclusion criteria for the study . A predefined secondary end point of the study was hospitalization for HF . The incidence of hospitalization for HF was 2.4 % in the 80-mg arm and 3.3 % in the 10-mg arm ( hazard ratio , 0.74 ; 95 % confidence interval , 0.59 to 0.94 ; P=0.0116 ) . The treatment effect of the higher dose was more marked in patients with a history of HF : 17.3 % versus 10.6 % in the 10- and 80-mg arms , respectively ( hazard ratio , 0.59 ; 95 % confidence interval , 0.4 to 0.88 ; P=0.009 ) . Among patients without a history of HF , the rates of hospitalization for HF were much lower : 1.8 % in the 80-mg group and 2.0 % in the 10-mg group ( hazard ratio , 0.87 ; 95 % confidence interval , 0.64 to 1.16 ; P=0.34 ) . Only one third of patients hospitalized for HF had evidence of preceding angina or myocardial infa rct ion during the study period . Blood pressure was almost identical during follow-up in the treatment groups . Conclusions — Compared with a lower dose , intensive treatment with atorvastatin in patients with stable coronary disease significantly reduces hospitalizations for HF . In a post hoc analysis , this benefit was observed only in patients with a history of HF . The mechanism accounting for this benefit is unlikely to be due primarily to a reduction in interim coronary events or differences in blood pressure BACKGROUND We previously reported urinary podocytes to be a marker of glomerular injury . The aim of the present study was to determine whether cerivastatin , a newly developed , potent synthetic statin , affects proteinuria and urinary podocyte excretion in patients with chronic glomerulonephritis ( CGN ) . METHODS We r and omly assigned 40 normotensive hypercholesterolemic patients with CGN to receive either cerivastatin 0.15 mg/day ( n=20 ) or placebo ( n=20 ) . Subjects comprised 24 men and 16 women , with a mean age of 40.8+/-14.4 years ; 27 had IgA nephropathy and 13 had non-IgA proliferative glomerulonephritis . Treatment was continued for 6 months . Plasma total cholesterol , HDL-cholesterol , LDL-cholesterol and triglycerides , urinary protein excretion and the number of podocytes were measured before treatment and at 3 and 6 months after treatment . RESULTS After 6 months , a significant reduction in total cholesterol ( P<0.001 ) , LDL-cholesterol ( P<0.001 ) and triglycerides ( P<0.05 ) , and a significant increase in HDL-cholesterol ( P<0.001 ) were observed in the group treated with cerivastatin .  Urinary protein excretion decreased from 1.8+/-0.6 to 0.8+/-0.4 g/day , ( P<0.01 ) in this group , and urinary podocyte excretion decreased from 1.6+/-0.6 to 0.9+/-0.4 cells/ml ( P<0.01 ) . However , placebo showed little effect on these lipid levels , urinary protein excretion and urinary podocyte excretion . The differences between the cerivastatin group and the placebo group were significant ( cholesterol , P<0.001 ; LDL-cholesterol , P<0.001 ; triglycerides , P<0.05 ; HDL-cholesterol , P<0.001 ; urinary protein , P<0.01 ; and urinary podocytes , P<0.01 ) . CONCLUSION Statins such as cerivastatin may be beneficial for restoration of injured podocytes in patients with CGN and hypercholesterolaemia BACKGROUND The effects of cholesterol-lowering treatment with statins on mortality and risk of cancer beyond the usual 5 - 6-year trial periods are unknown . We extended post-trial follow-up of participants in the Sc and inavian Simvastatin Survival Study ( 4S ) to investigate cause-specific mortality and incidence of cancer 5 years after closure of the trial . METHODS 4S was a r and omised double-blind trial of simvastatin or placebo in patients with coronary heart disease , serum total cholesterol 5.5 - 8.0 mmol/L , and serum triglycerides 2.5 mmol/L or lower . The double-blind period lasted for a median of 5.4 years ( range for survivors 4.9 - 6.3 ) and ended in 1994 . After the trial , most patients in both groups received open-label lipid-lowering treatment . National registers were used to assess mortality and causes of death and cancer incidence in the original treatment groups for a median total follow-up time of 10.4 years ( range for survivors 9.9 - 11.3 ) . Analysis was by intention to treat . FINDINGS 414 patients originally allocated simvastatin and 468 assigned placebo  died during the 10.4-year follow-up ( relative risk 0.85 [ 95 % CI 0.74 - 0.97 ] , p=0.02 ) , a difference largely attributable to lower coronary mortality in the simvastatin group ( 238 vs 300 deaths ; 0.76 [ 0.64 - 0.90 ] , p=0.0018 ) . 85 cancer deaths arose in the simvastatin group versus 100 in the placebo group ( 0.81 [ 0.60 - 1.08 ] , p=0.14 ) , and 227 incident cancers were reported in the simvastin group versus 248 in the placebo group ( 0.88 [ 0.73 - 1.05 ] , p=0.15 ) . Incidence of any specific type of cancer did not rise in the simvastatin group . INTERPRETATION Simvastatin treatment for 5 years in a placebo-controlled trial , followed by open-label statin therapy , was associated with survival benefit over 10 years of follow-up compared with open-label statin therapy for the past 5 years only . No difference was noted in mortality from and incidence of cancer between the original simvastatin group and placebo group BACKGROUND The PREVEND IT investigated whether treatment targeted at lowering urinary albumin excretion ( UAE ) would reduce adverse cardiovascular events . We obtained extended follow-up data to approximately 10 years to investigate the long-term effects of fosinopril 20 mg and pravastatin 40 mg on cardiovascular outcomes in subjects with UAE > 15 mg per 24 hours . METHODS The original PREVEND IT consisted of 864 participants and 839 survivors after 4 years . For every survivor , the primary end point determined by the combined incidence of cardiovascular mortality and hospitalization for cardiovascular morbidity was registered in several national data bases and electronic hospital systems . RESULTS Mean total follow-up of the extended PREVEND IT was 9.5 years ( range 9.4 - 10.7 years ) . Four years of treatment with fosinopril was not associated with a reduction in the primary end point compared with placebo ( hazard ratio 0.87 , 95 % CI 0.61 - 1.24 [ P = .42 ] ) during long-term follow-up . After 9.5 years , subjects with a baseline UAE in the upper quintile ( > 50 mg/24 hours ) had a total event rate of 29.5 % and were at a higher risk for developing cardiovascular disease compared with less UAE ( hazard ratio 2.03 , 95 % CI 1.38 - 2.97 [ P ≤ .01 ] ) . In addition , 4 years of fosinopril treatment result ed in a risk reduction of 45 % ( 95 % CI 6%-75 % [ P = .04 ] ) in this group compared with placebo . Subjects originally assigned to pravastatin had no overall risk reduction in the primary end point ( P = .99 ) . CONCLUSIONS Elevated UAE is associated with increased cardiovascular mortality and morbidity after 9.5 years of follow-up , with a doubling of the risk if the UAE is > 50 mg per 24 hours . In this group , the benefits of 4-year treatment with fosinopril were sustained during posttrial follow-up for cardiovascular mortality and morbidity . We propose that UAE be used to estimate risk in the general population and that large clinical trials be design ed to confirm the hypothesis that angiotensin-converting enzyme-inhibitor treatment may be beneficial in patients with mildly elevated UAE despite the absence of other comorbidities Aims Patients with Type 2 diabetes have an elevated risk of stroke . The role of lipid levels and diabetes‐specific factors in risk prediction of stroke is unclear , and estimates of efficacy of lipid‐lowering therapy vary between trials . We examined predictors of stroke and the effect of atorvastatin on specific stroke subtypes in Type 2 diabetes in the Collaborative Atorvastatin Diabetes Study ( CARDS ) [ a trial of 2838 participants with mean low‐density lipoprotein cholesterol < 4.14 mmol/l , no history of macrovascular disease and r and omized to atorvastatin 10 mg daily or placebo ] Background —Therapeutic decisions regarding pharmacological therapy should be based on safety and tolerability as well as efficacy data . Clinical trials design ed to assess efficacy are often insufficiently powered to generate reliable safety data . Methods and Results —The West of Scotl and Coronary Prevention Study ( WOSCOPS ) , the Cholesterol and Recurrent Events ( CARE ) , and Long-term Intervention with Pravastatin in Ischemic Disease ( LIPID ) studies collectively accumulated > 112 000 person-years of exposure in double-blind r and omized trials comparing  placebo and pravastatin ( 40 mg once daily ) . During 5 years of exposure , the incidence of fatal and nonfatal cancers was similar between pravastatin and placebo groups . No differences in noncardiovascular serious adverse events were detected . With > 243 000 blood sample analyses , the percentage of patients with any abnormal liver function test after baseline sampling was similar ( > 3 × the upper limit of normal for alanine aminotransferase : 128 [ 1.4 % ] versus 131 [ 1.4 % ] patients for pravastatin versus placebo , respectively ) . Study medication was withdrawn in 3 pravastatin and 7 placebo patients due to creatine phosphokinase elevations ; no cases of mild or severe myopathy were reported . A Cox regression model considering treatment group , age , diabetes , smoking , whether primary or secondary prevention study , and cardiovascular serious adverse events indicates that the likelihood of discontinuing pravastatin was less than placebo . Conclusions —This prospect i ve analysis indicates that during prolonged exposure , 40 mg of pravastatin is well tolerated , with no excess of noncardiovascular serious adverse events , including liver function abnormalities and laboratory and clinical evidence for myositis . These extensive safety and tolerability data provide important information for therapeutic decisions regarding this pharmacological agent BACKGROUND Although patients with chronic kidney disease ( CKD ) are at increased risk of cardiovascular disease ( CVD ) , the roles of lipid-modifying therapies in decreasing CVD risk are unclear . Our aim is to compare the effects of statin and fibrate therapy on arterial function as a risk marker of CVD . STUDY DESIGN Double-blind , r and omized , placebo-controlled , parallel-group study . SETTING & PARTICIPANTS Ambulatory patients with stages 3 to 5 CKD . INTERVENTION 6 weeks of atorvastatin , 40 mg/d , or gemfibrozil , 600 mg twice daily , with placebo . OUTCOMES & MEASUREMENTS Primary outcome was arterial function assessed by means of endothelial-dependent flow-mediated dilatation ( FMD ) and small-artery compliance ( C2 ) . Secondary outcomes included endothelial-independent glyceryl trinitrate-mediated dilatation ( GTNMD ) , large-artery compliance ( C1 ) , and levels of lipids , lipoproteins , and oxidized low-density lipoprotein , as well as markers of insulin resistance and inflammation . RESULTS Compared with placebo , atorvastatin significantly decreased low-density lipoprotein ( -52 % ) , triglyceride ( -30 % ) , and oxidized low-density lipoprotein levels ( -41 % ; P < 0.0001 ) . Gemfibrozil significantly decreased triglyceride levels ( -40 % ) and increased high-density lipoprote 
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Statins had uncertain effects on stroke ( 5 studies , 8658 participants ; RR 0.62 , 95 % CI 0.35 to 1.12).Potential harms from statin therapy were limited by lack of systematic reporting and were uncertain in analyses that had few events : elevated creatine kinase ( 7 studies , 4514 participants ; RR 0.84 , 95 % CI 0.20 to 3.48 ) , liver function abnormalities ( 7 studies , RR 0.76 , 95 % CI 0.39 to 1.50 ) , withdrawal due to adverse events ( 13 studies , 4219 participants ; RR 1.16 , 95 % CI 0.84 to 1.60 ) , and cancer ( 2 studies , 5581 participants ; RR 1.03 , 95 % CI 0.82 to 130).Statins had uncertain effects on progression of CKD .
Statins clearly reduced risks of death , major cardiovascular events , and MI in people with CKD who did not have CVD at baseline ( primary prevention ) .
Statins consistently lower death and major cardiovascular events by 20 % in people with CKD not requiring dialysis .
Statin-related effects on stroke and kidney function were found to be uncertain and adverse effects of treatment are incompletely understood .
Statins have an important role in primary prevention of cardiovascular events and mortality in people who have CKD