***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: Investigational product : Rosuvastatin ( Crestor ® ; Astra Zeneca ) . Active ingredients : Rosuvastatin ( 5 mg ) . Study title : Prevention of Atherosclerosis in Patients Living with HIV . Phase of study : Phase III . Aims : Primary aim : To assess whether rosuvastatin therapy could slow the progression of the carotid intima-media thickness ( C-IMT ; as measured by the change in the mean IMT of the near and far walls of the distal common carotid arteries ) over 2 years in HIV-infected patients ( HIV-IP ) . Secondary aims : To assess whether rosuvastatin therapy could reduce highly sensitive C reactive protein ( hs-CRP ) inflammatory marker that is increased in HIV-IP . To assess the effect of rosuvastatin therapy on serum lipid levels ( total cholesterol [ TC ] , low-density lipoprotein [ LDL ] cholesterol , high-density lipoprotein [ HDL ] cholesterol and triglycerides [ TG ] ) and apolipoproteins ( APO A1 , APO B and APO B/A1 ) . To assess the safety of rosuvastatin in HIV-IP through the evaluation of clinical laboratory analyses ( liver function tests and creatine kinase ) and adverse events ( AEs ) . Study design : Two-year r and omized , double-blind , placebo-controlled , parallel group study . Planned sample size : 320 HIV-IP . Summary of eligibility criteria : HIV-IP who are aged between 30 and 60 years , with a CD4 count . greater than 200 cells/mm3 . Patients must be stable on combination antiretroviral therapy ( cART ) for at least 12 months and have a 10-year CVD risk of less than 20 % ( using the Framingham risk score ) . Number of study centers : One . Duration of treatment : Two years ( 5 mg rosuvastatin or placebo once daily ) . Dose and route of administration : Oral rosuvastatin ( 5 mg ) once daily . The incidence of cardiovascular disease ( CVD ) in HIV-IP is at least three times higher than in the general population and further increases each year with combination anti-retroviral therapy ( cART ) . The carotid atherosclerosis progression rate is 10 times higher in HIV-IP than in uninfected individuals . The aim of this study is to assess whether therapy with 5 mg rosuvastatin could : 1 ) Slow the progression in the mean IMT of the distal common carotid arteries over two years in HIV-IP . 2 ) Change the concentration in the inflammatory marker – hs-CRP , which is increased in HIV-IP . 3 ) Change the concentrations of TC , LDL cholesterol , HDL cholesterol , TG , apolipoproteins ( APO ) B , APO A1 and APO B/A1 . 4 ) Be administered safely in the study population . Pharmacological intervention with rosuvastatin will be evaluated in a double-blind , placebo-controlled , r and omized clinical trial in HIV-IP treated with cART not matching the published selection criteria for lipid-lowering therapy . For the first time , this study will investigate anti-inflammatory and anti-atherogenic effects of a pharmacological lipid-lowering agent in HIV-IP that may lead to the reduction of CVD Background : Instability of carotid plaques has been reported to be associated with stroke and other cerebrovascular events . The purpose of this study was to examine whether cholesterol-lowering therapy with atorvastatin in nonhypercholesterolemic patients reduces carotid plaque instability as assessed by ultrasound integrated backscatter ( IBS ) analysis . Methods : Consecutive non- or slightly hypercholesterolemic patients with moderate carotid artery stenosis were r and omly assigned to a diet group ( n = 20 ) or a statin group ( atorvastatin ; n = 20 ) . Carotid plaques were monitored by measuring intima media thickness ( IMT ) and IBS values at baseline and after 6 months . Results : Three-dimensional IBS imaging showed that relative lipid volume of carotid plaques significantly decreased from 58.4 ± 25.6 to 47.8 ± 23.5 % in the statin group ( p < 0.01 ) , whereas there was no significant decrease in the diet group . Significant regression of IMT was not observed in either group . The changes of IBS values and relative lipid volume between baseline and 6 months were correlated with the change in low-density lipoprotein cholesterol ( r = 0.31 , p < 0.05 , and r = 0.34 , p < 0.05 , respectively ) . Conclusions : Lipid-lowering therapy by atorvastatin decreased relative lipid volume without significant regression of plaque volume during short-term follow-up in patients with moderate carotid artery stenosis . Quantitative assessment of carotid plaques by IBS analysis was clinical ly useful for monitoring atherosclerotic lesions OBJECTIVE Carotid intima media thickness ( IMT ) is a good indicator of the severity of atherosclerotic disease . Statins have been found to reduce carotid IMT in patients with hypercholesterolaemia . The aim of this study was to investigate if pravastatin is effective in reducing IMT in normocholesterolaemic patients with carotid artery disease . METHODS Patients with carotid artery stenosis and normal cholesterol levels who were not on a statin , were recruited . Patients were r and omised to receive pravastatin or placebo daily . Serum concentration of cholesterol and IMT of common carotid arteries were measured before r and omisation and at 3 monthly intervals thereafter , for 9 months . IMT was analysed to give the mean of a st and ardised 2 cm of the common carotid artery ( CCA ) . Results are expressed as median ( IQR ) and comparison made using the Wilcoxon signed ranks test . RESULTS Fifty-four patients were examined . Twenty-eight patients were r and omised to active treatment . There was no difference in demographic details and co-morbid states between the two groups . A significant reduction in cholesterol concentration was observed from 3 months in patients r and omised to the pravastatin group [ 5.14(4.72 - 5.88 ) vs. 4.11(3.44 - 5.33 ) , p < 0.05 ] , while there was also a significant decrease in combined IMT form 6 months [ 1.53(1.36 - 1.87 ) vs. 1.41 ( 1.33 - 1.78 ) , p < 0.05 ] . CONCLUSIONS The results demonstrate that pravastatin reduces intima media thickness of the common carotid artery in normocholesterolaemic patients with moderate carotid stenosis CONTEXT Atherosclerosis is often advanced before symptoms appear and it is not clear whether treatment is beneficial in middle-aged individuals with a low Framingham risk score ( FRS ) and mild to moderate sub clinical atherosclerosis . OBJECTIVE To assess whether statin therapy could slow progression and /or cause regression of carotid intima-media thickness ( CIMT ) over 2 years . DESIGN , SETTING , AND PARTICIPANTS R and omized , double-blind , placebo-controlled study ( Measuring Effects on Intima-Media Thickness : an Evaluation of Rosuvastatin [ METEOR ] ) of 984 individuals , with either age ( mean , 57 years ) as the only coronary heart disease risk factor or a 10-year FRS of less than 10 % , modest CIMT thickening ( 1.2-<3.5 mm ) , and elevated LDL cholesterol ( mean , 154 mg/dL ) ; conducted at 61 primary care centers in the United States and Europe between August 2002 and May 2006 . INTERVENTION Participants received either a 40-mg dose of rosuvastatin or placebo . MAIN OUTCOME MEASURES Rate of change in maximum CIMT ( assessed with B-mode ultrasound ) for 12 carotid sites ; changes in maximum CIMT of the common carotid artery , carotid bulb , and internal carotid artery sites and in mean CIMT of the common carotid artery sites . CIMT regression was assessed in the rosuvastatin group only . RESULTS Among participants in the rosuvastatin group , the mean ( SD ) baseline LDL cholesterol level of 155 ( 24.1 ) mg/dL declined to 78 ( 27.5 ) mg/dL , a mean reduction of 49 % ( P<.001 vs placebo group ) . The change in maximum CIMT for the 12 carotid sites was -0.0014 ( 95 % CI , -0.0041 to 0.0014 ) mm/y for the rosuvastatin group vs 0.0131 ( 95 % CI , 0.0087 - 0.0174 ) mm/y for the placebo group ( P<.001 ) . The change in maximum CIMT for the rosuvastatin group was -0.0038 ( 95 % CI , -0.0064 to -0.0013 ) mm/y for the common carotid artery sites ( P<.001 ) , -0.0040 ( 95 % CI , -0.0090 to 0.0010 ) mm/y for the carotid bulb sites ( P<.001 ) , and 0.0039 ( 95 % CI , -0.0009 to 0.0088 ) mm/y for the internal carotid artery sites ( P = .02 ) . The change in mean CIMT for the rosuvastatin group for the common carotid artery sites was 0.0004 ( 95 % CI , -0.0011 to 0.0019 ) mm/y ( P<.001 ) . All P values are vs placebo group . Overall , rosuvastatin was well tolerated with infrequent serious adverse cardiovascular events ( 6 participants [ 0.86 % ] had 8 events [ 1.1 % ] over 2 years ) . CONCLUSIONS In middle-aged adults with an FRS of less than 10 % and evidence of sub clinical atherosclerosis  , rosuvastatin result ed in statistically significant reductions in the rate of progression of maximum CIMT over 2 years vs placebo . Rosuvastatin did not induce disease regression . Larger , longer-term trials are needed to determine the clinical implication s of these findings . TRIAL REGISTRATION clinical trials.gov Identifier : OBJECTIVE To establish the diagnostic criteria of intima-media thickening ( IMT ) of the carotid artery , femoral artery and thoracic aorta in normal subjects and evaluate the effects of drugs on IMT in patients with atherosclerosis with high-frequency ultrasound imaging . METHODS 259 normal subjects and 102 patients with atherosclerosis ( AS ) were studied . 134 normal subjects were examined by transesophegeal echocardiography . 102 patients with AS were r and omly divided into 4 groups : simvastatin group , probucol group , captopril group , and placebo group . The values of IMT , including IMT of the normal segment ( IMT(A ) ) and the maximal IMT of each artery ( IMT(B ) ) of the carotid and femoral arteries , and thoracic aorta , the mean maximal IMT of the 4 arteries ( IMT(C ) ) , and the single maximal IMT among the 4 arteries ( IMT(D ) ) were measured . The examinations were repeated in 3 years after treatments . RESULTS In carotid , and femoral arteries and thoracic aorta , IMT increased with aging . The IMT values of the carotid and femoral arteries and thoracic aorta were 0.63 mm + /- 0.15 mm , 0.68 mm + /- 0.21 mm , 1.02 mm + /- 0.22 mm respectively with the upper limits of 0.93 mm , 1.10 mm , and 1.46 mm respectively . IMT(A ) increased 0.023 mm per year . The progression value of IMT(D ) in all therapeutic groups were significantly lower than that of the control group ( all P < 0.05 ) . CONCLUSION It is suggested that the IMT > 0.93 mm , > 1.10 mm , and > 1.46 mm is be defined as indicators of IMT in carotid and femoral arteries and thoracic aorta respectively . Drug therapy can decrease the progression of atherosclerosis but has no effects on the IMT in normal segment of arteries . High frequency ultrasound technique is reliable in monitoring the progression or regression of atherosclerosis in peripheral arteries Controlled clinical trials to assess the effects of therapy for atherosclerosis have generally used either clinical cardiovascular events or serial arterial imaging as end points . Serial coronary angiographic assessment of lesion change has been the most commonly used end point in arterial imaging trials [ 1 ] . Evidence now indicates that high-resolution B-mode ultrasonographic measurement of the combined thickness of the carotid arterial intima-media complex is a reliable end point for lipid-lowering interventional trials [ 1 ] . Unlike angiographic imaging 
    Output:
    
Meta-regression analysis showed a significant association between changes in mean CCA-IMT with decreasing triglyceride levels .
A similar , but not statistically significant trend was also found between CCA-IMT decrease and the decrease in LDL-C levels or increase in HDL-C levels .
CONCLUSION Statin therapy is associated with a favorable decrease in CCA-IMT , an effect that seems to be mainly driven by the CCA-IMT at baseline and the extent of lipid decrease , specifically triglycerides