18828702
Relationship Between Hyperuricemia and Cardiovascular Disease Risk Factors in a Chinese Population: A Cross-Sectional Study
Background To study the relationship between hyperuricemia and cardiovascular diseases (CVDs) risk factors in a Chinese population. Material/Methods Data analyzed in this study were from the Chinese Hyperuricemia and Gout Database. Indicators of serum uric acid (SUA) level, height, weight, systolic blood pressure (SBP), diastolic blood pressure (DBP), smoking status, alcohol consumption, blood glucose, cholesterol, and triglycerides were measured. T test, one-way analysis of variance, Pearson’s correlation, multivariate linear regression, and multivariate logistic regression were used. Results Compared with normouricemic men, hyperuricemic men had greater height (P<0.01), weight (P<0.001), body mass index (BMI) (P<0.001), SBP (P<0.01), DBP (P<0.001), cholesterol (P<0.01), and triglyceride (P<0.001). Compared with normouricemic women, hyperuricemic women were older (P<0.01) and had greater weight (P<0.05), BMI (P<0.01), SBP (P<0.01), DBP (P<0.05), glucose (P<0.05), and triglyceride (P<0.001). In men, an increase of 1 mg/dL in SUA was associated with a 0.279 kg/m2 increase in BMI (P<0.001), a 2.438 mg/dL increase in cholesterol (P<0.05), a 10.358 mg/dL increase in triglyceride (P<0.001), and a 3.1 mg/dL decrease in glucose (P<0.01). In women, an increase of 1 mg/dL SUA was associated with a 0.168 kg/m2 increase in BMI (P<0.01) and a 3.708 mg/dL increase in triglyceride (P<0.01). After adjustment, SUA was strongly associated with obesity and hyperlipidemia in both sexes. Conclusions Elevated serum uric acid concentration was strongly associated with obesity and hyperlipidemia in both men and women. These results indicated that, among hyperuricemia patients, we should pay more attention to the possibility of cardiovascular complications. These results might provide a novel target or a possible new treatment for cardiovascular diseases by lowering the level of serum uric acid.
6096396
Racial and Ethnic Differences in Mortality and Cardiovascular Events Among Patients With End‐Stage Renal Disease Due to Lupus Nephritis
To identify racial and ethnic differences in mortality and cardiovascular (CV) risk among patients with end‐stage renal disease (ESRD) due to lupus nephritis (LN).
21182504
Social determinants of cardiovascular disease risk factor presence among rural and urban Black and White men.
BACKGROUND: Social determinants of health are increasingly being addressed as a causal factor for disparities in health. The purpose of this study was to assess the effects of specified social determinants of health on cardiovascular disease (CVD) clinical risk factors in Black and White men residing in rural and urban Georgia. METHODS: Self-report data were collected on a total of 548 Black and White men aged >18 years from 2004-2005. Data were derived from a random telephone survey. Separate logistic regression models were conducted to examine the effects of specified social determinants on the presence of two or more CVD clinical risk factors. In addition, differences within rural and urban men were also assessed. RESULTS: Lower education, unemployment, lower income, and higher general stress were all significantly related to the presence of two or more CVD clinical risk factors. As expected, the covariates of age, race, and residential location also played a significant role in cardiovascular health. Rural men were nearly twice as likely to have two or more CVD risk factors compared to their urban men (P <0.01). Models examining location separately found urban Black men to be 2.6 times as likely to have more than two CVD risk factors (P <0.02). CONCLUSION: Findings reveal social determinants are associated with CVD risk factor differences between Black and White men and between rural and urban residents. It is important for policymakers and the healthcare industry to address these social determinants of health as they try to improve the health of the people they serve.
31176338
Anger, anxiety, and depression as risk factors for cardiovascular disease: the problems and implications of overlapping affective dispositions.
Several recent reviews have identified 3 affective dispositions--depression, anxiety, and anger-hostility--as putative risk factors for coronary heart disease. There are, however, mixed and negative results. Following a critical summary of epidemiological findings, the present article discusses the construct and measurement overlap among the 3 negative affects. Recognition of the overlap necessitates the development of more complex affect-disease models and has implications for the interpretation of prior studies, statistical analyses, prevention, and intervention in health psychology and behavioral medicine. The overlap among the 3 negative dispositions also leaves open the possibility that a general disposition toward negative affectivity may be more important for disease risk than any specific negative affect.
41169657
Carotid intima media-thickness and genes involved in lipid metabolism in diabetic patients using statins--a pathway toward personalized medicine.
The prognostic importance of large artery structure and function in relation to cardiovascular morbidity and mortality, together with the identification of new genetic risk factors have been two major areas of investigation in recent years. Carotid intima-media thickness (CIMT), as measured by B-mode ultrasound, is a surrogate marker for atherosclerosis and can be used to detect an accelerated disease process as well as subclinical disease. However, the genetic basis for CIMT variation is almost unknown. Cardiovascular genetics has led to numerous clinical studies generally focused on only one candidate gene and were frequently conducted in subjects with cardiovascular diseases and/or taking drugs that could affect CIMT. Pharmacogenetics is the study of the effect of a medication as it relates to single or defined sets of genes. An important goal of pharmacogenetics in cardiovascular disorders is to integrate the two (drugs plus genes) so that true personalized therapy can be delivered. In this paper, we will discuss the interaction between genes involved in lipid metabolism and statin therapy that affects intermediate phenotype (plasma lipid levels) and CIMT in patients with type 2 diabetes.
11951378
Serum uric acid in relation to age and physique in health and in coronary heart disease.
Excerpt The disease most frequently associated with an abnormal uric acid metabolism is gout.1, 2This association is based upon deposits of uric acid in the joints and connective tissue of gouty pa...
35797961
Association of serum uric acid with all-cause and cardiovascular disease mortality and incident myocardial infarction in the MONICA Augsburg cohort. World Health Organization Monitoring Trends and Determinants in Cardiovascular Diseases.
Because previous findings have been inconsistent, we explored the association of serum concentrations of uric acid with all-cause and cardiovascular disease mortality and myocardial infarction prospectively. We used data from 1,044 men who are members of the World Health Organization Monitoring Trends and Determinants in Cardiovascular Diseases (MONICA) Augsburg cohort. The men, 45-64 years of age in 1984-1985, were followed through 1992. There were 90 deaths, 44 of which were related to cardiovascular disease; 60 men developed incident nonfatal or fatal myocardial infarction. We estimated hazard rate ratios from Cox proportional hazard models. Uric acid levels > or =373 micromol/liter (fourth quartile) vs < or =319 micromol/liter (first and second quartile) independently predicted all-cause mortality [hazard rate ratio = 2.8; 95% confidence interval (CI) = 1.6-5.0] after adjustment for alcohol, total cholesterol/high-density lipoprotein cholesterol ratio, hypertension, use of diuretic drugs, smoking, body mass index, and education. The adjusted risk of cardiovascular disease mortality was 2.2 (95% CI = 1.0-4.8), and that of myocardial infarction was 1.7 (95% CI = 0.8-3.3). Although residual confounding cannot be excluded, our results are among the few, in men, demonstrating a strong positive association of elevated serum uric acid with all-cause mortality. Future investigations may be able to evaluate whether uric acid contributes independently to the development of cardiovascular disease or is simply a component of the atherogenic metabolic condition known as the insulin resistance syndrome.
16121354
Is there anything good in uric acid?
High uric acid (UA) levels can cause gout, urolithiasis and acute and chronic nephropathy, all of which are due to the deposit of urate crystals. There is also increasing evidence of relationships of hyperuricemia with other important disorders, including hypertension, chronic renal disease, metabolic syndrome and cardiovascular disease, as well as an increased mortality, although a causal relationship between these conditions has not been clearly established. On the other hand, low UA levels are not known to cause any disorder or disease. However, in the last few years a higher prevalence and progression of some neurological diseases have been associated with a low UA, and it is possible that they may predispose to some other disorders, mainly due to the decrease in its antioxidant activity. In this article, the known negative effects of UA are reviewed, as well as the much less-known possible positive actions, and their therapeutic implications.
2339229
Hyperuricemia and coronary heart disease: A systematic review and meta‐analysis
The role of serum uric acid as an independent risk factor for cardiovascular disease remains unclear, although hyperuricemia is associated with cardiovascular disease such as coronary heart disease (CHD), stroke, and hypertension.
21818629
Serum uric acid and its relation to cardiovascular disease risk factors in children and young adults from a biracial community: the Bogalusa Heart Study.
The distribution of serum uric acid and its relationship with cardiovascular risk variables have been studied in 3983 children and young adults, aged 5 to 26 years, drawn from a biracial (black and white) population. For two age groups, 5 to 11 years and 19 to 26 years, white subjects had significantly higher uric acid levels than black subjects, (4.02 mg/dl vs 3.57 mg/dl, p less than 0.0001, and 5.50 mg/dl vs 5.18 mg/dl, p less than 0.0001, respectively). Men in the 19 to 26 years age group had a significantly higher uric acid level than women (6.49 mg/dl vs 4.20 mg/dl, p less than 0.0001). White children and young adults were twice as likely to have levels above clinical limits than blacks, and males more likely to have hyperuricemia than females. Parents with a history of myocardial infarction were more likely to have children with hyperuricemia. Children and young adults with hyperuricemia had significantly higher plasma glucose (p less than 0.01) and insulin (p less than 0.001) levels, total cholesterol level (p less than 0.05), and serum triglyceride (p less than 0.0001), very-low-density lipoprotein cholesterol (p less than 0.01), low-density lipoprotein cholesterol (p less than 0.001), and total protein (p less than 0.0001) levels than subjects without hyperuricemia; high-density lipoprotein cholesterol level was significantly lower (p less than 0.0001) in subjects with hyperuricemia than in those without it.(ABSTRACT TRUNCATED AT 250 WORDS)
39644121
Uric acid and coronary heart disease risk: evidence for a role of uric acid in the obesity-insulin resistance syndrome. The Normative Aging Study.
Various epidemiologic studies have linked an increase in serum uric acid level to an increased risk of coronary heart disease. The reasons for this finding are unclear. The authors examined the influence of a number of cardiovascular disease risk factors on serum uric acid level in 886 middle-aged and older men participating in the Normative Aging Study. The men were examined between 1987 and 1991. In a multivariate regression model predicting serum uric acid level, uric acid was positively associated with body mass index (weight (kg)/height (m)2 beta = 0.041 mg/dl per kg/m2, p = 0.003), abdomen: hip circumference ratio (beta = 1.88 mg/dl per cm/cm, p = 0.048), log alcohol intake (beta = 0.150 mg/dl per g/week, p = 0.0001), and log postcarbohydrate insulin level (beta = 0.157 mg/dl per log(microIU/ml), p = 0.005). Serum uric acid level was negatively associated with age (beta = -0.012 mg/dl per year of age, p = 0.017) and log physical activity (beta = -0.152 mg/dl per kcal/week, p = 0.0001). The data suggest that serum uric acid may be involved in the obesity-insulin resistance syndrome, which in turn may explain the relation of serum uric acid to coronary atherosclerosis.
24534807
Relationship of uric acid concentration to cardiovascular risk factors in young men. Role of obesity and central fat distribution. The Verona Young Men Atherosclerosis Risk Factors Study.
OBJECTIVE
To examine the relationships of serum uric acid concentration with several risk factors of cardiovascular diseases (CVD).


SUBJECTS
957 men 18 y old participating in the Verona Young Men Atherosclerosis Risk Factors Study, a cross-sectional population-based study.


MEASUREMENTS
Body mass index (BMI), waist/hip ratio (WHR), serum uric acid, serum lipids, blood pressure, fasting insulin and behavioural variables.


RESULTS
Serum uric acid concentration showed positive associations with BMI (r = 0.24; P < 0.0001), WHR (r = 0.19; P < 0.0001) and serum triglyceride levels (r = 0.19; P < 0.0001); it was also significantly correlated to systolic (r = 0.08; P < 0.01) and diastolic (r = 0.11; P < 0.001) blood pressure, fasting insulin (r = 0.11; P < 0.001), total (r = 0.12; P < 0.001) and LDL cholesterol (r = 0.10; P < 0.01) plasma concentrations. Life-style characteristics, such as smoking and physical activity did not show any significant association, while daily alcohol intake was positively associated with uric acid concentration (r = 0.09; P < 0.01). While the adjustment for fasting insulin did not substantially change these results, the magnitude of the correlations between uric acid and CVD risk factors markedly decreased when allowance was made for BMI and WHR. Only triglycerides maintained an independent correlation with uric acid levels (r = 0.17; P < 0.0001). In multivariate regression analysis, serum triglycerides, BMI and WHR (at borderline significance) were independent positive predictors of uric acid (R2 of the model 0.122, P < 0.001), while fasting insulin concentration did not give any independent contribution to explain the variability uric acid levels.


CONCLUSIONS
These data indicate that, already in young, essentially health subjects, hyperuricaemia associates with several components of the so-called insulin resistance syndrome, thus suggesting that increased levels of uric acid might be another member of this syndrome. In addition, these data suggest that obesity and central body fat distribution, rather than hyperinsulinaemia/insulin resistance, play a major role in linking hyperuricaemia with CVD risk factors clustering in the insulin resistance syndrome. Nevertheless, hypertrigliceridemia is related to hyperuricemia independently of obesity and central body fat distribution.
18026313
Serum urate and the risk of major coronary heart disease events.
OBJECTIVE: To examine the relation between serum urate and the risk of major coronary heart disease events. DESIGN: A prospective study of a male cohort. SETTING: One general practice in each of 24 British towns. SUBJECTS: 7688 men aged 40-59 years at screening. MAIN OUTCOME MEASURES: Fatal and non-fatal coronary heart disease events. RESULTS: There were 1085 major coronary heart disease events during the average follow up period of 16.8 years. Serum urate was significantly associated with a wide range of cardiovascular risk factors including body mass index, alcohol intake, antihypertensive treatment, pre-existing coronary heart disease, serum triglycerides, cholesterol, and diastolic blood pressure. There was a significant positive association between serum urate and risk of coronary heart disease after adjustment for lifestyle factors and disease indicators. This relation was attenuated to non-significance upon additional adjustment for diastolic blood pressure and serum total cholesterol: cholesterol appeared to be the critical factor in attenuating this relation. When the association between serum urate and risk of coronary heart disease was examined by presence and grade of pre-existing coronary heart disease, a positive association was seen only in men with previous definite myocardial infarction, even after full adjustment (P = 0.07). CONCLUSIONS: The relation between serum urate and the risk of coronary heart disease depends heavily upon the presence of pre-existing myocardial infarction and widespread underlying atherosclerosis as well as the clustering of risk factors. Thus serum urate is not a truly independent risk factor for coronary heart disease. Raised serum urate appears to be an integral part of the cluster of risk factors associated with the insulin resistance syndrome that include obesity, raised serum triglycerides, and serum cholesterol.
9675267
Serum Uric Acid and Risk for Cardiovascular Disease and Death: The Framingham Heart Study
The association of serum uric acid with cardiovascular disease has been appreciated for nearly half a century (1). Several prospective studies have shown an association between baseline hyperuricemia and incident coronary heart disease, cardiovascular disease, and death (2-10). Despite the strength of these associations, uric acid has not been established as a causal risk factor for cardiovascular disease. Instead, uric acid seems inextricably linked to hypertension, dyslipidemia, and disordered glucose metabolism, which play a causal role in the pathogenesis of cardiovascular disease. As such, uric acid may be merely a marker of risk for cardiovascular disease. Several recent reports, however, have attempted to dispel this notion (3, 9, 11-14). Using data from the First National Health and Nutrition Examination Study (NHANES I), Freedman and colleagues (3) demonstrated that each 60-mol/L increment in uric acid level was associated with a 48% increase in risk for incident ischemic heart disease among women. Furthermore, a growing body of laboratory and clinical evidence suggests that uric acid plays a role in platelet adhesiveness (15-17), formation of free radicals (18), and oxidative stress (19, 20). As a result of this growing controversy, we revisited this question in the Framingham Heart Study sample. Longer and more contemporary follow-up and more outcome events allowed us to expand on a previous Framingham report [2]. In this paper, we describe the relation of baseline serum uric acid level to 1) incident coronary heart disease events [death from coronary heart disease, recognized myocardial infarction, and coronary insufficiency], 2) death from cardiovascular disease, and 3) death from all causes. Because previous studies (2, 3, 7, 21) have suggested that uric acid is more strongly associated with adverse events in women than in men, we chose a priori to perform sex-specific analyses. Methods Study Sample The selection criteria and study design of the Framingham Heart Study and the Framingham Offspring Study have been described elsewhere (22, 23). Original participants of the Framingham Heart Study who took part in the 13th biennial examination (1972 to 1976) and adult participants in the first examination of the Framingham Offspring Study (1971 to 1975) were eligible for this investigation (n=7940). Blood samples for uric acid measurement were obtained in 7650 (96.3%) persons. Participants were excluded (n=887) for the following reasons: use of more than 2 g of salicylates per day (n=17), missing covariate or follow-up data (n=117), and prevalent cardiovascular disease (n=753). The remaining 6763 participants were followed prospectively until 1994. Baseline Measurements and Definitions Medical histories and physical examinations were performed for each participant at every clinic visit. Systolic and diastolic blood pressure were measured twice in the left arm of seated participants by using a mercury-column sphygmomanometer positioned near eye level. The average of the two readings was used for each blood pressure variable. The diagnosis of hypertension was based on a systolic blood pressure of 140 mm Hg or higher, a diastolic blood pressure of 90 mm Hg or higher, or the current use of antihypertensive drugs (24). Height and weight were measured at each examination, and body mass index was calculated as the weight in kilograms divided by the square of the height in meters. Participants who reported smoking at least one cigarette per day during the year before the examination were classified as current smokers. Alcohol use was ascertained by self-report and was categorized as ounces of ethanol consumed per week. Menopause was defined as the absence of menses for 1 year or more. Diabetes was defined on the basis of a nonfasting blood glucose level of 11.1 mmol/L (200 mg/dL) or greater, a fasting blood glucose level of 7.8 mmol/L (140 mg/dL) or greater, or the use of insulin or an oral hypoglycemic agent. Serum uric acid levels were measured with an autoanalyzer that used a phosphotungstic acid reagent (25). Cholesterol levels were determined according to the Abell-Kendall method (26). Outcome Events The primary outcome measures were incident coronary heart disease events, death from cardiovascular disease (coronary heart disease, congestive heart failure, stroke, or other cardiovascular disease), and death from all causes. Coronary heart disease events included the following: death from coronary heart disease (available information suggested coronary heart disease as the probable cause), recognized myocardial infarction (serial electrocardiographic changes leading to development of new pathologic Q waves, characteristic increase and decrease in serum myocardial markers with a suggestive clinical history, or evidence at necropsy of new or recent infarction), and coronary insufficiency (prolonged ischemic chest discomfort associated with transient repolarization abnormality, without criteria for myocardial infarction). Events that were more equivocal, such as unrecognized myocardial infarction and angina pectoris, were not included as coronary heart disease events for this analysis. A panel of three physicians determined the outcome events according to previously published criteria (27) after reviewing Framingham Heart Study and outside hospital and physician records. Statistical Analysis Separate analyses were performed for men and women. All participants were divided according to sex-specific uric acid quintiles. Crude event rates were calculated for each quintile. Cox proportional-hazards regression models (28) were used to examine the relations of uric acid quintiles (with quintile 1 as the reference category) and the relation of uric acid level as a continuous variable to incidence of coronary heart disease events, cardiovascular disease mortality rates, and all-cause mortality rates. For comparative purposes, hazard ratios were calculated without adjustment. For inferential purposes, hazard ratios were calculated with adjustment for age only and also with adjustment for age and other clinical variables associated with uric acid level or atherosclerotic events: body mass index (kg/m2), diabetes (yes/no), systolic blood pressure (mm Hg), current diuretic use (yes/no), use of antihypertensive medications other than diuretics (yes/no), left ventricular hypertrophy shown on electrocardiography (yes/no), total cholesterol level (mmol/L), smoking status (yes/no), alcohol use (ounces consumed per week), and menopausal status in women (yes/no). Post hoc subgroup analyses were done to determine any possible relations between quintiles of uric acid and the outcome events in participants stratified according to diuretic use and hypertension status. All analyses were performed on a Sun UltraSPARC computer (Sun Microsystems, Mountain View, California) using SAS software (SAS Institute, Cary, North Carolina) (29). A two-sided P value less than 0.05 was the criterion for statistical significance. Results Participant Characteristics Table 1 shows the baseline clinical characteristics for men and women. The mean uric acid level was 379 mol/L in men (range, 119 to 738 mol/L) and 285 mol/L in women (range, 24 to 696 mol/L). The effect of age on mean serum uric acid level is illustrated in the Figure. In men, uric acid levels changed minimally with age. In women, mean serum uric acid levels gradually increased from the fourth to the seventh decades of life. Furthermore, among women 30 to 54 years of age, the mean serum uric acid level was 5 to 13 mol/L greater in those who were postmenopausal (data not shown). Table 1. Baseline Clinical Characteristics Figure. Mean serum uric acid level by sex and 5-year age group. Uric Acid Level and Outcome Events There were 117 376 person-years of follow-up. In men, 394 coronary heart disease events, 232 deaths due to cardiovascular disease, and 729 deaths from all causes occurred. As a continuous variable, baseline uric acid level was not associated with increased risk for any end point in men. In fully adjusted Cox models, for every 60-mol/L increase in serum uric acid level, hazard ratios were as follows: 0.91 (95% CI, 0.83 to 0.99) for coronary heart disease, 0.95 (CI, 0.86 to 1.06) for death from cardiovascular disease, and 0.97 (CI, 0.91 to 1.03) for death from all causes. In men, baseline quintile of serum uric acid level was also not associated with increased risk for any outcome measure. Uric acid level was inversely related to coronary heart disease in the full multivariable adjusted model (Table 2). Table 2. Relations of Serum Uric Acid Level to Coronary Heart Disease, Death from Cardiovascular Disease, and Death from All Causes In women, 223 coronary heart disease events, 197 deaths from cardiovascular disease, and 731 deaths from all causes occurred. From quintile 1 to quintile 5, crude rates increased more than threefold for coronary heart disease (from 1.9 to 7.5 per 1000 person-years), death from cardiovascular disease (from 1.3 to 7.0 per 1000 person-years) and death from all causes (from 6.3 to 21.8 per 1000 person-years) (Table 2). In unadjusted Cox models in which quintile 1 was the reference category, risk significantly increased with increasing uric acid quintile for all three outcome measures (P<0.001 for trend). This trend diminished after adjustment for age but remained significant for coronary heart disease (P=0.002), death from cardiovascular disease (P=0.009), and death from all causes (P=0.03). In fully adjusted Cox models, baseline uric acid level was no longer associated with increased risk for coronary heart disease (P>0.2 for trend), death from cardiovascular disease (P=0.23), or death from all causes (P>0.2). Similar relations were found when baseline uric acid level was assessed as a continuous variable. In the fully adjusted models, hazard ratios for every 60-mol/L increase in serum uric acid level were as follows: 1.05 (CI, 0.94 to 1.17) for coro
41298201
Serum uric acid: a risk factor and a target for treatment?
Serum uric acid was first noted to be associated with increased BP by Frederick Mohamed in the 1870s. Although the link was rediscovered periodically over the years, it generally was dismissed as a surrogate marker for decreased renal function that led to increased uric acid and increased risk for hypertension and cardiovascular (CV) disease. Recently, however, several lines of evidence suggest that increased serum uric acid may be a significant modifiable risk factor. Increased serum uric acid is associated with increased risk for future hypertension in several large longitudinal clinical trials as well as an independent risk factor for poor CV prognosis. Animal model experiments demonstrate that increased serum uric acid causes increased BP that initially is reversible but becomes irreversible, salt sensitive, and uric acid independent over time. The mechanisms include the direct action of uric acid on smooth muscle and vascular endothelial cells. Finally, in adolescents with new-onset essential hypertension, the prevalence of elevated serum uric acid is >90%, and preliminary clinical trial evidence suggests that agents that lower serum uric acid may lower BP in this select population. Although the investigations are still preliminary, serum uric acid represents a possible new and intriguing target for the reduction of morbidity and mortality associated with hypertension and CV disease.
9078434
Uric acid and oxidative stress: relative impact on cardiovascular risk?
Post-hoc analyses of the GREACE and the LIFE trials have renewed the interest in elevated serum uric acid (SUA) as a factor contributing to atherosclerotic cardiovascular disease (CVD) and in the possible benefit derived from its pharmacological reduction. The results of these trials are consistent with reports indicating favourable effects of SUA lowering treatment with allopurinol on the rate of cardiovascular complications in patients with coronary heart disease, congestive heart failure and dilated cardiomyopathy. Two recent overviews have concluded that, while in population samples at relatively low risk of CVD, SUA is at best a very weak predictor of CVD, by contrast it is a significant independent predictor among subjects at high or very high risk. This raises the question of a different meaning of excess SUA levels under different circumstances. Whereas in uncomplicated obese, insulin-resistant and hypertensive patients SUA levels increase mainly as a consequence of impaired renal excretion, in conditions of local ischemia an increased production of uric acid occurs in parallel with that of reactive oxygen species (ROS). Thus, although clinical and experimental evidence suggest that uric acid has actually antioxidant properties, it is conceivable that under these conditions its antioxidant activity is overcome by the pro-oxidant and pro-inflammatory effects of ROS accumulation. At present, there is no solid evidence to recommend treatment of the mild asymptomatic hyperuricemia associated with obesity, diabetes and/or hypertension (up to 10mg/dL). By contrast, similar SUA elevations in patients at higher cardiovascular risk should be taken more seriously. A controlled trial to investigate the effects of SUA reduction in these patients, while monitoring concomitant changes in parameters of oxidative stress and inflammation, is warranted.
551373
Relation Between Serum Uric Acid and Risk of Cardiovascular Disease in Essential Hypertension: The PIUMA Study
The question of serum uric acid as an independent risk factor in subjects with essential hypertension remains controversial. For up to 12 years (mean, 4.0) we followed 1720 subjects with essential hypertension. At entry, all subjects were untreated and all were carefully screened for absence of cardiovascular disease, renal disease, cancer, and other important disease. Outcome measures included total cardiovascular events, fatal cardiovascular events, and all-cause mortality. During 6841 person-years of follow-up there were 184 cardiovascular events (42 fatal) and 80 deaths from all causes. In the 4 quartiles of serum uric acid (division points: 0.268, 0.309, and 0.369 mmol/L [4.5, 5.2, and 6.2 mg/dL] in men; 0.190, 0.232, and 0.274 mmol/L [3.2, 3.9, and 4.6 mg/dL] in women), the rate (per 100 person-years) of cardiovascular events was 2.51, 1.48, 2.66, and 4.27, that of fatal cardiovascular events was 0.41, 0.33, 0.38, and 1.23, and that of all-cause deaths was 1.01, 0.55, 0.93, and 2.01, respectively. The relation between uric acid and event rate was J-shaped in both genders. After adjustment for age, gender, diabetes, total cholesterol/HDL cholesterol ratio, serum creatinine, left ventricular hypertrophy, ambulatory blood pressure, and use of diuretics during follow-up, uric acid levels in the highest quartile were associated with increased risk for cardiovascular events (relative risk, 1.73; 95% CI, 1.01 to 3.00), fatal cardiovascular events (relative risk, 1.96; 95% CI, 1.02 to 3.79), and all-cause mortality (relative risk, 1.63; 95% CI, 1.02 to 2.57) in relation to the second quartile. In untreated subjects with essential hypertension, raised uric acid is a powerful risk marker for subsequent cardiovascular disease and all-cause mortality.
13561608
Serum uric acid and cardiovascular disease: recent developments, and where do they leave us?
The relationship between serum uric acid (SUA) and cardiovascular disease has been controversial. Here we review recent literature assessing whether hyperuricemia is an independent risk factor for adverse cardiovascular outcomes. Studies from the past 6 years evaluating the association of SUA with cardiovascular disease were identified through MEDLINE, EMBASE, and Cochrane library searches, bibliography cross-referencing, and review articles. Twenty-one cohort studies in healthy and high-risk patients with cardiovascular disease were identified and reviewed. In studies of high-risk patients, in which more overall events were recorded, 10 of 11 studies were supportive of an independent association. In 10 studies of healthy patients, 6 suggested an independent association of SUA with adverse cardiovascular outcomes. Increasing SUA is likely an independent risk factor for cardiovascular disease in high-risk individuals. However, the magnitude of excess risk attributable to high SUA is likely to be small in healthy individuals. Trials of SUA-lowering therapy in hyperuricemic patients evaluating the effect on cardiovascular outcomes are justified in high-risk patients.
34252024
The impact of serum uric acid on cardiovascular outcomes in the LIFE study.
The impact of serum uric acid on cardiovascular outcomes in the LIFE study. Background The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study demonstrated the superiority of a losartan-based regimen over atenolol-based regimen for reduction of cardiovascular (CV) morbidity and mortality. It has been suggested that the LIFE study results may be related to the effects of losartan on serum uric acid (SUA). SUA has been proposed as an independent risk factor for CV morbidity and death. Methods Cox regression analysis was used to assess relationship of SUA and treatment regimens with the LIFE primary composite outcome (CV death, fatal or nonfatal myocardial infarction, fatal or nonfatal stroke). Results Baseline SUA was significantly associated with increased CV events [hazard ratio (HR) 1.024 (95% CI 1.017–1.032) per 10 μmol/L, P P P = 0.108]. After adjustment for Framingham risk score (FRS), SUA was no longer significant in the entire study population [HR = 1.006 (0.998–1.014), P = 0.122] or in men [HR = 1.006 (0.995–1.017), P = 0.291], but was significant in women [HR = 1.013 (1–1.025), P = 0.0457]. The baseline-to-end-of-study increase in SUA (standard deviation, SD) was greater ( P P P = 0.004. The association between time-varying SUA and increased CV risk tended to be stronger in women ( P P = 0.0658), although the gender-outcome interaction was not significant ( P = 0.079). Conclusion The increase in SUA over 4.8years in the LIFE study was attenuated by losartan compared with atenolol treatment, appearing to explain 29% of the treatment effect on the primary composite end point. The association between SUA and events was stronger in women than in men with or without adjustment of FRS.
12084403
Cardiovascular Tissue Engineering: Where We Come From and Where Are We Now?
Tissue engineering was introduced by Vacanti and Langer in the 80’s, exploring the potential of this new technology starting with the well-known “human ear on the mouse back”. The goal is to create a substitute which supplies an individual therapy for patients with regeneration, remodeling and growth potential. The growth potential of these subjects is of special interest in congenital cardiac surgery, avoiding repeated interventions and surgery. Initial applications of tissue engineered created substitutes were relatively simple cardiovascular grafts seeded initially by end-differentiated autologous endothelial cells. Important data were collected from these initial clinical autologous endothelial cell seeded grafts in peripheral and coronary vessel disease. After these initial successfully implantation bone marrow cell were used to seed patches and pulmonary conduits were implanted in patients. Driven by the positive results of tissue engineered material implanted under low pressure circumstances, first tissue engineered patches were implanted in the systemic circulation followed by the implantation of tissue engineered aortic heart valves. Tissue engineering is an extreme dynamic technology with continuously modifications and improvements to optimize clinical products. New technologies are unified and so this has also be done with tissue engineering and new application features, so called transcatheter valve intervention. First studies are initiated to apply tissue engineered heart valves with this new transcatheter delivery system less invasive. Simultaneously studies have been started on tissue engineering of so-called whole organs since organ transplantation is restricted due to donor shortage and tissue engineering could overcome this problem. Initial studies of whole heart engineering in the rat model are promising and larger size models are initiated.
25821261
Relations of hyperuricemia with the various components of the insulin resistance syndrome in young black and white adults: the CARDIA study. Coronary Artery Risk Development in Young Adults.
PURPOSE
To assess the association of hyperuricemia with the various components of the Insulin Resistance Syndrome (IRS) in a biracial cohort of young adults.


METHODS
Cross-sectional study in 4053 young black and white adults aged 18-30 years from the Coronary Artery Risk Development in Young Adults (CARDIA) study.


RESULTS
Body mass index (BMI), fasting insulin, and triglycerides were significantly higher, and high density lipoprotein (HDL)-cholesterol lower in subjects with hyperuricemia (uric acid > or = 7.0 mg/dl in males; > or = 6.0 mg/dl in females) (all p < 0.001). BMI showed the strongest positive correlation with uric acid among the IRS components. Significant associations of hyperuricemia with these risk factors were observed in all sex-race groups, which persisted after controlling for possible confounders including age, education, physical activity, smoking, alcohol intake, oral contraceptive use, and creatinine. Further adjustment for BMI and/or waist-to-hip ratio caused a large decrease in the strength of the associations. Adjustment for insulin also lead to decreases; however, the influence of fasting insulin appeared weaker than obesity. Even after controlling for obesity, insulin, and the other components of the IRS, male subjects in both races in the upper tertile of triglycerides were still more likely to have hyperuricemia.


CONCLUSIONS
The association of hyperuricemia with most aspects of the IRS may result predominantly from their covariation with adiposity and secondarily with insulin level. Elevated triglyceride level seems to have an independent relationship with hyperuricemia in males. The relationship between hyperuricemia and cardiovascular disease observed in previous studies may be secondary to its association with the IRS.
16433940
Prevalence of hyperuricemia and relation of serum uric acid with cardiovascular risk factors in a developing country
BackgroundThe prevalence of hyperuricemia has rarely been investigated in developing countries. The purpose of the present study was to investigate the prevalence of hyperuricemia and the association between uric acid levels and the various cardiovascular risk factors in a developing country with high average blood pressures (the Seychelles, Indian Ocean, population mainly of African origin).MethodsThis cross-sectional health examination survey was based on a population random sample from the Seychelles. It included 1011 subjects aged 25 to 64 years. Blood pressure (BP), body mass index (BMI), waist circumference, waist-to-hip ratio, total and HDL cholesterol, serum triglycerides and serum uric acid were measured. Data were analyzed using scatterplot smoothing techniques and gender-specific linear regression models.ResultsThe prevalence of a serum uric acid level >420 μmol/L in men was 35.2% and the prevalence of a serum uric acid level >360 μmol/L was 8.7% in women. Serum uric acid was strongly related to serum triglycerides in men as well as in women (r = 0.73 in men and r = 0.59 in women, p < 0.001). Uric acid levels were also significantly associated but to a lesser degree with age, BMI, blood pressure, alcohol and the use of antihypertensive therapy. In a regression model, triglycerides, age, BMI, antihypertensive therapy and alcohol consumption accounted for about 50% (R2) of the serum uric acid variations in men as well as in women.ConclusionsThis study shows that the prevalence of hyperuricemia can be high in a developing country such as the Seychelles. Besides alcohol consumption and the use of antihypertensive therapy, mainly diuretics, serum uric acid is markedly associated with parameters of the metabolic syndrome, in particular serum triglycerides. Considering the growing incidence of obesity and metabolic syndrome worldwide and the potential link between hyperuricemia and cardiovascular complications, more emphasis should be put on the evolving prevalence of hyperuricemia in developing countries.
24630655
Arsenic exposure, hyperuricemia, and gout in US adults.
BACKGROUND
There is very limited information on the association between arsenic and serum uric acid levels or gout. The aim of this study was to investigate the association of arsenic with hyperuricemia and gout in US adults.


METHODS
A cross-sectional study was conducted in 5632 adults aged 20years or older from the National Health and Nutrition Examination Survey (NHANES) 2003-2010 with determinations of serum uric acid and urine total arsenic and dimethylarsinate (DMA). Hyperuricemia was defined as serum uric acid higher than 7.0mg/dL for men and 6.0mg/dL for women. Gout was defined based on self-reported physician diagnosis and medication use.


RESULTS
After adjustment for sociodemographic factors, comorbidities and arsenobetaine levels, the increase in the geometric means of serum uric acid associated with one interquartile range increase in total arsenic and DMA levels was 3% (95% CI 2-5) and 3% (2-5), respectively, in men and 1% (0-3) and 2% (0-4), respectively, in women. In men, the adjusted odds ratio for hyperuricemia comparing the highest to lowest quartiles of total arsenic was 1.84 (95% CI, 1.26-2.68) and for DMA it was 1.41 (95% CI, 1.01-1.96). The corresponding odds ratios in women were 1.26 (0.77, 2.07) and 1.49 (0.96, 2.31), respectively. The odds ratio for gout comparing the highest to lowest tertiles was 5.46 (95% CI, 1.70-17.6) for total arsenic and 1.98 (0.64-6.15) for DMA among women older than 40years old. Urine arsenic was not associated with gout in men.


CONCLUSION
Low level arsenic exposures may be associated with the risk of hyperuricemia in men and with the prevalence of gout in women. Prospective research focusing on establishing the direction of the relationship among arsenic, hyperuricemia, and gout is needed.
73057679
Metabolic Syndrome among Undergraduate Students Attending Medical Clinics for Obligatory Medical Screening
Purpose : To determine the prevalence and risk factors for metabolic syndrome (MS) among first-year undergraduate students in three Sudanese universities. Methods : A total of 384 first-year students attending university medical clinics for obligatory medical checkup in Khartoum, Sudan participated in this cross-sectional study. Anthropometric parameters, including weight, height, body mass index (BMI) and waist circumference (WC) were measured with reference to National Cholesterol Education Program’s Adult Treatment Panel III (NCEP/ATP III) guidelines. Fasting blood samples were collected from all participants and assayed for fasting blood glucose (FBG), total cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL), and low density lipoprotein (LDL). Results : The overall prevalence of MS in the test group was 7.8 %. The prevalence of MS, though higher in females, was statistically not significant (p = 0.32). According to residential area (rural – urban), the prevalence was higher in urban than rural, 10.4 and 4.4 %, respectively (p = 0.25 and p = 0.25, respectively). In addition, frequency of MS was directly proportional to age. The weight of patients with MS was significantly different from that of non-MS subjects (p ˂ 0.001). Same was also observed when obese patients were compared with non-MS subjects. (p ˂ 0.001). Conclusion : The prevalence of MS among Sudanese first-year university students in Khartoum is moderately high. Incidence of MS among the students is directly proportional to BMI. Keywords : Metabolic syndrome, Obesity, Hypertension, Diabetes, Dyslipidemia, Anthropometric
30499896
Impact of Ambulatory Blood Pressure Monitoring on Control of Untreated, Undertreated, and Resistant Hypertension in Older People in Spain.
BACKGROUND AND OBJECTIVE
The impact of ambulatory blood pressure monitoring (ABPM) on hypertension control has not been fully assessed across the treatment spectrum in older community-living individuals and could have important implications; specifically, the number of untreated, undertreated, and treatment-resistant uncontrolled hypertensives in need of or with unnecessary drug treatment could vary with respect to studies based on conventional blood pressure (BP) measured in clinical settings.


DESIGN, SETTING, AND PARTICIPANTS
Cross-sectional study conducted in 2012 among 1118 community-living individuals aged ≥60 years in Spain.


MEASUREMENTS
Three conventional BP measurements at participants' homes and 24-hour ABPM were performed under standardized conditions. Uncontrolled hypertension (mean of the last 2 conventional BP readings ≥140/90 mm Hg) was considered undertreated if on 1 or 2 antihypertensive drugs, and apparently treatment-resistant if on ≥3 drugs. White-coat effect was defined as conventional BP ≥ 140/90 mm Hg and 24-hour BP <130/80 mm Hg.


RESULTS
Of 720 hypertensive patients (mean age, 72.3 ± 6.3 years; 51.3%, males), 64.4% had conventional BP ≥ 140/90 mm Hg, and from these 39.9% were untreated, 49.5% undertreated, and 10.6% apparently treatment-resistant. Among uncontrolled hypertensive patients, the white-coat effect was present in 52.4% of those untreated, in 53.5% of undertreated, and in 49% of apparent treatment-resistant. These white-coat results were similar or even higher across alternative BP thresholds.


CONCLUSIONS
One-half of older uncontrolled hypertensive patients studied at home were actually controlled according to ABPM, regardless of treatment status. This suggests reconsideration of treatment needs in these numerous white-coat hypertensive patients, who probably do not need drug treatment initiation or intensification.
35073725
Clinical evaluation of rosuvastatin in heart transplant patients with hypercholesterolemia and therapeutic failure of other statin regimens: short‐term and long‐term efficacy and safety results
We conducted an observational study of 30 heart transplant recipients with serum low‐density lipoprotein cholesterol (LDL‐c) >100 mg/dl despite previous statin therapy, who were treated with rosuvastatin 10 mg daily (5 mg in case of renal dysfunction). Serum lipids, creatine phosphokinase (CPK), bilirubin, and hepatic enzymes were prospectively measured 2, 4, and 12 weeks after the initiation of the drug. Clinical outcomes of patients who continued on long‐term rosuvastatin therapy beyond this 12‐week period were reviewed in February 2015. Over the 12‐week period following rosuvastatin initiation, serum levels of total cholesterol (TC) and LDL‐c and the ratio TC/high‐density lipoprotein cholesterol (HDL‐c) decreased steadily (P < 0.001). Average absolute reductions of these three parameters were –48.7 mg/dl, –46.6 mg/dl, and –0.9, respectively. Seventeen (57%) achieved a serum LDL‐c < 100 mg/dl. No significant changes from baseline were observed in serum levels of triglycerides, HDL‐c, hepatic enzymes, bilirubin, or CPK. Twenty‐seven (90%) patients continued on long‐term therapy with rosuvastatin over a median period of 3.6 years, with no further significant variation in lipid profile. The drug was suspended due to liver toxicity in 1 (3.3%) patient and due to muscle toxicity in 2 (6.7%) patients. All adverse reactions resolved rapidly after rosuvastatin withdrawal. Our study supports rosuvastatin as a reasonable alternative for heart transplant recipients with hypercholesterolemia and therapeutic failure of other statin regimens.
30599489
[Association of hyperuricemia with hyperlipidemia and obesity].
Various epidemiological evidences have shown the increased incidence of hyperuricemia in the subjects with hyperlipidemia and/or obesity. Our clinical study indicated the association was more close in hypertriglyceridemia to hyperuricemia than in hypercholesterolemia. Serum uric acid level increased more in Type IIb with elevated lipoprotein lipase (LPL) than those with low or normal LPL. Elevated LPL may be involved in the retarded uric acid clearance due to increased free fatty acids (FFA) in the serum, resulting in the elevation of uric acid and may be linked to the obesity-insulin resistance syndrome. Increased FFA may play an important role on the association of hyperuricemia with hypertriglyceridemia.
18242427
Relationship between Hyperuricemia and Lipid Profiles in US Adults
Background. Although the link between hyperuricemia and metabolic syndrome had been recognized, the association of the dyslipidemia among individuals with hyperuricemia remains not comprehensively assessed. Methods. Using NHANES III study, we examined the relation between serum lipid profiles and different serum uric acid levels, including serum total cholesterol, LDL cholesterol, triglycerides, HDL cholesterol, apolipoprotein-B, lipoprotein (a), apolipoprotein AI, ratio of triglycerides to HDL cholesterol, and ratio of apolipoprotein-B to AI. Results. After adjusting for potential confounders, average differences (95% confidence interval) comparing the top to the bottom (reference) serum uric acid were 0.29 (0.19, 0.39) mmol/L for total cholesterol, 0.33 (0.26, 0.41) mmol/L for triglycerides, 0.14 (0.01, 0.27) mmol/L for LDL cholesterol, −0.08 (−0.11, −0.05) mmol/L for HDL, and 0.09 (0.05, 0.12) g/L for serum apolipoprotein-B. Notably, ratios of triglycerides to HDL cholesterol and apolipoprotein-B to AI were also linearly associated with uric acid levels (P for trend < 0.001). Conclusions. This study suggested that serum LDL cholesterol, triglycerides, total cholesterol, apolipoprotein-B levels, ratio of triglycerides to HDL cholesterol, and ratio of apolipoprotein-B to AI are strongly associated with serum uric acid levels, whereas serum HDL cholesterol levels are significantly inversely associated. In the clinical practice, the more comprehensive strategic management to deal with dyslipidemia and hyperuricemia deserves further investigation.
3809151
Polymorphisms of the Peroxisome Proliferator-Activated Receptor-γ (rs1801282) and its coactivator-1 (rs8192673) are associated with obesity indexes in subjects with type 2 diabetes mellitus
AbstractᅟThe aim of this study was to clarify whether common single nucleotide polymorphisms (SNPs) of the Peroxisome Proliferator-Activated Receptor-γ (PPAR-γ) gene (rs1801282) and the Peroxisome Proliferator-Activated Receptor-γ Coactivator-1 (PGC-1α) gene (rs8192673) are associated with obesity indexes (BMI, waist circumference) in subjects with type 2 diabetes mellitus (T2DM) in Caucasian population. The second aim was to find an association of both polymorphisms with T2DM.MethodsTwo exonic SNPs of both genes rs1801282 of the PPAR-γ gene and rs8192673 of the PGC-1α gene) were genotyped in 881 unrelated Slovene subjects (Caucasians) with T2DM and in 348 subjects without T2DM (control subjects).ResultsFemale homozygotes with the CC genotype of the rs8192673 had higher waist circumference in comparison with subjects with other genotypes. Homozygotes (females, males) with wild allele (Pro) of the rs1801282 (Pro12Ala polymorphism) had higher waist circumference in comparison with subjects with other genotypes. In the study, there were no differences in the distributions of the rs8192673 and the rs1801282 genotypes between patients with T2DM and controls. Linear regression analyses for both polymorphisms were performed and demonstrated an independent effect of the rs1801282 of the PPAR-γ on waist circumference in subjects with T2DM, whereas an independent effect on waist circumference was not demonstrated for the rs8192673 of the PGC-1α gene.ConclusionsIn a large sample of the Caucasians the rs8192673 of the PGC-1α gene and the rs1801282 of the PPAR-γ gene were associated with waist circumference in subjects with T2DM.