***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 There have been no r and omized trials of cardioprotective therapy after acute myocardial infa rct ion in patients with chronic kidney disease who should be largely eligible for aspirin ( acetylsalicylic acid ; ASA ) and beta-blockers ( BB ) as a base of therapy . METHODS We analyzed a prospect i ve coronary care unit registry of 1724 patients with ST-segment elevation myocardial infa rct ion . RESULTS Usage rates were 52.3 % , 19.0 % , 15.2 % , and 13.5 % for ASA and BB ( ASA+BB ) , BB alone , ASA alone , and no ASA or BB therapy . Patients who received ASA+BB were more likely to be male , free of earlier cardiac disease , and recipients of thrombolysis . Conversely , the absence of ASA+BB was observed in patients with heart failure on admission , left bundle branch block , atrial and ventricular arrhythmias , and shock . The combination of ASA+BB was used in 63.9 % , 55.8 % , 48.2 % , and 35.5 % of patients with corrected creatinine clearance values of > 81.5 , 81.5 to 63.1 , 63.1 to 46.2 , and < 46.2 mL/min/72 kg ( P < .0001 ) . ASA+BB was used in 40.4 % of patients undergoing dialysis . The age-adjusted relative risk reduction for the inhospital mortality rate was similar among all renal groups and ranged from 64.3 % to 80.0 % ( all P < .0001 ) . CONCLUSION ASA+BB is an underused therapy in patients with acute myocardial infa rct ion who have underlying kidney disease Cardiovascular events ( CVEs ) are the leading cause of death in chronic hemodialysis patients . Results of trials in non-end-stage renal disease ( ESRD ) patients can not be extrapolated to patients with ESRD . It is critical to test cardiovascular therapies in these high-risk patients who are usually excluded from major cardiovascular trials . The study objective was to evaluate the effect of fosinopril on CVEs in patients with ESRD . Eligible patients were r and omized to fosinopril 5 mg titrated to 20 mg daily ( n=196 ) or placebo ( n=201 ) plus conventional therapy for 24 months . The primary end point was combined fatal and nonfatal first major CVEs ( cardiovascular death , resuscitated death , nonfatal stroke , heart failure , myocardial infa rct ion , or revascularization ) . No significant benefit for fosinopril was observed in the intent to treat analysis ( n=397 ) after adjusting for independent predictors of CVEs ( RR=0.93 , 95 % confidence interval ( CI ) 0.68 - 1.26 , P=0.35 ) . The per protocol secondary supportive analysis ( n=380 ) found a trend towards benefit for fosinopril ( adjusted RR=0.79 ( 95 % CI 0.59 - 1.1 , P=0.099 ) ) . In the patients who were hypertensive at baseline , systolic and diastolic blood pressures were significantly decreased in the fosinopril as compared to the placebo group . After adjustment for risk factors , trends were observed suggesting fosinopril may be associated with a lower risk of CVEs . These trends may have become statistically significant had the sample size been larger , and these findings warrant further study OBJECTIVES We sought to evaluate the effects of carvedilol on mortality and morbidity in dialysis patients with dilated cardiomyopathy . BACKGROUND Several lines of evidence support the concept that therapy with beta-blocking agents reduces morbidity and mortality in patients with congestive heart failure ( HF ) , but the demonstration of such a survival benefit in dialysis patients with dilated cardiomyopathy is still lacking . METHODS A total of 114 dialysis patients with dilated cardiomyopathy were r and omized to receive either carvedilol or placebo in addition to st and ard therapy . A first analysis was performed at one year and was followed by an additional follow-up period of 12 months . RESULTS Two-year echocardiographic data revealed a significant attenuation of pathologic remodeling , with smaller cavity diameters and higher ejection fractions in the active treatment group than in the placebo group . At two years , 51.7 % of the patients died in the carvedilol group , compared with 73.2 % in the placebo group ( p < 0.01 ) . Furthermore , there were significantly fewer cardiovascular deaths ( 29.3 % ) and hospital admissions ( 34.5 % ) among patients receiving carvedilol than among those receiving a placebo ( 67.9 % and 58.9 % , respectively ; p < 0.00001 ) . The exploratory analyses revealed that fatal myocardial infa rct ions , fatal strokes , and hospital admissions for worsening HF were lower in the carvedilol group than in the placebo group . A reduction in sudden deaths and pump-failure deaths was also observed , though it did not reach statistical significance . CONCLUSIONS Carvedilol reduced morbidity and mortality in dialysis patients with dilated cardiomyopathy . These data suggest the use of carvedilol in all dialysis patients with chronic HF Aim To determine the safety and efficacy of nebivolol in elderly heart failure ( HF ) patients with renal dysfunction . Methods and results SENIORS recruited patients aged 70 years or older with symptomatic HF , irrespective of ejection fraction , and r and omized them to nebivolol or placebo .  Patients ( n = 2112 ) were divided by tertile of estimated glomerular filtration rate ( eGFR ) . Mean age of patients was 76.1 years , 35 % of patients had an ejection fraction of > 35 % , and 37 % were women result ing in a unique cohort , far more representative of clinical practice than previous trials . eGFR was strongly associated with outcomes and nebivolol was similarly efficacious across eGFR tertiles . The primary outcome rate ( all-cause mortality or cardiovascular hospital admission ) and adjusted hazard ratio for nebivolol use in those with low eGFR was 40 % and 0.84 ( 95 % CI 0.67–1.07 ) , 31 % and 0.79 ( 0.60–1.04 ) in the middle tertile , and 29 % and 0.86 ( 0.65–1.14 ) in the highest eGFR tertile . There was no interaction noted between renal function and the treatment effect ( P = 0.442 ) . Nebivolol use in patients with moderate renal impairment ( eGFR < 60 ) was not associated with major safety concerns , apart from higher rates of drug-discontinuation due to bradycardia . Conclusion Nebivolol is safe and has a similar effect in elderly HF patients with mild or moderate renal impairment Given the high prevalence of cardiovascular disease in people with chronic kidney disease ( CKD ) and the clear benefits of mortality reduction observed for most β−blockers in clinical trials , they are relatively underused in CKD patients [ 1,2 ] . The rationale for use of β-blockers in patients with CKD is review ed in detail elsewhere [ 2,3 ] but is summarized in this editorial . Alterations in β- and α-receptor responsiveness are associated with sympathetic over-activity in CKD . This increased sympathetic activity is involved in the genesis of hypertension , and contributes to cardiac complications seen in CKD [ 2,3 ] . The contribution of the sympathetic nervous system to nephropathy progression is documented in sub-totally nephrectomized rats where non-hypotensive doses of β-blockers ameliorate development of glomerulosclerosis and cardiac injury [ 4 ] . In men ,  sympathetic over-activity  , as assessed by sural nerve microneurography , was present in patients on haemodialysis [ 5 ] , stage 4 nephropathy [ 6 ] and in early stage 2 nephropathy among patients with polycystic kidney disease [ 7 ] . The role of the damaged kidney in causing sympathetic over-activity is illustrated by normalization of sympathetic over-activity in haemodialysis patients following bilateral nephrectomy [ 5 ] and in renal allograft recipients when their shrunken native kidneys are removed [ 8 ] . The most common cause of death in stage 3 and higher CKD results from complications of cardiovascular disease . This may be due , in part , to inadequate treatment of blood pressure , where blood pressure goals were not attained and agents known to reduce mortality secondary to cardiovascular causes , i.e. aspirin , ACE inhibitors and β-blockers were not used [ 9 ] . In a separate study , β-blockers were used in fewer than 30 % of haemodialysis patients [ 10 ] . This is surprising , since β-blockers are well-established , evidence -based therapy for reducing cardiovascular risk in hypertension associated with diabetes and after myocardial infa rct ion [ 11,12 ] . Observational studies support definite survival benefits derived from β-blocker use in patients with advanced CKD [ 13,14 ] . Furthermore , a prospect i ve CONTEXT Hypertension is a leading cause of end-stage renal disease ( ESRD ) in the United States , with no known treatment to prevent progressive declines leading to ESRD . OBJECTIVE To compare the effects of 2 levels of blood pressure ( BP ) control and 3 antihypertensive drug classes on glomerular filtration rate ( GFR ) decline in hypertension . DESIGN R and omized 3 x 2 factorial trial with enrollment from February 1995 to September 1998 . SETTING AND PARTICIPANTS A total of 1094 African Americans aged 18 to 70 years with hypertensive renal disease ( GFR , 20 - 65 mL/min per 1.73 m(2 ) ) were recruited from 21 clinical centers throughout the United States and followed up for 3 to 6.4 years . INTERVENTIONS Participants were r and omly assigned to 1 of 2 mean arterial pressure goals , 102 to 107 mm Hg ( usual ; n = 554 ) or 92 mm Hg or less ( lower ; n = 540 ) , and to initial treatment with either a beta-blocker ( metoprolol 50 - 200 mg/d ; n = 441 ) , an angiotensin-converting enzyme inhibitor ( ramipril 2.5 - 10 mg/d ; n = 436 ) or a dihydropyridine calcium channel blocker , ( amlodipine 5 - 10 mg/d ; n = 217 ) . Open-label agents were added to achieve the assigned BP goals . MAIN OUTCOME MEASURES Rate of change in GFR ( GFR slope ) ; clinical composite outcome of reduction in GFR by 50 % or more ( or > or = 25 mL/min per 1.73 m2 ) from baseline , ESRD , or death . Three primary treatment comparisons were specified : lower vs usual BP goal ; ramipril vs metoprolol ; and amlodipine vs metoprolol . RESULTS Achieved BP averaged ( SD ) 128/78 ( 12/8 ) mm Hg in the lower BP group and 141/85 ( 12/7 ) mm Hg in the usual BP group . The mean ( SE ) GFR slope from baseline through 4 years did not differ significantly between the lower BP group ( -2.21 [ 0.17 ] mL/min per 1.73 m2 per year ) and the usual BP group ( -1.95 [ 0.17 ] mL/min per 1.73 m2 per year ; P = .24 ) , and the lower BP goal did not significantly reduce the rate of the clinical composite outcome ( risk reduction for lower BP group = 2 % ; 95 % confidence interval [ CI ] , -22 % to 21 % ; P = .85 ) . None of the drug group comparisons showed consistent significant differences in the GFR slope . However , compared with the metoprolol and amlodipine groups , the ramipril group manifested risk reductions in the clinical composite outcome of 22 % ( 95 % CI , 1%-38 % ; P = .04 ) and 38 % ( 95 % CI , 14%-56 % ; P = .004 ) , respectively . There was no significant difference in the clinical composite outcome between the amlodipine and metoprolol groups . CONCLUSIONS No additional benefit of slowing progression of hypertensive nephrosclerosis was observed with the lower BP goal . Angiotensin-converting enzyme inhibitors appear to be more effective than beta-blockers or dihydropyridine calcium channel blockers in slowing GFR decline Abstract Objective : To compare the ability of angiotensin converting enzyme inhibitors and β blockers to slow the development of end stage renal failure in non-diabetic patients with chronic renal failure . Design : Open r and omised multicentre trial with three year follow up . Setting : Outpatient departments of six French hospitals . Patients : 100 hypertensive patients with chronic renal failure ( initial serum creatinine 200 - 400 
    Output:
    
Treatment with beta-blockers improved all-cause mortality in patients with CKD and chronic systolic heart failure .
There is insufficient evidence to conclude whether people with CKD who are not known to have heart failure derive benefit from beta-blockers