***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 —Whether marked LDL reduction to levels well below 100 mg/dL would further reduce the burden of cardiovascular disease is controversial . We compared the effects of 2 statins with widely differing potencies for LDL reduction  ( pravastatin 40 mg/d and atorvastatin 80 mg/d ) on carotid intima-media thickness ( CIMT ) . Methods and Results —This was a single-center , r and omized , clinical trial of 161 patients ( mean age , 60 years ; 71.4 % male ; 46 % with known cardiovascular disease ) that met National Cholesterol Education Program ( NCEP ) II criteria for lipid-lowering therapy . The effects of atorvastatin ( 80 mg/d ; n=79 ) and pravastatin ( 40 mg/d ; n=82 ) on CIMT were compared using blinded , serial assessment s of the far wall of the distal common carotid artery . Baseline CIMT and other characteristics were similar between study groups . As anticipated , atorvastatin was substantially more potent for LDL reduction after 12 months : in the atorvastatin group , LDL cholesterol was 76±23 mg/dL after 12 months ( −48.5 % ) ; LDL cholesterol was 110±30 mg/dL in the pravastatin group ( −27.2%;P < 0.001 ) . Atorvastatin  induced progressive CIMT regression over 12 months ( change in CIMT , −0.034±0.021 mm ) , whereas CIMT was stable in the pravastatin group ( change of 0.025± 0.017 mm;P = 0.03 ) . Conclusions —Marked LDL reduction ( < 100 mg/dL ) with a high-potency statin provides superior efficacy for atherosclerosis regression at 1 year . This early effect on CIMT , a surrogate for clinical benefit , suggests that marked LDL reduction  with synthetic statins may provide enhanced reduction in clinical coronary event rates Background and Purpose — Multifocal signal loss lesions ( MSLLs ) on T2 * -weighted gradient-echo ( GE ) MRI are believed to be microbleeds histopathologically . Previous epidemiological studies suggested that low serum cholesterol is associated with the increased risk of intracerebral hemorrhage . We investigated risk factors of MSLLs and the relationship between lipid profiles and MSLLs on GE-MRI . Methods — We included consecutively 172 patients who underwent brain MRI .  MSLLs on GE-MRI were counted by 2 neurologists separately and grade d by consensus . The concentrations of lipid profiles were categorized as quartiles , and the MSLLs were grade d as absent ( total count , 0 ) , mild ( 1 to 2 ) , moderate ( 3 to 10 ) , and severe ( > 10 ) . Results — The mean concentrations of total cholesterol and low-density lipoprotein cholesterol were significantly lower in patients with a severe degree of MSLLs than in those without MSLL ( P < 0.05 ) . By multivariate analysis , MSLLs were significantly correlated with hypertension ( odds ratio [ OR ] , 3.42 ; 95 % CI , 1.17 to 9.97 ) , leukoaraiosis ( OR , 4.62 ; 95 % CI , 2.87 to 7.41 ) , the lowest quartile of serum total cholesterol ( < 4.27 mmol/L ; OR , 10.91 ; 95 % CI , 3.98 to 25.57 ) , and the highest quartile of high-density lipoprotein ( > 1.47 mmol/L ; OR , 3.5 ; 95 % CI , 1.45 to 8.29 ) . Conclusions — Our results suggest that both the lipid profile levels and the severity of hypertension may be closely associated with MSLLs on GE-MRI The Pravastatin , Lipids , and Atherosclerosis in the Carotids trial ( PLAC-II ) was initiated in 1987 and is the first double-masked r and omized clinical trial with progression of early extracranial carotid atherosclerosis as an outcome variable . The trial will compare a lipid-lowering agent ( pravastatin , a hydroxymethylglutaryl CoA reductase inhibitor ) with placebo for ability to retard the rate of progression of extracranial carotid atherosclerosis over 3 years . Inclusion criteria consisted of prevalent coronary artery disease , moderately elevated low-density lipoprotein ( LDL ) cholesterol ( between the 60th and 90th percentiles ) , and the presence of at least one extracranial carotid artery atherosclerotic plaque that had an intimal-medial thickness ( IMT ) > or = 1.3 mm as visualized by B-mode ultrasound . Of approximately 650 patients who qualified on the basis of coronary disease and elevated LDL cholesterol , 55 % were excluded because of B-mode criteria . One hundred and fifty-one males and females 50 - 75 years of age were recruited . R and om allocation produced placebo-treated and test-treated groups that were similar for baseline historical data , physical findings , laboratory tests , lipid values , and B-mode characteristics . Baseline concentrations of plasma total cholesterol , LDL cholesterol , and high-density lipoprotein ( HDL ) cholesterol were 234 , 166 , and 41 mg/dl , respectively . Baseline plasma concentration of triglyceride was 170 mg/dl . Despite selection of participants whose arteries , overall , were suitable for the trial , individual segments in some participants could not be visualized . Ninety-seven percent of the individual carotid artery segments were visualized in the common carotid , 88 % in the bifurcation , and 63 % in the internal carotid artery . Far walls were slightly more often visualized than near walls , and nonvisualization was most common for the near wall of the internal carotid . Nonvisualized segments were comparable between both treatment groups . The distribution of arterial walls with qualifying plaque of > or = 1.3 mm IMT was similar for the two groups , and the two groups were also comparable for the primary outcome determinant , mean maximum IMT ( mean of maximum of all visualizable sites , 1.32 mm for each treatment group ) . There are special problems related to recruitment and evaluation of patients for a clinical trial such as this , but the atherosclerosis outcome measurement markedly enhances power and compensates for difficulty in recruitment BACKGROUND Although statins reduce coronary and cerebrovascular morbidity and mortality in middle-aged individuals , their efficacy and safety in elderly people is not fully established . Our aim was to test the benefits of pravastatin treatment in an elderly cohort of men and women with , or at high risk of developing , cardiovascular disease and stroke . METHODS We did a r and omised controlled trial in which we assigned 5804 men ( n=2804 ) and women ( n=3000 ) aged 70 - 82 years with a history of , or risk factors for , vascular disease to pravastatin ( 40 mg per day ; n=2891 ) or placebo ( n=2913 ) . Baseline cholesterol concentrations ranged from 4.0 mmol/L to 9.0 mmol/L. Follow-up was 3.2 years on average and our primary endpoint was a composite of coronary death , non-fatal myocardial infa rct ion , and fatal or non-fatal stroke . Analysis was by intention-to-treat . FINDINGS Pravastatin lowered LDL cholesterol concentrations by 34 % and reduced the incidence of the primary endpoint to 408 events compared with 473 on placebo ( hazard ratio 0.85 , 95 % CI 0.74 - 0.97 , p=0.014 ) . Coronary heart disease death and non-fatal myocardial infa rct ion risk was also reduced ( 0.81 , 0.69 - 0.94 , p=0.006 ) . Stroke risk was unaffected ( 1.03 , 0.81 - 1.31 , p=0.8 ) , but the hazard ratio for transient ischaemic attack was 0.75 ( 0.55 - 1.00 , p=0.051 ) . New cancer diagnoses were more frequent on pravastatin than on placebo ( 1.25 , 1.04 - 1.51 , p=0.020 ) . However , incorporation of this finding in a meta- analysis of all pravastatin and all statin trials showed no overall increase in risk . Mortality from coronary disease fell by 24 % ( p=0.043 ) in the pravastatin group . Pravastatin had no significant effect on cognitive function or disability . INTERPRETATION Pravastatin given for 3 years reduced the risk of coronary disease in elderly individuals . PROSPER therefore extends to elderly individuals the treatment strategy currently used in middle aged people Drug therapy for hypercholesterolaemia has remained controversial mainly because of insufficient clinical trial evidence for improved survival . The present trial was design ed to evaluate the effect of cholesterol lowering with simvastatin on mortality and morbidity in patients with coronary heart disease ( CHD ) . 4444 patients with angina pectoris or previous myocardial infa rct ion and serum cholesterol 5.5 - 8.0 mmol/L on a lipid-lowering diet were r and omised to double-blind treatment with simvastatin or placebo . Over the 5.4 years median follow-up period , simvastatin produced mean changes in total cholesterol , low-density-lipoprotein cholesterol , and high-density-lipoprotein cholesterol of -25 % , -35 % , and + 8 % , respectively , with few adverse effects . 256 patients ( 12 % ) in the placebo group died , compared with 182 ( 8 % ) in the simvastatin group . The relative risk of death in the simvastatin group was 0.70 ( 95 % CI 0.58 - 0.85 , p = 0.0003 ) . The 6-year probabilities of survival in the placebo and simvastatin groups were 87.6 % and 91.3 % , respectively . There were 189 coronary deaths in the placebo group and 111 in the simvastatin group ( relative risk 0.58 , 95 % CI 0.46 - 0.73 ) , while noncardiovascular causes accounted for 49 and 46 deaths , respectively . 622 patients ( 28 % ) in the placebo group and 431 ( 19 % ) in the simvastatin group had one or more major coronary events . The relative risk was 0.66 ( 95 % CI 0.59 - 0.75 , p < 0.00001 ) , and the respective probabilities of escaping such events were 70.5 % and 79.6 % . This risk was also significantly reduced in subgroups consisting of women and patients of both sexes aged 60 or more . Other benefits of treatment included a 37 % reduction ( p < 0.00001 ) in the risk of undergoing myocardial revascularisation procedures . This study shows that long-term treatment with simvastatin is safe and improves survival in CHD patients BACKGROUND Elevated levels of C-reactive protein , even in the absence of hyperlipidemia , are associated with an increased risk of coronary events . Statin therapy reduces the level of C-reactive protein independently of its effect on lipid levels . We hypothesized that statins might prevent coronary events in persons with elevated C-reactive protein levels who did not have overt hyperlipidemia . METHODS The level of C-reactive protein was measured at base line and after one year in 5742 participants in a five-year r and omized trial of lovastatin for the primary prevention of acute coronary events . RESULTS The rates of coronary events increased significantly with increases in the base-line levels of C-reactive protein . Lovastatin therapy reduced the C-reactive protein level by 14.8 percent ( P<0.001 ) , an effect not explained by lovastatin-induced changes in the lipid profile . As expected , lovastatin was effective in preventing coronary events in participants whose base-line ratio of total cholesterol to high-density lipoprotein ( HDL ) cholesterol was higher than the median ratio , regardless of the level of C-reactive protein ( number needed to treat for five years to prevent 1 event , 47 ; P=0.005 ) . However , lovastatin was also effective among those with a ratio of total to HDL cholesterol that was lower than the median and a C-reactive protein level higher than the median ( number needed to treat , 43 ; P=0.02 ) . In contrast , lovastatin was ineffective among participants with a ratio of total to HDL cholesterol and a C-reactive protein level that were both lower than the median ( number needed to treat , 983 ; P=0.80 ) . CONCLUSIONS Statin therapy may be effective in the primary prevention of coronary events among subjects with relatively low lipid levels but with elevated levels of C-reactive protein CONTEXT Patients experience the highest rate of death and recurrent ischemic events during the early period after an acute coronary syndrome , but it is not known whether early initiation of treatment with a statin can reduce the occurrence of these early events . OBJECTIVE To determine whether treatment with atorvastatin , 80 mg/d , 
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Statin size effect was closely associated with LDL-C reduction .
Statins may reduce the incidence of all strokes without any increase in hemorrhagic strokes , and this effect is mainly driven by the extent of between-group LDL-C reduction .
Carotid IMT progression also strongly correlated with LDL-C reduction