***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 The role of serum uric acid ( SUA ) as a risk factor for cardiovascular disease ( CVD ) remains controversial . Little is known about its predictive value for mortality from congestive heart failure ( CHF ) and stroke , particularly in elderly , post-menopausal women . METHODS The relation of SUA to risk of death from total CVD , CHF , stroke and coronary heart disease ( CHD ) was examined prospect ively in a large cohort of 28613 elderly Austrian women ( mean age 62.3 years ) , followed-up for a median of 15.2 years . Adjusted Cox proportional hazards models were calculated to evaluate SUA as an independent predictor for fatal CVD events . RESULTS SUA in the highest quartile ( > or=5.41 mg/dL ) was significantly associated with mortality from total CVD ( p<0.0001 ) , showing a clear dose-response relationship ; the adjusted hazard ratio ( 95%CI ) in comparison to the lowest SUA quartile was 1.35 ( 1.20 - 1.52 ) . In subgroup analyses SUA was independently predictive for deaths from acute and subacute ( p<0.0001 ) and chronic forms ( p=0.035 ) of CHD , yielding adjusted hazard ratios for the highest versus lowest SUA quartile of 1.58 ( 1.19 - 2.10 ) and 1.25 ( 1.01 - 1.56 ) , respectively . SUA was further significantly related to fatal CHF ( p<0.0001 ) and stroke ( p=0.018 ) ; the adjusted hazard ratios for the highest versus lowest SUA quartile were 1.50 ( 1.04 - 2.17 ) and 1.37 ( 1.09 - 1.74 ) , respectively . CONCLUSIONS These findings , for the first time , demonstrate that SUA is an independent predictor for all major forms of death from CVD including acute , subacute and chronic forms of CHD , CHF and stroke in elderly , post-menopausal women We examined the relation of serum creatinine and uric acid to  mortality and cardiovascular disease in older ( aged ≥60 years ) Chinese patients with isolated systolic hypertension ( systolic/diastolic blood pressure ≥160/<95 mmHg ) . We used Cox regression to correlate outcome with baseline serum creatinine and uric acid measured in 1880 and 1873 , respectively , of the 2394 patients enrolled in the placebo-controlled Systolic Hypertension in China ( Syst-China ) Trial . Median follow-up was 3 years . In multiple Cox regression analysis with adjustment for gender , age , active treatment , and other significant covariates , serum creatinine was significantly associated with a worse prognosis . The relative hazard rates ( 95 % CIs ) associated with a 20-&mgr;mol/L increase in serum creatinine for all-cause , cardiovascular , and stroke mortality were 1.16 ( 1.05 to 1.27 , P = 0.003 ) , 1.15 ( 1.01 to 1.31 , P = 0.03 ) , and 1.37 ( 1.13 to 1.65 , P = 0.001 ) , respectively . In a similar analysis , which also accounted for serum creatinine , serum uric acid was also significantly and independently associated with excess mortality of cardiovascular disease and stroke . The relative hazard rates associated with a 50-&mgr;mol/L increase of serum uric acid were 1.14 ( 1.02 to 1.27 , P = 0.02 ) for cardiovascular mortality and 1.34 ( 1.14 to 1.57 , P < 0.001 ) for fatal stroke . In conclusion , in older Chinese patients with isolated systolic hypertension , serum creatinine and serum uric acid were predictors of mortality BACKGROUND The role of serum uric acid ( SUA ) as an independent risk factor for cardiovascular disease ( CVD ) remains controversial , and little is known about its prognostic importance for mortality from congestive heart failure ( CHF ) and stroke . Few large-scale epidemiologic studies with sufficient follow-up have addressed the association of SUA and CVD mortality in apparently healthy men across a wide age range . METHODS A cohort of 83 683 Austrian men ( mean age , 41.6 years ) was prospect ively followed for a median of 13.6 years . We used Cox proportional hazards models adjusted for established risk factors to evaluate SUA as an independent predictor for CVD mortality . RESULTS The highest quintile of SUA concentration ( > 398.81 mumol/L ) was significantly related to mortality from CHF ( P = 0.03 ) and stroke ( P < 0.0001 ) ; adjusted hazard ratios ( 95 % confidence interval ) for the highest vs lowest quintiles of SUA were 1.51 ( 1.03 - 2.22 ) and 1.59 ( 1.23 - 2.04 ) , respectively . SUA was not associated , however , with mortality from acute , subacute , or chronic forms of coronary heart disease ( CHD ) after adjustment for potential confounding factors ( P = 0.12 ) . Age was a significant effect modifier for the relation of SUA to fatal CHF ( P = 0.05 ) , with markedly stronger associations found in younger individuals . CONCLUSIONS Our study demonstrates for the first time in a large prospect i ve male cohort that SUA is independently related to mortality from CHF and stroke . Although increased SUA is not necessarily a causal risk factor , our results suggest the clinical importance of monitoring and intervention based on the presence of an increased SUA concentration , especially because SUA is routinely measured Background —Hyperuricemia , a known correlate of oxidative stress , is a marker for adverse prognosis among individuals with heart failure . However , the relationship between hyperuricemia and the risk for incidence of heart failure in a community-based population has not been studied . Methods and Results —We prospect ively analyzed the relationship between serum uric acid concentration at baseline and subsequent heart failure among the participants of the Framingham Offspring cohort ( n=4912 ; mean baseline age , 36 years ; 52 % women ) . By using Cox regressions , we calculated the risk of heart failure with increasing serum uric acid after adjusting for sex , age , smoking , body mass index , renal dysfunction , diuretics , systolic blood pressure , valvular heart disease , diabetes , alcohol , and use of antihypertensive medications . The incidence rates of heart failure were ≈6-fold higher among those at the highest quartile of serum uric acid ( > 6.3 mg/dL ) compared with those at the lowest quartile ( < 3.4 mg/dL ) . The adjusted hazard ratio for the highest quartile of serum uric acid compared with the lowest was 2.1 ( 1.04 to 4.22 ) . The relationship between hyperuricemia and heart failure was found in participants without metabolic syndrome and other subgroups as well . Conclusions —Hyperuricemia is a novel , independent risk factor for heart failure in a group of young general community dwellers . This has implication s for development of preventive strategies for heart failure Background —In patients with chronic heart failure ( CHF ) , hyperuricemia is a common finding and is associated with reduced vasodilator capacity and impaired peripheral blood flow . It has been suggested that the causal link of this association is increased xanthine oxidase (XO)–derived oxygen free radical production and endothelial dysfunction . We therefore studied the effects of XO inhibition with allopurinol on endothelial function and peripheral blood flow in CHF patients after intra-arterial infusion and after oral administration in 2 independent placebo-controlled studies . Methods and Results —In 10 CHF patients with normal serum uric acid ( UA ) levels ( 315±42 & mgr;mol/L ) and 9 patients with elevated UA ( 535±54 & mgr;mol/L ) , endothelium-dependent ( acetylcholine infusion ) and endothelium-independent  ( nitroglycerin infusion ) vasodilation of the radial artery was determined . Coinfusion of allopurinol ( 600 & mgr;g/min ) improved endothelium-dependent but not endothelium-independent vasodilation in hyperuricemic patients ( P < 0.05 ) . In a double-blind , crossover design , hyperuricemic CHF patients were r and omly allocated to allopurinol 300 mg/d or placebo for 1 week . In 14 patients ( UA 558±21 & mgr;mol/L , range 455 to 743 & mgr;mol/L ) , treatment reduced UA by > 120 & mgr;mol/L in all patients ( mean reduction 217±15 & mgr;mol/L , P < 0.0001 ) . Compared with placebo , allopurinol  improved peak blood flow ( venous occlusion plethysmography ) in arms ( + 24 % , P = 0.027 ) and legs ( + 23 % , P = 0.029 ) . Flow-dependent flow improved by 58 % in arms ( P = 0.011 ) . Allantoin , a marker of oxygen free radical generation , decreased by 20 % after allopurinol treatment ( P < 0.001 ) . There was a direct relation between change of UA and improvement of flow-dependent flow  after allopurinol treatment ( r = 0.63 , P < 0.05 ) . Conclusions —In hyperuricemic CHF patients , XO inhibition with allopurinol improves peripheral vasodilator capacity and blood flow both locally and systemically Background —Hyperuricemia is common in chronic heart failure ( CHF ) , and it is a strong independent marker of prognosis . Upregulated xanthine oxidase ( XO ) activity and impaired renal excretion have been shown to account for increased serum uric acid ( UA ) levels in CHF . Therapeutic interventions with allopurinol to reduce UA levels by XO inhibition have been shown to be beneficial . Discussion s are ongoing whether UA itself is actively involved or it is a mere marker of upregulated XO activity within CHF pathophysiology . Therefore , the aim of this study was to test the effect of lowering UA by uricosuric treatment without XO inhibition on hemodynamic and metabolic characteristics of CHF . Impaired renal excretion of UA was taken into account . Methods and Results —Serum UA ( SUA ) , urinary UA ( uUA ) excretion , and renal clearance test for UA ( ClUA ) were measured in 82 patients with CHF .  SUA was significantly increased compared with controls of similar age ( control , 5.45±0.70 mg/dL ; New York Heart Association I , 6.48±1.70 mg/dL ; New York Heart Association II , 7.34±1.94 mg/dL ; New York Heart Association III , 7.61±2.11 mg/dL ; P<0.01 ) . Patients with CHF showed lower uUA excretion and ClUA . On multivariate analysis , insulin , brain natriuretic peptide ( P<0.01 ) , and creatinine levels ( P=0.05 ) showed independent correlation with SUA . The treatment effect of the uricosuric agent benzbromarone was tested in 14 patients with CHF with hyperuricemia in a double-blind , placebo-controlled , r and omized crossover study design . Benzbromarone significantly decreased SUA ( P<0.01 ) . Brain natriuretic peptide , left ventricular ejection fraction , and dimensions in echocardiographic assessment did not change after benzbromarone therapy . In contrast , fasting insulin  ( placebo , 18.8±8.9 & mgr;U/mL ; benzbromarone , 11.0±6.2 & mgr;U/mL ; P<0.05 ) , homeostasis model assessment of insulin resistance index  ( placebo , 5.4±2.6 ; benzbromarone , 3.0±1.7 ; P<0.05 ) , and tumor necrosis factor-&agr ;  ( placebo , 2.59±0.63 pg/mL ; benzbromarone , 2.14±0.51 pg/mL ; P<0.05 ) improved after benzbromarone , and the changes in tumor necrosis factor-&agr ; levels were correlated with reduction of SUA ( P<0.05 ) . Conclusions —These results show that UA lowering without XO inhibition may not have an effect on hemodynamic impairment in CHF pathophysiology . To the extent that these data are correct , this finding suggests that upregulated XO activity rather than UA itself is actively involved in hemodynamic impairment in CHF . Clinical Trial Registration — clinical trials.gov . Identifier : NCT00422318 The aim of the present prospect i ve , single centre observational study was to describe the profile and prognosis of patients hospitalised with chronic heart failure and to determine the value of discharge blood pressure and cholesterol for long-term survival . From among 2,346 hospitalised patients , 320 ( 13.6 % ) suffered from chron 
    Output:
    
Elevated serum uric acid is associated with an increased risk of incident HF and adverse outcomes in HF patients