***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: Statin treatment in patients with coronary heart disease is associated with a reduced incidence of short-term adverse events and endpoint cardiac events . However , the effects of statin treatment on atherosclerotic plaques , particularly stable plaques , remain poorly defined . In total , 228 consecutive patients with stable atherosclerotic plaques who had undergone coronary arteriography ( CAG ) and intravascular ultrasound ( IVUS ) were r and omly assigned to receive placebo ( placebo group , n=54 ) or atorvastatin ( ATOR ) at a single daily dose of 10 mg ( ATOR 10 mg group , n=47 ) , 20 mg ( ATOR 20 mg group , n=45 ) , 40 mg ( ATOR 40 mg group , n=43 ) or 80 mg ( ATOR 80 mg group , n=39 ) . Endpoints , including serum lipids , serum inflammation , plaque volume and percentage of plaque necrosis were assessed after 3–6 months . At baseline , mean low-density lipoprotein ( LDL ) , high-density lipoprotein ( HDL ) and high-sensitivity C-reactive protein ( hs-CRP ) levels , as well as plaque volumes and percentages of plaque necrosis , were similar between all groups . At 6 months of follow-up , the LDL levels in the ATOR groups were below those at their respective baselines ( P<0.01 ) . HDL levels in the ATOR 80 mg group following treatment were significantly higher compared with baseline ( P=0.001 ) . Additionally , they were significantly higher compared with those in the placebo , ATOR 10 , 20 and 40 mg groups ( P<0.01 , P=0.001 , P=0.048 , P=0.047 , respectively ) . Hs-CRP levels in the placebo group following treatment were higher compared with baseline levels ( 6.87±2.62 vs. 5.07±1.80 , P<0.01 ) , but hs-CRP levels in the ATOR 80 mg group following treatment were lower compared with baseline ( 3.59±1.07 vs. 6.10±2.12 , P<0.01 ) . According to the virtual histology ( VH ) of IVUS , the percentages of plaque necrosis following treatment in the placebo and ATOR 10 mg groups rose above baseline levels ( 15.51±12.56 vs. 7.69±1.31 % , 13.54±11.76 vs. 7.83±1.43 % , P<0.01 ) and conformed to the diagnostic criteria for unstable plaques ( 15.51±12.56 , 13.54±11.76 % ) . By contrast , in the ATOR 20 , 40 and 80 mg groups , percentages of plaque necrosis remained stable following treatment compared with baseline ( P=0.069 , 0.846 and 0.643 , respectively ) . Plaque volumes following treatment in the placebo , ATOR 10 and 20 mg groups were similar to baseline levels . However , in the ATOR 40 and 80 mg groups , plaque volumes decreased following treatment compared with baseline plaque volumes ( 30.69±8.12 vs. 37.09±12.01 mm3 , 24.99±1.01 vs. 36.47±14.68 mm3 , P=0.019 , P<0.01 , respectively ) . ATOR ( 20 mg/day ) is able to lower LDL to st and ard levels while ATOR 40 mg/day was superior to 20 mg/day and had similar effects to 80 mg/day . Only ATOR 80 mg/day was able to increase HDL levels . Hs-CRP in patients without ATOR was higher and ATOR 80 mg/day decreased levels . ATOR ≥20 mg/day is able to stabilize plaques and ATOR 80 mg/day was superior to 20 and 40 mg/day . Thus , ATOR 40–80 mg/day reduces the volume of plaques Background —Recent clinical trials have demonstrated that aggressive lipid lowering by statins could prevent recurrent events after acute coronary syndrome ( ACS ) . We hypothesized that this efficacy was caused by a significant reduction in plaque volume by aggressive LDL cholesterol ( LCL-C ) lowering . The present study investigated the effect of early statin treatment on plaque volume of a nonculprit lesion by serial volumetric intravascular ultrasound in patients with ACS . Methods and Results —Seventy patients with ACS were enrolled . All patients underwent emergency coronary angiography and percutaneous coronary intervention ( PCI ) .  They were r and omized to intensive lipid-lowering therapy ( n=35 ; atorvastatin 20 mg/d ) or control ( n=35 ) groups after PCI . Volumetric intravascular ultrasound analyses were performed at baseline and 6-month follow-up for a non-PCI site in 48 patients ( atorvastatin , n=24 ; control , n=24 ) . LDL-C level was significantly decreased by 41.7 % in the atorvastatin group compared with the control group , in which LDL-C was increased by 0.7 % ( P<0.0001 ) . Plaque volume was significantly reduced in the atorvastatin group ( 13.1±12.8 % decrease ) compared with the control group ( 8.7±14.9 % increase ; P<0.0001 ) . Percent change in plaque volume showed a significant positive correlation with follow-up LDL-C level ( R=0.456 , P=0.0011 ) and percent LDL-C reduction ( R=0.612 , P<0.0001 ) , even in patients with baseline LDL-C < 125 mg/dL. Conclusions —Early aggressive lipid-lowering therapy by atorvastatin for 6 months significantly reduced the plaque volume in patients with ACS . Percent change in plaque volume showed a significant positive correlation with percent LDL-C reduction , even in patients with low baseline Purpose The aim of this study was to demonstrate the early effects of statin treatment on plaque composition according to plaque stability on Intravascular Ultrasound-Virtual Histology at 6 months after a coronary event . Previous trials have demonstrated that lipid lowering therapy with statins decreases plaque volume and increases plaque echogenicity in patients with coronary artery disease . Material s and Methods Fifty-four patients ( 54 lesions ) with acute coronary syndrome were prospect ively enrolled . We classified and analyzed the target plaques into two types according to plaque stability : thin-cap fibroatheroma ( TCFA , n=14 ) and non-TCFA ( n=40 ) . The primary end point was change in percent necrotic core in the 10-mm subsegment with the most disease . Results After 6 months of statin therapy , no change was demonstrated in the mean percentage of necrotic core ( 18.7±8.5 % to 20.0±11.0 % , p=0.38 ) . There was a significant reduction in necrotic core percentage in patients with TCFA ( 21.3±7.2 % to 14.4±8.9 % , p=0.017 ) , but not in patients with non-TCFA . Moreover , change in percent necrotic core was significantly correlated with change in high-sensitivity C-reactive protein levels ( r=0.4 , p=0.003 ) . Changes in low-density lipoprotein cholesterol levels and lipid core percentage demonstrated no significant associations . Conclusion A clear reduction of lipid core was observed only for the TCFA plaque type , suggesting that changes in plaque composition following statin therapy might occur earlier in vulnerable plaque than in stable plaque ; the effect may be related to the anti-inflammatory effects of statins CONTEXT Prior intravascular ultrasound ( IVUS ) trials have demonstrated slowing or halting of atherosclerosis progression with statin therapy but have not shown convincing evidence of regression using percent atheroma volume ( PAV ) , the most rigorous IVUS measure of disease progression and regression . OBJECTIVE To assess whether very intensive statin therapy could regress coronary atherosclerosis as determined by IVUS imaging . DESIGN AND SETTING Prospect i ve , open-label blinded end-points trial ( A Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound-Derived Coronary Atheroma Burden [ ASTEROID ] ) was performed at 53 community and tertiary care centers in the United States , Canada , Europe , and Australia . A motorized IVUS pullback was used to assess coronary atheroma burden at baseline and after 24 months of treatment . Each pair of baseline and follow-up IVUS assessment s was analyzed in a blinded fashion . PATIENTS Between November 2002 and October 2003 , 507 patients had a baseline IVUS examination and received at least 1 dose of study drug . After 24 months , 349 patients had evaluable serial IVUS examinations . INTERVENTION All patients received intensive statin therapy with rosuvastatin , 40 mg/d . MAIN OUTCOME MEASURES Two primary efficacy parameters were prespecified : the change in PAV and the change in nominal atheroma volume in the 10-mm subsegment with the greatest disease severity at baseline . A secondary efficacy variable , change in normalized total atheroma volume for the entire artery , was also prespecified . RESULTS The mean ( SD ) baseline low-density lipoprotein cholesterol ( LDL-C ) level of 130.4 ( 34.3 ) mg/dL declined to 60.8 ( 20.0 ) mg/dL , a mean reduction of 53.2 % ( P<.001 ) . Mean ( SD ) high-density lipoprotein cholesterol ( HDL-C ) level at baseline was 43.1 ( 11.1 ) mg/dL , increasing to 49.0 ( 12.6 ) mg/dL , an increase of 14.7 % ( P<.001 ) . The mean ( SD ) change in PAV for the entire vessel was -0.98 % ( 3.15 % ) , with a median of -0.79 % ( 97.5 % CI , -1.21 % to -0.53 % ) ( P<.001 vs baseline ) . The mean ( SD ) change in atheroma volume in the most diseased 10-mm subsegment was -6.1 ( 10.1 ) mm3 , with a median of -5.6 mm3 ( 97.5 % CI , -6.8 to -4.0 mm3 ) ( P<.001 vs baseline ) . Change in total atheroma volume showed a 6.8 % median reduction ; with a mean ( SD ) reduction of -14.7 ( 25.7 ) mm3 , with a median of -12.5 mm3 ( 95 % CI , -15.1 to -10.5 mm3 ) ( P<.001 vs baseline ) . Adverse events were infrequent and similar to other statin trials . CONCLUSIONS Very high-intensity statin therapy using rosuvastatin 40 mg/d achieved an average LDL-C of 60.8 mg/dL and increased HDL-C by 14.7 % , result ing in significant regression of atherosclerosis for all 3 prespecified IVUS measures of disease burden . Treatment to LDL-C levels below currently accepted guidelines , when accompanied by significant HDL-C increases , can regress atherosclerosis in coronary disease patients . Further studies are needed to determine the effect of the observed changes on clinical outcome . TRIAL REGISTRATION Clinical Trials.gov Identifier : NCT00240318 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 , initiated 24 to 96 hours after an acute coronary syndrome , reduces death and nonfatal ischemic events . DESIGN AND SETTING A r and omized , double-blind trial conducted from May 1997 to September 1999 , with follow-up through 16 weeks at 122 clinical centers in Europe , North America , South Africa , and Australasia . PATIENTS A total of 3086 adults aged 18 years or older with unstable angina or non-Q-wave acute myocardial infa rct ion . INTERVENTIONS Patients were stratified by center and r and omly assigned to receive treatment with atorvastatin ( 80 mg/d ) or matching placebo between 24 and 96 hours after hospital admission . MAIN OUTCOME MEASURES Primary end point event defined as death , nonfatal acute myocardial infa rct ion , cardiac arrest with resuscitation , or recurrent symptomatic myocardial ischemia with objective evidence and requiring emergency rehospitalization . RESULTS A primary end point event occurred in 228 patients ( 14.8 % ) in the atorvastatin group and 269 patients ( 17.4 % ) in the placebo group ( relative risk [ RR ] , 0.84 ; 95 % confidence interval [ CI ] , 0.70 - 1.00 ; P = .048 ) 
    Output:
    
Conclusions This meta- analysis indicates a significant effect of statin therapy  on plaque and external elastic membrane volumes and fibrous and dense calcium volumes .
There was no effect on lumen volume , fibro-fatty and necrotic tissue volumes