Serum uric acid (SUA) is a suggested biomarker for established coronary artery disease, but the role of SUA in early phases of atherosclerosis is controversial. The relations of SUA with vascular markers of subclinical atherosclerosis, including carotid artery intima-media thickness (cIMT), carotid plaque, carotid distensibility (Cdist) and brachial flow-mediated dilatation (FMD) were examined in 1985 young adults aged 30-45 years. In addition to ordinary regression, we used Mendelian randomization techniques to infer causal associations.
In women, the independent multivariate correlates of SUA included BMI, creatinine, alcohol use, triglycerides, glucose and adiponectin (inverse association) (Model R(2) = 0.30). In men, the correlates were BMI, creatinine, triglycerides, C-reactive protein, alcohol use, total cholesterol and adiponectin (inverse) (Model R(2) = 0.33). BMI alone explained most of the variation of SUA levels both in women and men (Partial R(2) ~ 0.2). When SUA was modeled as an explanatory variable for vascular markers, it directly associated with cIMT and inversely with Cdist in age- and sex-adjusted analysis. After further adjustments for BMI or glomerular filtration rate, these relations were reduced to non-significance. No associations were found between SUA and FMD or the presence of a carotid plaque. Mendelian randomization analyses using known genetic variants for BMI and SUA confirmed that BMI is causally linked to SUA and that BMI is a significant confounder in the association between SUA and cIMT.
SUA is associated with cardiovascular risk markers in young adults, especially BMI, but we found no evidence that SUA would have an independent role in the pathophysiology of early atherosclerosis.
Many epidemiologic and experimental animal studies support the hypothesis of there being a causal association between lead exposure and increased blood pressure/cardiovascular disease. This study includes 1,052 men and women from Copenhagen County, Denmark, who were examined in 1976 and 1981; in 1987, only the men were examined. Blood lead fell by approximately 40% for the men during the 11-year period and by approximately 30% for the women during the first 5-year period. There was a univariate association between systolic blood pressure and blood lead for both sexes in 1976, but it disappeared at the following examinations. For women, there was also a significant association with diastolic blood pressure, even after confounders were controlled for at the two examinations. Moreover, the authors found a significant univariate association between changes in blood lead and changes in systolic blood pressure from 1976 to 1987 in the males. All participants taking part in the study in 1976 were followed regarding hospital admissions and deaths throughout a follow-up period lasting for 14 years. There was a significant univariate association with total mortality, coronary heart disease, and cardiovascular disease. However, with regard to coronary heart disease and cardiovascular disease, the associations disappeared when confounders were controlled for. Blood lead was a significant predictor of total mortality after control for relevant confounders. This study supports the hypothesis of there being a weak causal association between blood lead and blood pressure, total mortality, coronary heart disease, and cardiovascular disease. The importance of this association is very modest for the individual, but the population attributable risk may be considerable.
Comment In: Am J Epidemiol. 1994 Mar 1;139(5):543-48154481
OBJECTIVE: The objective of the study was to describe the distribution of cardiovascular disease (CVD) risk factors, and to evaluate the extent of clustering of CVD risk factors in Norwegian children and adolescents. MATERIAL AND METHODS: A randomly selected cohort of 9-year-olds and 15-year-olds from all regions of the country was sampled. Of 2,818 subjects invited to participate, 2,299 accepted, giving an overall participation rate of 82%. RESULTS: Mean (SD) values for the main risk factors for 9-year-old and 15-year-old girls and boys were: total cholesterol (TC) (mmol/L) 4.49 (0.73), 4.37 (0.68), 4.19 (0.76) and 3.80 (0.69), respectively; triglycerides (TG) (mmol/L) 0.72 (0.33), 0.63 (0.32), 0.79 (0.32) and 0.82 (0.47), respectively; high density lipoprotein cholesterol (HDL-c) (mmol/L) 1.70 (0.35), 1.79 (0.40), 1.61 (0.34) and 1.42 (0.30), respectively; systolic blood pressure (mmHg) 102.6 (7.7), 103.3 (7.7), 109.0 (8.8) and 115.3 (9.0), respectively; and homeostasis model assessment score (HOMA) 1.29 (0.83), 1.19 (0.78), 2.10 (1.37) and 2.14 (1.49), respectively. At least five risk factors were found in 11.1 (95% confidence interval (CI) 8.76 to 13.44) times as many participants as expected. A significant degree of clustering of CVD risk factors was found in 11.4% (95% CI, 9.8 to 13.0) of the study population, and these had mean Z scores of 1.24 (0.06) and 1.04 (0.08) for the 9-year-olds and 15-year-olds, respectively. CONCLUSION: This study presents national reference data on selected CVD risk factors in children and adolescents.
Patients with inflammatory joint diseases (IJD) have increased risk of cardiovascular disease (CVD). Our aim was to compare CVD risk profiles in patients with IJD, including rheumatoid arthritis (RA), axial spondyloarthritis (axSpA) and psoriatic arthritis (PsA) and evaluate the future risk of CVD.
The prevalence and numbers of major CVD risk factors (CVD-RFs) (hypertension, elevated cholesterol, obesity, smoking, and diabetes mellitus) were estimated in patients with RA, axSpA and PsA. Relative and absolute risk of CVD according to Systematic Coronary Risk Evaluation (SCORE) was calculated.
In total, 3791 patients were included. CVD was present in 274 patients (7.2%). Of those without established CVD; hypertension and elevated cholesterol were the most frequent CVD-RFs, occurring in 49.8% and 32.8% of patients. Patients with PsA were more often hypertensive and obese. Overall, 73.6% of patients had a minimum of one CVD-RF, which increased from 53.2% among patients aged 30 to
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To investigate changes in cardiovascular risk factors over 14 years in relation to diabetes status.
The study is based on 10,327 subjects who attended the Tromsø Study in 1994 and were screened again in 2007-8. At baseline there were 79 prevalent cases, and 397 incident cases of type 2 diabetes mellitus (DM2) were diagnosed between 1994 and 2008.
Cases with DM2 had decreasing levels of high-density lipoprotein cholesterol (HDL-C), total cholesterol and blood pressure (BP) and increasing levels of triglycerides, body mass index (BMI), and anti-hypertensive treatment during 14 years of follow-up. Despite decreasing BP, more than 75% of the treated cases had BP above 135/80 at the end of follow-up. Similarly, less than 35% of incident cases using statins had low-density lipoprotein cholesterol (LDL-C) below the recommended threshold value of 2.6?mmol/l.
Despite greater relative reduction in cardiovascular risk factors among people with DM2 compared to those without, treatment targets were met in less than 50% of subjects with DM2. Thirteen percent reached the combined targets for glucose, BP and LDL-C control. This indicates a need for more effective strategies to control cardiovascular risk factors especially among individuals with DM2.
The value of lifestyle modification in reducing physiological cardiovascular disease (CVD) risk factors remains controversial because changes in patient behaviour following CVD prevention counseling have failed to correlate with or impact reductions in physiological variables.
To determine whether nonpharmacological CVD prevention counselling significantly reduces behavioural and physiological risk factors, and to examine correlations between changes in these variables.
At baseline, dyslipidemic individuals with or at risk of developing CVD completed CVD risk factor questionnaires. At baseline and three months, participants submitted dietary logs, self-classified their readiness for behaviour change for eight lifestyles, and had their blood lipid profiles, weight and height assessed. Following CVD risk factor screening, lower and higher risk participants were recommended for multidisciplinary group counselling (GC) or group plus individual counselling (GIC), respectively. A prospective time series design assessed behavioural and physiological risk factor changes.
Preeclampsia is a long-term cardiovascular risk factor for the mother and possibly the offspring. Preeclampsia and cardiovascular diseases share common pathophysiological features, including endothelial dysfunction. We explored whether endothelial function, measured noninvasively, as well as circulating biomarkers reflecting lipid metabolism, angiogenesis, and inflammation, differed in paired mothers and offspring 5 to 8 years after delivery. Twenty-six mother and child pairs after pregnancies complicated by preeclampsia were compared with 17 mother and child pairs after uncomplicated pregnancies. In addition, we assessed whether concentrations of maternal circulating biomarkers at delivery predicted findings 5 to 8 years postpartum. We also included an assessment of early onset preeclampsia and specifically addressed the effects of small for gestational age. Endothelial function was significantly reduced in both mothers and children after preeclampsia when combined with a small-for-gestational-age infant compared with mothers and children after pregnancies without a small-for-gestational-age infant (mothers: P
A subsample of the population-based Northern Sweden MONICA Study. This subsample underwent an oral glucose tolerance test after an overnight fast, and consisted of 354 men and 404 women in the 25-64-year age range.
Delineation of low insulin sensitivity and high serum insulin by the diagnostic test technique, prevalence of these variables and their associations with cardiovascular risk factors.
The participants were classified into four subgroups by an insulin sensitivity index and fasting serum insulin. The combination of low insulin sensitivity and high serum insulin was present in 17% of the male and in 18% of the female 25-64-year-old population. In both sexes this combination was closely associated (P
Limited and partly controversial data are available regarding the relationship of arterial pulse wave velocity and childhood cardiovascular risk factors. We studied how risk factors identified in childhood and adulthood predict pulse wave velocity assessed in adulthood. The study cohort consisted of 1691 white adults aged 30 to 45 years who had risk factor data available since childhood. Pulse wave velocity was assessed noninvasively by whole-body impedance cardiography. The number of conventional childhood and adulthood risk factors (extreme quintiles for low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, body mass index, and smoking) was directly associated with pulse wave velocity in adulthood (P=0.005 and P
Sedentary behaviour has recently emerged as a unique risk factor for chronic disease morbidity and mortality. One factor that may explain this relationship is visceral adiposity, which is prospectively associated with increased cardiometabolic risk and mortality. The objective of the present study was to determine whether sedentary behaviour was associated with increased accumulation of visceral fat or other deleterious changes in cardiometabolic risk over a 6-year follow-up period among adult participants in the Quebec Family Study.
The current study included 123 men and 153 women between the ages of 18 and 65. Total sedentary time and physical activity were assessed by self-report questionnaire. Cross-sectional areas of visceral and subcutaneous abdominal adipose tissue were assessed using computed tomography. Cardiometabolic biomarkers including fasting insulin, glucose, blood lipids, HOMA-Insulin Resistance, and oral glucose tolerance were also measured. All variables of interest were collected at both baseline and follow-up.
After adjustment for age, sex, baseline BMI, physical activity, energy intake, smoking, education, income and menopausal status, baseline sedentary behaviour was not associated with changes in visceral adiposity or any other marker of cardiometabolic risk. In the longitudinal model which adjusted for all studied covariates, every 15-minute increase in sedentary behaviour from baseline to follow-up was associated with a 0.13 cm increase in waist circumference (95% CI?=?0.02, 0.25). However, there was no association between changes in sedentary behaviour and changes in visceral adiposity or other markers of cardiometabolic risk.
These results suggest that neither baseline sedentary behaviour nor changes in sedentary behaviour are associated with longitudinal changes in visceral adiposity in adult men and women. With the exception of waist circumference, the present study did not find evidence of a relationship between sedentary behaviour and any marker of cardiometabolic risk in this population.