***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 
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    ***EXAMPLES*** 
    Input: Background : TORCH ( Towards a Revolution in COPD Health ) is an international multicentre , r and omised , placebo-controlled clinical trial of inhaled fluticasone propionate/salmeterol combination treatment and its monotherapy components for maintenance treatment of moderately to severely impaired patients with chronic obstructive pulmonary disease ( COPD ) . The primary outcome is all-cause mortality . Cause-specific mortality and deaths related to COPD are additional outcome measures , but systematic methods for ascertainment of these outcomes have not previously been described . Methods : A Clinical Endpoint Committee ( CEC ) was tasked with categorising the cause of death and the relationship of deaths to COPD in a systematic , unbiased and independent manner . The key elements of the operation of the committee were the use of predefined principles of operation and definitions of cause of death and COPD -relatedness ; the independent review of cases by all members with development of a consensus opinion ; and a substantial infrastructure to collect medical information . Results : 911 deaths were review ed and consensus was reached in all . Cause-specific mortality was : cardiovascular 27 % , respiratory 35 % , cancer 21 % , other 10 % and unknown 8 % . 40 % of deaths were definitely or probably related to COPD . Adjudications were identical in 83 % of blindly re-adjudicated cases ( κ = 0.80 ) . COPD -relatedness was reproduced 84 % of the time ( κ = 0.73 ) . The CEC adjudication was equivalent to the primary cause of death recorded by the site investigator in 52 % of cases . Conclusion : A CEC can provide st and ardised , reliable and informative adjudication of COPD mortality that provides information which frequently differs from data collected from assessment by site investigators OBJECTIVES We investigated whether plasma amino-terminal pro-brain natriuretic peptide ( NT-proBNP ) , a marker of cardiac dysfunction and prognosis measured in CORONA ( Controlled Rosuvastatin Multinational Trial in Heart Failure ) , could be used to identify the severity of heart failure at which statins become ineffective . BACKGROUND Statins reduce cardiovascular morbidity and mortality in many patients with ischemic heart disease but not , overall , those with heart failure . There must be a transition point at which treatment with a statin becomes futile . METHODS In CORONA , patients with heart failure , reduced left ventricular ejection fraction , and ischemic heart disease were r and omly assigned to 10 mg/day rosuvastatin or placebo . The primary composite outcome was cardiovascular death , nonfatal myocardial infa rct ion , or stroke . RESULTS Of 5,011 patients enrolled , NT-proBNP was measured in 3,664 ( 73 % ) . The midtertile included values between 103 pmol/l ( 868 pg/ml ) and 277 pmol/l ( 2,348 pg/ml ) . Log NT-proBNP was the strongest predictor ( per log unit ) of every outcome assessed but was strongest for death from worsening heart failure ( hazard ratio [ HR ] : 1.99 ; 95 % confidence interval [ CI ] : 1.71 to 2.30 ) , was weaker for sudden death ( HR : 1.69 ; 95 % CI : 1.52 to 1.88 ) , and was weakest for atherothrombotic events ( HR : 1.24 ; 95 % CI : 1.10 to 1.40 ) . Patients in the lowest tertile of NT-proBNP had the best prognosis and , if assigned to rosuvastatin rather than placebo , had a greater reduction in the primary end point ( HR : 0.65 ; 95 % CI : 0.47 to 0.88 ) than patients in the other tertiles ( heterogeneity test , p = 0.0192 ) . This reflected fewer atherothrombotic events and sudden deaths with rosuvastatin . CONCLUSIONS Patients with heart failure due to ischemic heart disease who have NT-proBNP values < 103 pmol/l ( 868 pg/ml ) may benefit from rosuvastatin Background Elevated plasma B-type natriuretic peptide ( BNP ) levels and their association with heart failure have been reported in subjects with acute exacerbations of chronic obstructive pulmonary disease ( AE COPD ) . Purpose To examine and compare plasma BNP levels and diastolic and systolic dysfunction in subjects with AE COPD and stable chronic obstructive pulmonary disease ( COPD ) . Methods In all , 87 unselected consecutive hospitalizations due to AE COPD in 61 subjects and a total of 190 consecutive subjects with stable COPD were recruited .  Plasma BNP levels  were compared cross-sectionally and longitudinally .  Transthoracic echocardiographic examinations were also performed in the hospitalized subjects . Results In the hospitalized subjects , the median plasma BNP level ( interquartile range ) was 55.4 ( 26.9–129.3 ) pg/mL and was higher than that of patients with stable COPD : 18.3 ( 10.0–45.3 ) for Global Initiative for Chronic Obstructive Lung Disease grade I ; 25.8 ( 11.0–53.7 ) for grade II ; 22.1 ( 9.1–52.6 ) for grade III ; and 17.2 ( 9.6–22.9 ) pg/mL for grade I V , all P<0.001 . In 15 subjects studied prospect ively , the median plasma BNP level was 19.4 ( 9.8–32.2 ) pg/mL before AE COPD , 72.7 ( 27.7–146.3 ) pg/mL during AE COPD , and 14.6 ( 12.9–39.0 ) pg/mL after AE COPD ( P<0.0033 and P<0.0013 , respectively ) . Median plasma BNP levels during AE COPD were significantly higher in ten unsuccessfully discharged subjects 260.5 ( 59.4–555.0 ) than in 48 successfully discharged subjects 48.5 ( 24.2–104.0 ) pg/mL ( P=0.0066 ) . Only 5.6 % of AE COPD subjects were associated with systolic dysfunction defined as a left ventricular ejection fraction ( LVEF ) < 50 % ; a further 7.4 % were considered to have impaired relaxation defined as an E/A wave velocity ratio < 0.8 and a deceleration time of E > 240 ms . BNP levels were weakly correlated with the E/peak early diastolic velocity of the mitral annulus ( Ea ) ratio ( Spearman ’s rank correlation coefficient = 0.353 , P=0.018 ) , but they were not correlated with the LVEF ( Spearman ’s rank correlation coefficient = −0.221 , P=0.108 ) . Conclusion A modest elevation of plasma BNP is observed during AE COPD . It appears that AE COPD may have an impact on plasma BNP levels that is not attributable to heart failure Background Cardiovascular disease is prevalent and frequently unrecognized in patients with chronic obstructive pulmonary disease ( COPD ) . NT-proBNP is an established risk factor in patients with heart failure . NT-proBNP may also be released from the right ventricle . Thus serum NT-proBNP may be elevated during acute exacerbations of COPD ( AE COPD ) . The prognostic value of NT-proBNP in patients hospitalized with AE COPD is sparsely studied . Our objective was to test the hypothesis that NT-proBNP independently predicts long term mortality following AE COPD . Methods A prospect i ve cohort study of 99 patients with 217 admissions with AE COPD .  Clinical , electrocardiographic , radiological and biochemical data were collected at index and repeat admissions and analyzed in an extended survival analysis with time-dependent covariables . Results Median follow-up time was 1.9 years , and 57 patients died during follow-up . NT-proBNP tertile limits were 264.4 and 909 pg/mL , and NT-proBNP in tertiles 1 through 3 was associated with mortality rates of 8.6 , 35 and 62 per 100 patient-years , respectively ( age-adjusted log-rank p<0.0001 ) . After adjustment for age , gender , peripheral edema , cephalization and cTnT in a multivariable survival model , the corresponding hazard ratios for dying were 2.4 ( 0.95 - 6.0 ) and 3.2 ( 1.3 - 8.1 ) ( with 95 % confidence intervals in parentheses , p-value for trend 0.013 ) . Conclusions NT-proBNP is a strong and independent determinant of mortality after AE COPD Flaws in the design , conduct , analysis , and reporting of r and omised trials can cause the effect of an intervention to be underestimated or overestimated . The Cochrane Collaboration ’s tool for assessing risk of bias aims to make the process clearer and more BACKGROUND Brain natriuretic peptide ( BNP ) is associated with increased myocardial stretching . This study aims to assess the effect of mild diuretics on plasma BNP levels in patients with an acute exacerbation of chronic obstructive pulmonary disease ( COPD ) who have high plasma concentrations of BNP . METHODS Thirty consecutive patients with an acute exacerbation of COPD without any clinical evidence of cor pulmonale who had elevated plasma BNP concentrations ( group 1 ) and 15 patients with stable COPD as controls ( group 2 ) participated in this study . A mild diuretic treatment in addition to the st and ard treatment for an acute attack of COPD was r and omised to 15 patients in group 1 ( group 1A ) . The remaining patients in group 1 only took st and ard treatment for acute COPD exacerbation ( group 1B ) . Plasma BNP concentrations were measured on admission and repeated on the 5th and 10th days . RESULTS There was a significant decrease in plasma BNP concentrations , more striking in group 1A than 1B . Both in group 1A and 1B , the fall in plasma BNP concentrations was independent of either presence or absence of right ventricular dysfunction on echo evaluation . CONCLUSION Adding mild diuretics to the st and ard treatment for an acute attack of COPD may rapidly reduce plasma BNP levels in COPD patients with acute exacerbations who have high plasma BNP levels without any clinical evidence of cor pulmonale BACKGROUND Amino-terminal pro-brain natriuretic peptide ( NT-proBNP ) testing is useful for diagnosis or exclusion of heart failure ( HF ) in dyspneic patients .  Atrial fibrillation ( AF ) may cause dyspnea in the absence of acute HF and may also affect plasma levels of NT-proBNP . METHODS We prospect ively enrolled 599 patients presenting with dyspnea to the emergency department and obtained a blood sample for NT-proBNP measurement . The diagnosis of AF was identified via presentation electrocardiogram . A final diagnosis of HF was determined by blinded study physicians using all available hospital records for each subject through 60 days of follow-up . We assessed the association between the presence of  AF  and level of NT-proBNP in subsets of patients with and without HF . RESULTS Of 599 dyspneic patients , 75 ( 13 % ) were in AF at presentation ; these patients had significantly higher median NT-proBNP levels when compared with those without AF ( 2934 vs 294 pg/mL , P < .0001 ) . Among patients with acute HF , AF was present in 28 % ; NT-proBNP levels were lower in those with AF versus those without ( 3488 vs 4492 pg/mL , P < .001 ) , but AF was not independently associated with NT-proBNP after multivariable adjustment . In patients without acute HF , median NT-proBNP concentrations were significantly higher in those with AF than in those without ( 932 vs 121 pg/mL , P = .02 ) ; in these subjects , AF was the strongest predictor of an NT-proBNP concentration in a range consistent with acute HF ( odds ratio 9.94 , 95 % CI 2.97 - 33.3 , P < .001 ) . CONCLUSION Atrial fibrillation is associated with higher NT-proBNP concentrations in dyspneic patients , particularly in those without acute HF STUDY OBJECTIVES In dyspneic patients without left ventricular enlargement , it may be difficult to differentiate between obstructive lung disease and diastolic heart failure . Determination of  plasma brain natriuretic peptide ( BNP ) levels  , known to increase with ventricular stretch , may be of clinical relevance in this situation . We compared the discriminant power of BNP blood levels and of echocardiography in patients with either chronic obstructive lung disease or diastolic heart failure . PATIENTS Twenty-six New York Heart Association class III dyspneic patients with normal left ventricular systolic function were enrolled : 17 patients with chronic obstruct 
    Output:
    
NP levels were lower in stable compared to exacerbation of COPD , and significantly increased with concomitant left ventricular systolic dysfunction or cor pulmonale .
Cardiovascular comorbidities were associated with increased levels .
Levels consistently correlated with pulmonary artery pressure and left ventricular ejection fraction , but not pulmonary function or oxygen saturation .
NP demonstrated high negative predictive values ( 0.80 to 0.98 ) to exclude left ventricular dysfunction in both stable and exacerbation of COPD , but relatively low positive predictive values .
NP elevation predicted early adverse outcomes , but the association with long term mortality was inconsistent .