***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 This study sought to assess the acute hemodynamic effect of vasopressin V(2 ) receptor antagonism . BACKGROUND In decompensated heart failure ( HF ) , tolvaptan , a vasopressin V(2 ) receptor antagonist , has been shown to improve congestion . It has not yet been established whether these improvements may be associated with the hemodynamic effects of tolvaptan . METHODS A total of 181 patients with advanced HF on st and ard therapy were r and omized to double-blind treatment with tolvaptan at a single oral dose ( 15 , 30 , or 60 mg ) or placebo . RESULTS Tolvaptan at all doses significantly reduced pulmonary capillary wedge pressure ( -6.4 + /- 4.1 mm Hg , -5.7 + /- 4.6 mm Hg , -5.7 + /- 4.3 mm Hg , and -4.2 + /- 4.6 mm Hg for the 15-mg , 30-mg , 60-mg , and placebo groups , respectively ; p < 0.05 for all tolvaptan vs. placebo ) . Tolvaptan also reduced right atrial pressure ( -4.4 + /- 6.9 mm Hg [ p < 0.05 ] , -4.3 + /- 4.0 mm Hg [ p < 0.05 ] , -3.5 + /- 3.6 mm Hg , and -3.0 + /- 3.0 mm Hg for the 15-mg , 30-mg , 60-mg , and placebo groups , respectively ) and pulmonary artery pressure ( -5.6 + /- 4.2 mm Hg , -5.5 + /- 4.1 mm Hg , -5.2 + /- 6.1 mm Hg , and -3.0 + /- 4.7 mm Hg for the 15-mg , 30-mg , 60-mg , and placebo groups , respectively ; p < 0.05 ) . Tolvaptan increased urine output by 3 h in a dose-dependent manner ( p < 0.0001 ) , without changes in renal function . CONCLUSIONS In patients with advanced HF , tolvaptan result ed in favorable but modest changes in filling pressures associated with a significant increase in urine output . These data provide mechanistic support for the symptomatic improvements noted with tolvaptan in patients with decompensated HF . ( Heart Pressure Assessment Study With Tolvaptan to Treat Congestive Heart Failure ; NCT00132886 ) 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 Although tolvaptan is a recently approved drug for heart failure and causes aquaresis without affecting renal function , its clinical efficacy for patients with acute decompensated heart failure ( ADHF ) is yet to be eluci date d. METHODS AND RESULTS We conducted a prospect i ve observational study in patients with ADHF and high risk for worsening renal function ( WRF ) . Risk stratification for WRF was done by scoring system . Of 174 patients , 114 patients were included as high-risk population for WRF .  Incidence of WRF , urine output within 24h and 48 h , and changes in brain natriuretic peptide ( BNP ) were recorded in 44 patients treated with tolvaptan plus conventional therapy , and 70 patients with only conventional therapy . Urine output at 24h and 48 h after admission were both significantly higher in the tolvaptan group ( p=0.001 and < 0.001 , respectively ) , and changes in BNP were not significantly different ( p=0.351 ) . However , the incidence of WRF was significantly lower in the tolvaptan group compared to the conventional group ( 22.7 % vs 41.4 % , p=0.045 ) . Logistic regression analysis showed that treatment with tolvaptan was an independent factor for reducing WRF ( hazard ratio 0.28 , 95 % confidence interval ; 0.10 - 0.84 ; p=0.023 ) . CONCLUSION In patients with ADHF with high risk of WRF , treatment with tolvaptan could prevent WRF compared to conventional therapy Abstract Aims Loop diuretics are first‐line medications for congestive heart failure ( CHF ) ; however , they are associated with serious adverse effects , including decreased renal function , and sympathetic nervous and renin – angiotensin system activation . We tested whether tolvaptan , a vasopressin V2‐receptor antagonist , could reduce unfavourable furosemide‐induced effects during CHF treatment . Methods and results Sixty patients emergently hospitalized owing to CHF‐induced dyspnea were r and omly assigned to receive either 40 mg intravenous furosemide daily or 7.5 mg oral tolvaptan for 5 days after admission . Both groups also received intravenous carperitide and canrenoate potassium . As results , baseline patient characteristics were similar between the furosemide ( n = 30 ) and the tolvaptan ( n = 30 ) groups , with no significant difference in 5 day urine volume or fluid balance . Brain natriuretic peptide and body weight improvements were similar between groups . However , serum creatinine ( Cr ) level did not increase , and the incidence of worsening renal function was significantly lower in the tolvaptan group . Consequently , the Cr increase to gain 1000 mL urine was 2.5‐fold lower in the tolvaptan group . Furthermore , the blood urea nitrogen (BUN)/Cr ratio significantly decreased in the tolvaptan group , suggesting that renal perfusion was preserved , and urea reuptake and passive water reabsorption were suppressed following tolvaptan treatment . Although catecholamine improvements after treatment were not significantly different , plasma renin activity was enhanced in the furosemide group . Conclusions As compared with furosemide , tolvaptan in patients with acute heart failure is associated with comparable decongestion , better preservation of renal function and less activation of renin – angiotensin system . ( UMIN 000014134 ) OBJECTIVES We sought to determine whether non-potassium-sparing diuretics ( PSDs ) in the absence of a PSD may result in  progressive heart failure ( HF ) . BACKGROUND Angiotensin-converting enzyme ( ACE ) inhibitors incompletely suppress ACE activity in HF patients . Furthermore , non-PSDs are activators of aldosterone secretion . We reasoned that non-PSDs , in the absence of a PSD , might result in progressive HF . METHODS In the 6,797 patients in the Studies Of Left Ventricular Dysfunction ( SOLVD ) , we compared the risk of hospitalization for , or death from , HF between those taking a PSD  and those who were not , adjusting for known covariates . RESULTS The risk of hospitalization from worsening HF in those taking a PSD relative to those taking only a non-PSD was 0.74 ( 95 % confidence interval [ CI ] 0.55 to 0.99 ; p = 0.047 ) . The relative risk for cardiovascular death was 0.74 ( 95 % CI 0.59 to 0.93 ; p = 0.011 ) , for death from all causes 0.73 ( 95 % CI 0.59 to 0.90 ; p = 0.004 ) , and for hospitalization for , or death from , HF 0.75 ( 95 % CI 0.58 to 0.97 ; p = 0.030 ) . Compared with patients not taking any diuretic , the risk of hospitalization or death due to worsening HF in patients  taking non-PSDs alone was significantly increased ( risk ratio [ RR ] = 1.31 , 95 % CI 1.09 to 1.57 ; p = 0.0004 ) ; this was not observed in patients  taking PSDs with or without a non-PSD ( RR = 0.99 , 95 % CI 0.76 to 1.30 ; p = 0.95 ) . CONCLUSIONS The use of  PSDs in HF patients is associated with a reduced risk of death from , or hospitalization for , progressive HF or all-cause or cardiovascular death , compared with patients taking only a non-PSD BACKGROUND More efficacious and /or safer decongestive therapy is clearly needed in acute heart failure ( AHF ) patients complicated by renal dysfunction . We tested the hypothesis that adding tolvaptan , an oral vasopressin-2 receptor antagonist , to conventional therapy with loop diuretics would be more effective treatment in this population . METHODS AND RESULTS A multicenter , open-label , r and omized control trial was performed , and 217 AHF patients with renal dysfunction ( estimated glomerular filtration rate 15 - 60 mL • min(-1 ) • 1.73 m(-2 ) ) were r and omized 1:1 to treatment with tolvaptan ( n=108 ) or conventional treatment ( n=109 ) . The primary end point was 48-hour urine volume . The tolvaptan group showed more diuresis than the conventional treatment group ( 6464.4 vs 4999.2 mL ; P < .001 ) despite significantly lower amounts of loop diuretic use ( 80 mg vs 120 mg ; P < .001 ) . Dyspnea relief was achieved significantly more frequently in the tolvaptan group at all time points within 48 hours except 6 hours after enrollment . The rate of worsening of renal function ( ≥0.3 mg/dL increase from baseline ) was similar between the tolvaptan and conventional treatment groups ( 24.1 % vs 27.8 % , respectively ; P = .642 ) . CONCLUSIONS Adding tolvaptan to conventional treatment achieved more diuresis and relieved dyspnea symptoms in AHF patients with renal dysfunction . CLINICAL TRIAL REGISTRATION URL : http://www.umin.ac.jp/ctr/index/htm/ Unique identifier : UMIN000007109 Objectives To assess the efficacy of tolvaptan in acute heart failure with hyponatremia using a r and omized double-blinded placebo-controlled study design . Background Tolvaptan is a selective vasopressin receptor 2 antagonist . There are no published clinical trials on the utility of tolvaptan in acute heart failure with hyponatremia in the Indian population . Methods After screening and informed consent , 51 HF patients with hyponatremia were r and omized using computer-generated r and omization sequence to receive placebo or 15 mg of tolvaptan for 5 days along with conventional medical therapy . The patient 's perception of dyspnea using Likert score and the plasma sodium was measured at baseline and for the next 4 days . Results There was a mean improvement in sodium concentration by 5 mEq/L ( p = 0.001 ) in patients receiving tolvaptan , whereas no significant improvement was seen in the placebo group ( p = 0.33 ) . Significant improvement in Likert score was observed in both the groups ( p = 0.001 ) , even though there was no difference between both the groups . Dry mouth and thirst were the most commonly occurring adverse effects observed in both the groups . There were no significant hemodynamic changes with tolvaptan therapy . Conclusion Tolvaptan at a dose of 15 mg is effective in reversing hyponatremia in acute heart failure and may be a suitable option in these patients CONTEXT Vasopressin mediates fluid retention in heart failure .  Tolvaptan , a vasopressin V2 receptor blocker , shows promise for management of heart failure . OBJECTIVE To investigate the effects of tolvaptan initiated in patients hospitalized with heart failure . DESIGN , SETTING , AND PARTICIPANTS The Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study With Tolvaptan ( EVEREST ) , an event-driven , r and omized , double-blind , placebo-controlled study . The outcome trial comprised 4133 patients within 2 short-term clinical status studies , who were hospitalized with heart failure , r and omized at 359 North American , South American , and European sites between October 7 , 2003 , and February 3 , 2006 , and followed up during long-term treatment . INTERVENTION Within 48 hours of admission , patients were r and omly assigned to receive oral tolvaptan , 30 mg once per day ( n = 2072 ) , or placebo ( n = 2061 ) for a minimum of 60 days , in addition to st and ard therapy . MAIN OUTCOME MEASURES Dual primary end points were all-cause mortality ( superiority and noninferiority ) and cardiovascular death or hospitalization for heart failure ( superiority only ) . Secondary end points included changes in dyspnea , body weight , and edema . RESULTS During a median follow-up of 9.9 months , 537 patients ( 25.9 % ) in the tolvaptan group and 543 ( 26.3 % ) in the placebo group died ( hazard ratio , 0. 
    Output:
    
Conclusion Tolvaptan can decrease body weight , increase serum sodium level , and ameliorate some of the congestion symptoms in patients with acute heart failure , which may help avoid the overdose of loop diuretics , especially in patients with renal dysfunction