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Background: Excess adipose tissue has been implicated in the pathogenesis of insulin resistance and atherosclerosis and is a key risk factor for blood pressure (BP) elevation. However, circulating levels of adiponectin, a protein produced by adipose tissue and widely implicated in the pathogenesis of insulin resistance and atherosclerosis, are inversely proportional to adiposity. The relationship between adiponectin and incident hypertension has not been determined in the general US population.Methods: Normotensive participants (n = 1233) enrolled in the Dallas Heart Study, a multiethnic, probability-based population sample of Dallas County adults were followed for median of 7 years. Retroperitoneal, intraperitoneal, visceral, and subcutaneous adipose tissue were measured at baseline by magnetic resonance imaging. Liver fat content was measured by 1 H-magnetic resonance spectroscopy. Relative risk regression was used to determine the association of adiponectin with incident hypertension after adjustment for age, race, sex, BMI, smoking, diabetes, baseline systolic BP, total cholesterol, and regional fat depot.Results: Of the 1233 study participants (median age 40 years, 40% black, and 56% women), 391 (32%) had developed hypertension over a median follow-up of 7 years. Adiponectin levels were associated with reduced risk of incident hypertension (RR 0.81, 95% CI [0.68-0.96]) in the fully adjusted model, which included liver fat. Similar results were observed after adjustment for subcutaneous or visceral fat depots when tested individually or simultaneously in the model.Conclusion: Our study suggested a protective role of adiponectin against incident hypertension independent of body fat distribution. [ABSTRACT FROM AUTHOR]

Background: Previous studies that reported an association of dietary Na+ intake with metabolic syndrome were limited by the use of imprecise measures of obesity, Na+ intake, or exclusion of multiethnic populations. The effect of dietary K+ intake on obesity is less well described. Objective: We hypothesized that high dietary Na+ and low K+, based on the ratio of urinary Na+ to K+ (U[Na+]/[K+]) in a first-void morning urinary sample, is independently associated with total body fat. Design: In a prospective population-based cohort, 2782 participants in the community-dwelling, probability-sampled, multiethnic Dallas Heart Study were analyzed. The primary outcome established a priori was total-body percentage fat (TBPF) measured by dual-energy X-ray absorptiometry. The main predictor was U[Na+]/[K+]. Robust linear regression was used to explore an independent association between U[Na+]/[K+] and TBPF. The analyses were stratified by sex and race after their effect modifications were analyzed. Results: Of the cohort, 55.4% were female, 49.8% African American, 30.8% white, 17.2% Hispanic, and 2.2% other races. The mean (6SD) age was 44 6 10 y, BMI (in kg/m2) was 30 6 7, TBPF was 32 6 10%, and U[Na+]/[K+] was 4.2 6 2.6; 12% had diabetes. In the unadjusted and adjusted models, TBPF increased by 0.75 (95% CI: 0.25, 1.25) and 0.43 (0.15, 0.72), respectively (P = 0.003 for both), for every 3-unit increase in U[Na+]/[K+]. A statistically significant interaction was found between race and U[Na+] /[K+], so that the non-African American races had a higher TBPF than did the African Americans per unit increase in U[Na+]/[K+] (P-interaction, 0.0001 for both). No interaction was found between sex and U[Na+]/[K+]. Conclusions: The ratio of dietary Na+ to K+ intake may be independently associated with TBPF, and this association may be more pronounced in non-African Americans. Future studies should explore whether easily measured spot U[Na+]/[K+] can be used to monitor dietary patterns and guide strategies for obesity management. [ABSTRACT FROM AUTHOR]

The few available population-based longitudinal studies examining the link between change in neighborhood condition and weight change to date have only examined neighborhood changes generated by residential mobility. Applying a difference-in-difference analytic framework to data from the Dallas Heart Study (DHS), a multi-ethnic, population-based cohort in Dallas County, TX, we evaluated the relationship between changes in neighborhood condition and weight change for both movers and non-movers over an approximate seven-year follow-up period. We employed a novel measure of neighborhood condition based on property appraisal data to capture temporally consistent measures of change in neighborhood condition regardless of residential mobility. We observed an inverse relationship between weight change and change in neighborhood condition which was more pronounced for non-movers (1.9 fewer kilograms gained per 1-standard deviation improvement in neighborhood condition) than for movers (1.5 fewer kilograms gained per 1-standard deviation improvement in neighborhood condition). [ABSTRACT FROM AUTHOR]

Adiponectin is a key component in multiple metabolic pathways. Studies evaluating associations of adiponectin with clinical outcomes in older adults have reported conflicting results. We investigated the association of adiponectin with mortality and cardiovascular disease (CVD) morbidity in a young, multiethnic adult population. We analyzed data from participants in the Dallas Heart Study without baseline CVD who underwent assessment of total adiponectin from 2000 to 2002. The primary outcome of all-cause mortality was assessed over median 10.4 years of follow-up using multivariable-adjusted Cox proportional hazards models. Secondary outcomes included CVD mortality, major adverse cardiovascular and cerebrovascular events (MACCE), and heart failure (HF). The study cohort included 3,263 participants, mean age 43.4 years, 44% women, and 50% black. There were 184 deaths (63 CVD), 207 MACCE, and 46 HF events. In multivariable models adjusted for age, gender, race, hypertension, diabetes, smoking, high-density lipoprotein cholesterol-C, hyperlipidemia, high-sensitivity C-reactive protein level, estimated glomerular filtration rate, and body mass index, increasing adiponectin quartiles were positively associated with all-cause mortality Q4 versus Q1 (hazard ratio [HR] = 2.27; 95% confidence interval [CI] 1.47, 3.50); CVD mortality Q4 versus Q1 (HR = 2.43; 95% CI 1.15, 5.15); MACCE Q4 versus Q1 (HR = 1.71; 95% CI 1.13, 2.60); and HF Q4 versus Q1 (HR = 2.95; 95% CI 1.14, 7.67). Findings were similar with adiponectin as a continuous variable and consistent across subgroups defined by age, gender, race, obesity, diabetes, metabolic syndrome, or elevated high-sensitivity C-reactive protein. In conclusion, higher adiponectin was associated with increased mortality and CVD morbidity in a young, multiethnic population. These findings may have implications for strategies aimed at lowering adiponectin to prevent adverse outcomes. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular disease is a leading economic and medical burden in the United States (US). As an important risk factor for cardiovascular disease, hypertension represents a critical point of intervention. Less is known about longitudinal effects of neighborhood deprivation on blood pressure outcomes, especially in light of new hypertension guidelines., Methods: Longitudinal data from the Dallas Heart Study facilitated multilevel regression analysis of the relationship between neighborhood deprivation, blood pressure change, and incident hypertension over a 9-year period. Factor analysis explored neighborhood perception, which was controlled for in all analyses. Neighborhood deprivation was derived from US Census data and divided into tertiles for analysis. Hypertension status was compared using pre-2017 and 2017 hypertension guidelines., Results: After adjusting for covariates, including moving status and residential self-selection, we observed significant associations between residing in the more deprived neighborhoods and 1) increasing blood pressure over time and 2) incident hypertension. In the fully adjusted model of continuous blood pressure change, significant relationships were seen for both medium (SBP: β = 4.81, SE = 1.39, P = .0005; DBP: β = 2.61, SE = 0.71, P = .0003) and high deprivation (SBP: β = 7.64, SE = 1.55, P < .0001; DBP: β = 4.64, SE = 0.78, P < .0001). In the fully adjusted model of incident hypertension, participants in areas of high deprivation had 1.69 higher odds of developing HTN (OR 1.69; 95% CI 1.02, 2.82), as defined by 2017 hypertension guidelines. Results varied based on definition of hypertension used (pre-2017 vs. 2017 guidelines)., Conclusion: These findings highlight the potential impact of adverse neighborhood conditions on cardiometabolic outcomes, such as hypertension., (Published by Elsevier Inc.)

Background: Although contributors to remodeling of the left ventricle (LV) have been well studied in general population cohorts, few data are available describing factors influencing changes in left atrial (LA) structure., Methods and Results: Maximum LA volume was determined by cardiac magnetic resonance imaging among 748 participants in the Dallas Heart Study at 2 visits a mean of 8 years apart. Associations of changes in LA volume (ΔLAV) with traditional risk factors, biomarkers, LV geometry, and remodeling by cardiac magnetic resonance imaging and detailed measurements of global and regional adiposity (by magnetic resonance imaging and dual-energy x ray absorptiometry) were assessed using multivariable linear regression. Greater ΔLAV was independently associated with black and Hispanic race/ethnicity, change in systolic blood pressure, LV mass and ΔLV mass, N-terminal probrain natriuretic peptide and change in N-terminal probrain natriuretic peptide, and body mass index (P<0.05 for each). In subanalyses, the associations of ΔLAV with LV mass parameters were driven by associations with baseline and ΔLV end diastolic volume (P<0.0001 for each) and not wall thickness (P=0.21). Associations of ΔLAV with body mass index were explained exclusively by associations with visceral fat mass (P=0.002), with no association seen between ΔLAV and subcutaneous abdominal fat (P=0.47) or lower body fat (P=0.30)., Conclusions: Left atrial dilatation in the population is more common in black and Hispanic than in white individuals and is associated with parallel changes in the LV. LA dilatation may be mediated by blood pressure control and the development of visceral adiposity., (© 2017 American Heart Association, Inc.)

Therapies targeting high-density lipoprotein cholesterol content (HDL-C) have not improved coronary heart disease (CHD) outcomes. High-density lipoprotein particle concentration (HDL-P) may better predict CHD. However, the impact of race/ethnicity on the relations between HDL-P and subclinical atherosclerosis and incident CHD events has not been described. Participants from the Dallas Heart Study (DHS), a multiethnic, probability-based, population cohort of Dallas County adults, underwent the following baseline measurements: HDL-C, HDL-P by nuclear magnetic resonance imaging, and coronary artery calcium by electron-beam computed tomography. Participants were followed for a median of 9.3 years for incident CHD events (composite of first myocardial infarction, stroke, coronary revascularization, or cardiovascular death). The study comprised 1,977 participants free of CHD (51% women, 46% black). In adjusted models, HDL-C was not associated with prevalent coronary artery calcium (p = 0.13) or incident CHD overall (hazard ratio [HR] per 1 SD 0.89, 95% confidence interval [CI] 0.76 to 1.05). However, HDL-C was inversely associated with incident CHD among nonblack (adjusted HR per 1 SD 0.67, 95% CI 0.46 to 0.97) but not black participants (HR 0.94, 95% CI 0.78 to 1.13, pinteraction = 0.05). Conversely, HDL-P, adjusted for risk factors and HDL-C, was inversely associated with prevalent coronary artery calcium (p = 0.009) and with incident CHD overall (adjusted HR per 1 SD 0.73, 95% CI 0.62 to 0.86), with no interaction by black race/ethnicity (pinteraction = 0.57). In conclusion, in contrast to HDL-C, the inverse relation between HDL-P and incident CHD events is consistent across ethnicities. These findings suggest that HDL-P is superior to HDL-C in predicting prevalent atherosclerosis as well as incident CHD events across a diverse population and should be considered as a therapeutic target., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Background: Obesity has been linked to the development of hypertension, but whether total adiposity or site-specific fat accumulation underpins this relationship is unclear., Objectives: This study sought to determine the relationship between adipose tissue distribution and incident hypertension., Methods: Normotensive participants enrolled in the Dallas Heart Study were followed for a median of 7 years for the development of hypertension (systolic blood pressure [SBP] ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or initiation of blood pressure medications). Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) was quantified by magnetic resonance imaging and proton-spectroscopic imaging, and lower body fat (LBF) was imaged by dual-energy x-ray absorptiometry. Multivariable relative risk regression was performed to test the association between individual fat depots and incident hypertension, adjusting for age, sex, race/ethnicity, diabetes, smoking, SBP, and body mass index (BMI)., Results: Among 903 participants (median age, 40 years; 57% women; 60% nonwhite; median BMI 27.5 kg/m(2)), 230 (25%) developed incident hypertension. In multivariable analyses, higher BMI was significantly associated with incident hypertension (relative risk: 1.24; 95% confidence interval: 1.12 to 1.36, per 1-SD increase). However, when VAT, SAT, and LBF were added to the model, only VAT remained independently associated with incident hypertension (relative risk: 1.22; 95% confidence interval: 1.06 to 1.39, per 1-SD increase)., Conclusions: Increased visceral adiposity, but not total or subcutaneous adiposity, was robustly associated with incident hypertension. Additional studies will be needed to elucidate the mechanisms behind this association., (Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objectives: This study aimed to investigate the independent and joint associations between family history of myocardial infarction (FH) and coronary artery calcification (CAC) with incident coronary heart disease (CHD)., Background: FH and CAC are associated with each other and with incident CHD. It is not known whether FH retains its predictive value after CAC results are accounted for., Methods: Among 2,390 participants without cardiovascular disease enrolled in the Dallas Heart Study, we assessed FH (myocardial infarction in a first-degree relative) and prevalent CAC by electron-beam computed tomography. The primary outcome, a composite of CHD-related death, myocardial infarction, and percutaneous or surgical coronary revascularization, was assessed over a mean follow-up of 8.0 ± 1.2 years. The individual and joint associations with the CHD composite outcome were determined for FH and CAC., Results: The mean age of the population was 44 ± 9 years; 32% had FH and 47% had a CAC score of 0. In multivariate models adjusted for traditional risk factors, FH was independently associated with CHD (adjusted hazard ratio: 2.6; 95% confidence interval: 1.6 to 4.2; p < 0.001). Further adjustment for prevalent CAC did not diminish this association (adjusted hazard ratio: 2.6; 95% confidence interval: 1.6 to 4.2; p < 0.001). FH and CAC were additive: CHD event rates in those with both FH and CAC were 8.8% vs. 3.3% in those with prevalent CAC alone (p < 0.001). CHD rates were 1.9% in those with FH alone compared with 0.4% in those with neither FH nor CAC (p < 0.017). Among subjects without CAC, FH characterized a group with a more unfavorable cardiometabolic profile., Conclusions: FH provided prognostic information that was independent of and additive to CAC. Among those with CAC, FH identified subjects at particularly high short-term risk, and, among those without it, selected a group with an adverse risk-factor profile., (Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

This study examines intercorrelations among waist circumference (WC), intraperitoneal fat (IPF), and subcutaneous abdominal fat (SAF) in ethnically diverse Dallas Heart Study consisting of 1538 women and 1212 men (50% Black). Correlations between fat depots and triglyceride or HOMA2-IR, biomarkers of metabolic syndrome, are also reported. Total abdominal fat (TAF), ASF, and IPF masses were measured by magnetic resonance imaging. The highest correlations with WC according to ethnicity and gender were noted for TAF (R (2) = 0.81 - 0.88) with progressively lower correlations with ASF (0.65-0.82) and IPF (0.29-0.85). The percentage of IPF relative to TAF was not significantly correlated with WC. For all WC categories, higher IPF/ASF ratios were associated with higher triglyceride levels. In contrast, differences in ratios had little or no association with HOMA2-IR. However, when all data were pooled, IPF was positively correlated with both triglyceride (r = 0.358 (men) and 0.363 (women)) and HOMA2-IR (r = 0.480 (men) and 0.517 (women)); after adjustment for ASF, IPF was still correlated with triglyceride (r = 0.353 (men) and 0.348 (women)) and HOMA2-IR (r = 0.290 (men) and 0.221 (women)). WC measures TAF reliably, but its association with IPF depends on IPF/ASF ratios that vary by gender and ethnicity.