***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 and Purpose — The role of uric acid as a risk factor for myocardial infa rct ion is controversial , and little is known about its role as a risk factor for stroke . Recent evidence suggests that uric acid may be an important causal agent in cardiovascular disease , for example , by inducing renal disease and hence hypertension . We investigated the association between serum uric acid and coronary heart disease and stroke in a large prospect i ve population -based study . Methods — The study was based on 4385 participants of the Rotterdam Study who , at baseline ( 1990 to 1993 ) , were ≥55 years of age , free from stroke and coronary heart disease , and had blood taken . Follow-up for incident stroke and myocardial infa rct ion was complete until January 1 , 2002 . Data were analyzed with Cox proportional hazards models with adjustment for relevant confounders . Results — Average follow-up was 8.4 years . High serum uric acid levels were associated with risk of myocardial infa rct ion and stroke ; age- and sex-adjusted hazard ratios ( 95 % CIs ) for highest versus lowest quintile of uric acid were 1.68 ( 1.24 to 2.27 ) for cardiovascular disease ( 515 cases ) , 1.87 ( 1.12 to 3.13 ) for myocardial infa rct ion ( 194 cases ) , 1.57 ( 1.11 to 2.22 ) for stroke ( 381 cases ) , 1.77 ( 1.10 to 2.83 ) for ischemic stroke ( 205 cases ) , and 1.68 ( 0.68 to 4.15 ) for hemorrhagic stroke ( 46 cases ) . Adjustment for other vascular risk factors only slightly attenuated these associations . Associations were stronger in persons without hypertension than in those with hypertension . Conclusions — Uric acid is a strong risk factor for myocardial infa rct ion and stroke 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 Background — Although gout and hyperuricemia are related to several conditions that are associated with reduced survival , no prospect i ve data are available on the independent impact of gout on mortality . Furthermore , although many studies have suggested that hyperuricemia is associated with cardiovascular disease ( CVD ) , limited data are available on the impact of gout on CVD . Methods and Results — Over a 12-year period , we prospect ively examined the relation between a history of gout  and the risk of death and myocardial infa rct ion in 51 297 male participants of the Health Professionals Follow-Up Study . During the 12 years of follow-up , we documented 5825 deaths from all causes , which included 2132 deaths from CVD and 1576 deaths from coronary heart disease ( CHD ) . Compared with men without history of gout and CHD at baseline , the multivariate relative risks among men with history of gout were 1.28 ( 95 % confidence interval [ CI ] , 1.15 to 1.41 ) for total mortality , 1.38 ( 95 % CI , 1.15 to 1.66 ) for CVD deaths , and 1.55 ( 95 % CI , 1.24 to 1.93 ) for fatal CHD . The corresponding relative risks among men with preexisting CHD were 1.25 ( 95 % CI , 1.09 to 1.45 ) , 1.26 ( 95 % CI , 1.07 to 1.50 ) , and 1.24 ( 95 % CI , 1.04 to 1.49 ) , respectively . In addition , men with gout had a higher risk of nonfatal myocardial infa rct ion than men without gout ( multivariate relative risk , 1.59 ; 95 % CI , 1.04 to 2.41 ) . Conclusions — These prospect i ve data indicate that men with gout have a higher risk of death from all causes . Among men without preexisting CHD , the increased mortality risk is primarily a result of an elevated risk of CVD death , particularly from CHD Study objective : To investigate the association of  residence in mountainous or lowl and areas  with  total and coronary mortality  , in a cohort with 15 years of follow up . Design and setting : Prospect i ve study , based on the adult population of two lowl and and one mountainous village in rural Greece . Baseline measurements on sociodemographic , lifestyle , somatometric , clinical , and biochemical variables were recorded in 1981 during a health survey and total and coronary deaths were ascertained on the basis of death certificates up to 1996 . Participants : 1198 men and women , who had participated in the 1981 survey . Analyses are based on 504 men and 646 women with complete data . Main results : There were 150 deaths among men and 140 among women ( coronary deaths : 34 and 33 respectively ) . In multivariate analysis with Cox regression , after adjustment for age , education , body weight , smoking , alcohol consumption , systolic blood pressure , serum total cholesterol , blood glucose , serum triglycerides , and serum uric acid , total and coronary mortality were lower for residents of the mountainous village in comparison with residents of the lowl and villages ( hazard ratios ( 95 % confidence intervals ) for men and women , respectively : total mortality , 0.57 ( 0.38 to 0.84 ) and 0.69 ( 0.47 to 1.02 ) ; coronary mortality , 0.39 ( 0.16 to 0.98 ) and 0.46 ( 0.20 to 1.05 ) ) . Conclusions : Residence in mountainous areas seems to have a “ protective effect ” from total and coronary mortality . Increased physical activity from walking on rugged terrains under conditions of moderate hypoxia among the mountain residents could explain these findings PURPOSE Approximately half of previous studies on serum uric acid have reported it to be an independent risk factor for coronary heart disease ( CHD ) . We tested this hypothesis in the Atherosclerosis Risk in Communities ( ARIC ) Study . METHODS A total of 13,504 healthy middle-aged men and women were followed prospect ively for up to eight years . We identified 128 fatal and nonfatal CHD events in women and 264 in men . RESULTS The age- , race- , and ARIC field center-adjusted relative risk of CHD for sex-specific quartiles of serum uric acid were 1.0 , 1.39 , 1.08 , and 2.35 in women ( p for trend = 0.009 ) and 1.0 , 1.03 , 0.89 , and 1.21 in men ( p for trend = 0.44 ) , respectively . However , serum uric acid was correlated positively with many risk factors , and after multivariable adjustment , there was little evidence of an association of uric acid with CHD in either sex . CONCLUSIONS Our results are not consistent with serum uric acid being an independent risk factor for CHD 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 Increased blood and plasma viscosity , hematocrit , fibrinogen , and activation of coagulation and leukocytes have been reported in patients with claudication ; however , their associations with symptomatic and asymptomatic peripheral arterial disease have not been reported in an epidemiological study Methods and Results Blood and plasma viscosity , hematocrit , fibrinogen , urinary fibrinopeptide A , plasma leukocyte elastase , and uric acid were measured in a r and om sample of 1,581 men and women aged 55 - 74 years in Edinburgh , Scotl and , and related to peripheral arterial stenosis ( ankle-brachial systolic pressure index , ABPI ) and to lower limb ischemia ( intermittent claudication and reactive hyperemia test ) . Each variable ( except fibrinopeptide A ) was significantly related to prevalent symptomatic and asymptomatic peripheral arterial disease . On multivariate analysis , blood viscosity ( p<0.05 ) and fibrinogen ( p<0.01 ) were independently associated with peripheral arterial narrowing ( ABPI ) ; a positive interaction was found between fibrinogen and smoking in the association with ABPI . Plasma viscosity was associated with claudication in the presence of a given degree of arterial narrowing ( odds ratio of claudication in top quintile compared with bottom quintile of plasma viscosity , 3.35 ; 95 % CI , 1.32 , 8.51 ) . Leukocyte elastase and uric acid were each associated with reactive hyperemia independently of arterial narrowing ( p<0.01 ) . Conclusion Blood rheological factors and leukocyte activation as well as arterial narrowing are associated with lower limb ischemia in the general population and may be implicated in its pathogenesis Low serum cholesterol concentrations are associated with deaths from cancer . This association was found in a prospect i ve study of middle aged men in Malmö and consideration of possible explanations for the lowering of serum cholesterol prompted an analysis of serum urate in relation to deaths from cancer . A total of 127 of the 7725 participants in the Malmö study had died since screening . A weakly positive but significant correlation between raised serum urate concentration and total mortality was found . This correlation was wholly explained by neoplastic deaths ( p less than 0.01 ) , while there were no associations with alcohol related deaths or with deaths from coronary heart disease . When the deaths from cancer were classified as " early " or " late "-- that is , occurring less than or more than 2.5 years after the screening -- the correlation between raised urate concentr 
    Output:
    
Hyperuricemia may marginally increase the risk of CHD events , independently of traditional CHD risk factors .