***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: OBJECTIVES The objective of this study was to examine whether statin therapy is associated with enhanced endothelium-dependent vascular function , improved pulmonary function and reduced systemic inflammation in patients with chronic obstructive pulmonary disease ( COPD ) . DESIGN AND SETTING This r and omized , placebo-controlled , double-blind , parallel trial including patients with COPD was performed at two University hospitals in Norway . SUBJECTS , INTERVENTION AND MEASUREMENTS Patients with stable COPD ( n = 99 ) were assigned r and omly to receive rosuvastatin 10 mg ( n = 49 ) or matching placebo ( n = 50 ) once daily for 12 weeks . The primary outcome measure was change in endothelium-dependent vascular function measured using peripheral arterial tonometry and expressed as the reactive hyperaemia index . Secondary end-points were change in pulmonary function , as assessed by forced expiratory volume in 1 s ( FEV1 ) and FEV1/forced vital capacity ( FVC ) , and change in the circulating levels of the inflammatory markers interleukin-6 ( IL6 ) and high-sensitivity C-reactive protein ( hsCRP ) . RESULTS In the overall study population , no significant between-group difference in change in endothelium-dependent vascular or pulmonary function was observed . Rosuvastatin therapy was associated with a reduction in hsCRP ( -20 % vs. 11 % , P = 0.017 ) and an attenuation of the rise in IL6 concentration ( 8 % vs. 30 % , P = 0.028 ) compared with placebo . In a prespecified subgroup analysis of patients with a supra-median circulating hsCRP concentration ( > 1.7 mg L(-1 ) ) , rosuvastatin was associated with improved endothelium-dependent vascular function ( 13 % vs. 2 % , P = 0.026 ) . CONCLUSIONS In stable COPD patients without the st and ard indications for statin therapy  , rosuvastatin treatment is associated with a significant attenuation of systemic inflammation and improvement in endothelial-dependent vascular function in patients with evidence of systemic inflammation Inflammation is increased in chronic obstructive pulmonary disease ( COPD ) and plays a role in exercise intolerance . We investigated whether pravastatin administration is effective in improving exercise capacity in patients with COPD , and whether baseline or serial changes in high-sensitivity C-reactive protein ( hs-CRP ) over time are associated with corresponding changes in exercise capacity . In a r and omized , double-blinded , and parallel design , 125 patients with clinical ly stable COPD were r and omly assigned to receive placebo or pravastatin ( 40 mg/day ) over a period of 6 months . Plasma hs-CRP levels were measured before r and omization and during follow-up . Baseline characteristics were similar in the 2 groups . Exercise time remained stable throughout the study in the placebo group . Exercise time increased by 54 % from 599 + /- 323 seconds at baseline to 922 + /- 328 seconds at the end ( p < 0.0001 ) in pravastatin-treated patients . A decrease in hs-CRP over baseline values was observed in 79 % of patients ( 42 of 53 ) treated with pravastatin . Pravastatin-treated patients with a greater percent decrease in hs-CRP had a significant improvement in exercise time compared with those without hs-CRP decrease . A significant correlation was found in univariate analysis between decrease of log-transformed hs-CRP and increase of exercise time . Baseline hs-CRP and change of hs-CRP were significantly correlated with exercise time , even after adjustment for lipid profiles and hemodynamics . In conclusion , these data reinforce hs-CRP as a significant surrogate marker in COPD and underscore an important guide to the efficacy of treatment in COPD trials Objectives : Chronic obstructive pulmonary disease ( COPD ) is more prevalent in HIV-infected individuals and is associated with persistent inflammation . Therapies unique to HIV are lacking . We performed a pilot study of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor rosuvastatin to determine effects on lung function . Design : R and omized , placebo-controlled , triple-blinded trial . Methods : HIV-infected individuals with abnormal lung function were recruited from an ongoing lung function study . Participants were r and omized to 24 weeks of placebo  ( n = 11 ) or rosuvastatin  ( n = 11 ) using an adaptive r and omization based on change in peripheral C-reactive protein levels at 30 days of treatment . Forced expiratory volume in 1 s ( FEV1 ) and diffusing capacity for carbon monoxide (DLco)%-predicted were compared to baseline at 24 weeks in the two groups using a Wilcoxon rank-sum test . The % -predicted change at 24 weeks in pulmonary function variables was compared between groups using simulated r and omization tests . Results : The placebo group experienced a significant decline in FEV1%-predicted ( P = 0.027 ) , and no change in DLco%-predicted over 24 weeks . In contrast , FEV1%-predicted remained stable in the rosuvastatin group , and DLco%-predicted increased significantly ( P = 0.027 ) . There was no significant difference in absolute change in either measure between placebo and rosuvastatin groups . Conclusion : In a pilot study , the use of rosuvastatin for 24 weeks appeared to slow worsening of airflow obstruction and to improve DLco in HIV-infected individuals with abnormal lung function , although comparison of absolute changes between the groups did not reach significance . This study is the first to test a therapy for COPD in an HIV-infected population , and large-scale clinical trials are needed OBJECTIVES Rising evidence s showed a possible protective role of statins in chronic obstructive pulmonary disease ( COPD ) . We aim ed to evaluate in a post-hoc analysis of the GISSI-HF trial the prognostic effect of the use of rosuvastatin in patients with co-existing COPD and HF , assuming that the anti-inflammatory properties of these drugs may imply a potential beneficial effect in these associated chronic inflammatory conditions . METHODS We analyzed patients with chronic HF and history of COPD deriving from the GISSI-HF study . Of all 4574 patients eligible to statin , 1060 ambulatory patients with HF and concomitant COPD were enrolled and r and omly assigned to rosuvastatin 10 mg daily ( 538 patients ) or placebo ( 522 patients ) . The primary end-point was to compare all cause death rate in patients r and omized to rosuvastatin or placebo . Further , we assessed the effects of rosuvastatin ( 10 mg daily ) on cardiovascular ( CV ) death , non-CV death and hospital admissions . Median follow-up was 3.9 years with an interquartile range ( IQR ) of 3.0 - 4.4 . RESULTS During the follow-up 438 ( 41.3 % ) patients died , 304 ( 28.6 % ) for CV death and 687 ( 64.8 % ) had at least one hospitalization . The two patient groups had similar outcome , irrespective of r and omization , in terms of all-cause mortality ( log-rank test p = 0.30 ) CV , non CV-death ( p = 0.88 and 0.09 respectively ) and all-cause hospitalization ( p = 0.82 ) . Cox regression analysis did not show a favorable association between the use of statin and the examined end-points both on unadjusted and adjusted models . CONCLUSIONS Statin use is not associated with a beneficial effects on all cause , CV , non CV mortality and hospitalization in patients with coexistent chronic HF and history of COPD . Clinical Trials.gov Identifier : NCT00336336 UNLABELLED Observational studies have suggested that statins may have beneficial effects on outcomes in chronic obstructive pulmonary disease ( COPD ) patients . These effects may be mediated through an anti-inflammatory effect of statins . The purpose of this pilot- study was to determine whether statins have an anti-inflammatory effect on the lungs of COPD patients . We conducted r and omized , controlled , parallel group pilot- study to compare the effects of  atorvastatin ( n=12 ) or placebo ( n=6 ) on lung inflammation in patients with mild to moderate COPD . The primary endpoint was change in CD45 + cells expression measured by immunohistochemistry and changes in expression of genes measured using microarrays in lung biopsy ( TBB ) sample s before and after 12 weeks of treatment with atorvastatin 40 mg/day . All subjects had spirometry , lung volumes , diffusing capacity of the lungs for carbon monoxide ( DLCO ) ,  St George 's Respiratory Question naire ( SGRQ )  , 6 minute walk distance ( 6 MWD ) , serum lipids , hs-CRP , induced sputum ( IS ) , bronchoscopy and TBB carried out at baseline and after treatment . TBB specimens were processed for histology , immunohistochemistry and genome-wide association studies ( GWAS ) profiling . Seventeen subjects completed the study . There was a significant improvement in SGRQ with mean SGRQ decreased by 12 points after treatment with atorvastatin ( P=0.012 ) . Atorvastatin treatment produced a significant 34 % reduction in sputum neutrophil count , and a 57 % reduction in CD45 + cells in lung biopsies ( expressed as integrated optical density -IOD ; median IOD 62.51 % before , 27.01 % after atorvastatin treatment , P=0.008 ) . In patients ' lung tissue atorvastatin treatment produced downregulation of key genes involved in inflammatory processes , immune response , and leukocyte activation . These data demonstrate the pulmonary anti-inflammatory effects of  atorvastatin in COPD patients with the potential for beneficial clinical effects . TRIAL REGISTRATION Clinical Trials.gov : NCT01748279 BACKGROUND Retrospective studies have shown that statins decrease the rate and severity of exacerbations , the rate of hospitalization , and mortality in chronic obstructive pulmonary disease ( COPD ) . We prospect ively studied the efficacy of simvastatin in preventing exacerbations in a large , multicenter , r and omized trial . METHODS We design ed the Prospect i ve R and omized Placebo-Controlled Trial of Simvastatin in the Prevention of COPD Exacerbations ( STATCOPE ) as a r and omized , controlled trial of simvastatin ( at a daily dose of 40 mg ) versus placebo , with annual exacerbation rates as the primary outcome . Patients were eligible if they were 40 to 80 years of age , had COPD ( defined by a forced expiratory volume in 1 second [ FEV1 ] of less than 80 % and a ratio of FEV1 to forced vital capacity of less than 70 % ) , and had a smoking history of 10 or more pack-years , were receiving supplemental oxygen or treatment with glucocorticoids or antibiotic agents , or had had an emergency department visit or hospitalization for COPD within the past year . Patients with diabetes or cardiovascular disease and those who were taking statins or who required statins on the basis of Adult Treatment Panel III criteria were excluded . Participants were treated from 12 to 36 months at 45 centers . RESULTS A total of 885 participants with COPD were enrolled for approximately 641 days ; 44 % of the patients were women . The patients had a mean ( ±SD ) age of 62.2±8.4 years , an FEV1 that was 41.6±17.7 % of the predicted value , and a smoking history of 50.6±27.4 pack-years . At the time of study closeout , the low-density lipoprotein cholesterol levels were lower in the simvastatin-treated patients than in those who received placebo . The mean number of exacerbations per person-year was similar in the simvastatin and placebo groups : 1.36±1.61 exacerbations and 1.39±1.73 exacerbations , respectively ( P=0.54 ) . The median number of days to the first exacerbation was also similar : 223 days ( 95 % confidence interval [ CI ] , 195 to 275 ) and 231 days ( 95 % CI , 193 to 303 ) , respectively ( P=0.34 ) . The number of nonfatal serious adverse events per person-year was similar , as well : 0.63 events with simvastatin and 0.62 events with placebo . There were 30 deaths in the placebo group and 28 in the simvastatin group ( P=0.89 ) . CONCLUSIONS Simvastatin at a daily dose of 40 mg did not affect exacerbation rates or the time to a first exacerbation in patients with COPD who were at high risk for exacerbations . ( Funded by the National Heart , Lung , and Blood Institute and the Canadian Institutes of Health Research ; STATCOPE Clinical Trials.gov number , NCT01061671 . ) Background : Statins have anti-inflammatory effects in patients with chronic obstructive pulmonary disease ( COPD ) . This study design 
    Output:
    
Statin treatment was associated with a larger improvement in exercise capacity , lung function , and St. George 's Respiratory Question naire score compared with placebo , but there were no statistically significant differences in inflammatory markers , all‐cause mortality , and safety outcomes ; however , subgroup analysis indicated that statin drugs improved clinical outcomes in the subjects from trials enrolling patients with overt cardiovascular disease ( CVD ) , elevated baseline C‐reactive protein levels , or a high cholesterol level .
: The findings from this systematic review suggest a role for statin drugs in patients with COPD and coexisting CVD , evidence of  increased systemic inflammation , or hyperlipidemia with respect to improving exercise tolerance and pulmonary function .