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Background: Obesity may contribute to adverse outcomes in coronavirus disease 2019 (COVID-19). However, studies of large, broadly generalizable patient populations are lacking, and the effect of body mass index (BMI) on COVID-19 outcomes- particularly in younger adults-remains uncertain., Methods: We analyzed data from patients hospitalized with COVID-19 at 88 US hospitals enrolled in the American Heart Association's COVID-19 Cardiovascular Disease Registry with data collection through July 22, 2020. BMI was stratified by World Health Organization obesity class, with normal weight prespecified as the reference group., Results: Obesity, and, in particular, class III obesity, was overrepresented in the registry in comparison with the US population, with the largest differences among adults ≤50 years. Among 7606 patients, in-hospital death or mechanical ventilation occurred in 2109 (27.7%), in-hospital death in 1302 (17.1%), and mechanical ventilation in 1602 (21.1%). After multivariable adjustment, classes I to III obesity were associated with higher risks of in-hospital death or mechanical ventilation (odds ratio, 1.28 [95% CI, 1.09-1.51], 1.57 [1.29-1.91], 1.80 [1.47-2.20], respectively), and class III obesity was associated with a higher risk of in-hospital death (hazard ratio, 1.26 [95% CI, 1.00-1.58]). Overweight and class I to III obese individuals were at higher risk for mechanical ventilation (odds ratio, 1.28 [95% CI, 1.09-1.51], 1.54 [1.29-1.84], 1.88 [1.52-2.32], and 2.08 [1.68-2.58], respectively). Significant BMI by age interactions were seen for all primary end points ( P -interaction<0.05 for each), such that the association of BMI with death or mechanical ventilation was strongest in adults ≤50 years, intermediate in adults 51 to 70 years, and weakest in adults >70 years. Severe obesity (BMI ≥40 kg/m 2 ) was associated with an increased risk of in-hospital death only in those ≤50 years (hazard ratio, 1.36 [1.01-1.84]). In adjusted analyses, higher BMI was associated with dialysis initiation and with venous thromboembolism but not with major adverse cardiac events., Conclusions: Obese patients are more likely to be hospitalized with COVID-19, and are at higher risk of in-hospital death or mechanical ventilation, in particular, if young (age ≤50 years). Obese patients are also at higher risk for venous thromboembolism and dialysis. These observations support clear public health messaging and rigorous adherence to COVID-19 prevention strategies in all obese individuals regardless of age.

Importance: Obesity is a global health challenge and a risk factor for atherosclerotic cardiovascular disease (ASVCD). Performance of the pooled cohort equations (PCE) for ASCVD risk by body mass index (BMI; calculated as weight in kilograms divided by height in meters squared) is unknown., Objective: To assess performance of the PCE across clinical BMI categories., Design, Setting, and Participants: This cohort study used pooled individual-level data from 8 community-based, prospective, longitudinal cohort studies with 10-year ASCVD event follow-up from 1996 to 2016. We included all adults ages 40 to 79 years without baseline ASCVD or statin use, resulting in a sample size of 37 311 participants. Data were analyzed from August 2017 to July 2020., Exposures: Participant BMI category: underweight (<18.5), normal weight (18.5 to <25), overweight (25 to <30), mild obesity (30 to <35), and moderate to severe obesity (≥35)., Main Outcomes and Measures: Discrimination (Harrell C statistic) and calibration (Nam-D'Agostino χ2 goodness-of-fit test) of the PCE across BMI categories. Improvement in discrimination and net reclassification with addition of BMI, waist circumference, and high-sensitivity C-reactive protein (hsCRP) to the PCE., Results: Among 37 311 participants (mean [SD] age, 58.6 [11.8] years; 21 897 [58.7%] women), 380 604 person-years of follow-up were conducted. Mean (SD) baseline BMI was 29.0 (6.2), and 360 individuals (1.0%) were in the underweight category, 9937 individuals (26.6%) were in the normal weight category, 13 601 individuals (36.4%) were in the overweight category, 7783 individuals (20.9%) were in the mild obesity category, and 5630 individuals (15.1%) were in the moderate to severe obesity category. Median (interquartile range [IQR]) 10-year estimated ASCVD risk was 7.1% (2.5%-15.4%), and 3709 individuals (9.9%) developed ASCVD over a median (IQR) 10.8 [8.5-12.6] years. The PCE overestimated ASCVD risk in the overall cohort (estimated/observed [E/O] risk ratio, 1.22; 95% CI, 1.18-1.26) and across all BMI categories except the underweight category. Calibration was better near the clinical decision threshold in all BMI groups but worse among individuals with moderate or severe obesity (E/O risk ratio, 1.36; 95% CI, 1.25-1.47) and among those with the highest estimated ASCVD risk ≥20%. The PCE C statistic overall was 0.760 (95% CI, 0.753-0.767), with lower discrimination in the moderate or severe obesity group (C statistic, 0.742; 95% CI, 0.721-0.763) compared with the normal-range BMI group (C statistic, 0.785; 95% CI, 0.772-0.798). Waist circumference (hazard ratio, 1.07 per 1-SD increase; 95% CI, 1.03-1.11) and hsCRP (hazard ratio, 1.07 per 1-SD increase; 95% CI, 1.05-1.09), but not BMI, were associated with increased ASCVD risk when added to the PCE. However, these factors did not improve model performance (C statistic, 0.760; 95% CI, 0.753-0.767) with or without added metrics., Conclusions and Relevance: These findings suggest that the PCE had acceptable model discrimination and were well calibrated at clinical decision thresholds but overestimated risk of ASCVD for individuals in overweight and obese categories, particularly individuals with high estimated risk. Incorporation of the usual clinical measures of obesity did not improve risk estimation of the PCE. Future research is needed to determine whether incorporation of alternative high-risk obesity markers (eg, weight trajectory or measures of visceral or ectopic fat) into the PCE may improve risk prediction.

Objectives: This study evaluated the contributions of obesity and changes in body mass index (BMI) in mid-life to long-term heart failure (HF) risk independent of cardiorespiratory fitness (CRF) levels., Background: Obesity and low CRF are well-established risk factors for HF. However, given the inverse association between CRF and obesity, the independent contributions of BMI toward HF risk are not fully understood., Methods: We included 19,485 participants from the Cooper Center Longitudinal Study who survived to receive Medicare coverage, from 1999 to 2009. CRF was estimated in metabolic equivalents (METS) according to Balke treadmill time. Associations of BMI and BMI change with HF hospitalization after age 65 were assessed by applying a proportional hazards recurrent events model to the failure time data., Results: After 127,110 person-years of follow-up, we observed 1,038 HF hospitalization events. Higher mid-life BMI was significantly associated with greater risk of HF hospitalization after adjusting for established HF risk factors (hazard ratio [HR]: 1.19; 95% confidence interval [CI]: 1.12 to 1.26 per 3 kg/m 2 higher BMI). This association was attenuated after adjusting for CRF (HR: 1.10; 95% CI: 1.03 to 1.17 per 3 kg/m 2 higher BMI). CRF accounted for 47% of the HF risk associated with BMI. BMI change was not significantly associated with risk of HF in older age after adjustment for CRF change., Conclusions: Higher BMI-associated risk of HF is explained largely by differences in CRF levels. Furthermore, BMI change is not significantly associated with HF risk after adjusting for CRF changes. These findings highlight the importance of CRF in mediating BMI-associated HF risk., (Copyright © 2017 American College of Cardiology Foundation. Published by 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.)

Visceral adipose tissue (VAT) is a strong prognostic factor for cardiovascular disease and a potential target for cardiovascular risk stratification. Because VAT is difficult to measure in clinical practice, we estimated prediction models with predictors routinely measured in general practice and VAT as outcome using ridge regression in 2,501 middle-aged participants from the Netherlands Epidemiology of Obesity study, 2008-2012. Adding waist circumference and other anthropometric measurements on top of the routinely measured variables improved the optimism-adjusted R2 from 0.50 to 0.58 with a decrease in the root-mean-square error (RMSE) from 45.6 to 41.5 cm2 and with overall good calibration. Further addition of predominantly lipoprotein-related metabolites from the Nightingale platform did not improve the optimism-corrected R2 and RMSE. The models were externally validated in 370 participants from the Prospective Investigation of Vasculature in Uppsala Seniors (PIVUS, 2006-2009) and 1,901 participants from the Multi-Ethnic Study of Atherosclerosis (MESA, 2000-2007). Performance was comparable to the development setting in PIVUS (R2 = 0.63, RMSE = 42.4 cm2, calibration slope = 0.94) but lower in MESA (R2 = 0.44, RMSE = 60.7 cm2, calibration slope = 0.75). Our findings indicate that the estimation of VAT with routine clinical measurements can be substantially improved by incorporating waist circumference but not by metabolite measurements.

Aims: To describe the overall fat distribution patterns independent of body mass index (BMI) in participants with type 2 diabetes (T2D) in the SURPASS‐3 MRI substudy by comparison with sex‐ and BMI‐matched virtual control groups (VCGs) derived from the UK Biobank imaging study at baseline and Week 52. Methods: For each study participant at baseline and Week 52 (N = 296), a VCG of ≥150 participants with the same sex and similar BMI was identified from the UK Biobank imaging study (N = 40 172). Average visceral adipose tissue (VAT), abdominal subcutaneous adipose tissue (aSAT) and liver fat (LF) levels and the observed standard deviations (SDs; standardized normal z‐scores: z‐VAT, z‐aSAT and z‐LF) were calculated based on the matched VCGs. Differences in z‐scores between baseline and Week 52 were calculated to describe potential shifts in fat distribution pattern independent of weight change. Results: Baseline fat distribution patterns were similar across pooled tirzepatide (5, 10 and 15 mg) and insulin degludec (IDeg) arms. Compared with matched VCGs, SURPASS‐3 participants had higher baseline VAT (mean [SD] z‐VAT +0.42 [1.23]; p < 0.001) and LF (z‐LF +1.24 [0.92]; p < 0.001) but similar aSAT (z‐aSAT −0.13 [1.11]; p = 0.083). Tirzepatide‐treated participants had significant decreases in z‐VAT (−0.18 [0.58]; p < 0.001) and z‐LF (−0.54 [0.84]; p < 0.001) but increased z‐aSAT (+0.11 [0.50]; p = 0.012). Participants treated with IDeg had a significant change in z‐LF only (−0.46 [0.90]; p = 0.001), while no significant changes were observed for z‐VAT (+0.13 [0.52]; p = 0.096) and z‐aSAT (+0.09 [0.61]; p = 0.303). Conclusion: In this exploratory analysis, treatment with tirzepatide in people with T2D resulted in a significant reduction of z‐VAT and z‐LF, while z‐aSAT was increased from an initially negative value, suggesting a possible treatment‐related shift towards a more balanced fat distribution pattern with prominent VAT and LF loss. [ABSTRACT FROM AUTHOR]

Aim: The effects of weight loss with a partial or total meal replacement programme (MRP) on atherosclerotic cardiovascular disease (ASCVD) risk factors are not fully understood, in particular in people at higher CV risk. In the 52‐week randomized controlled OPTIWIN study in men and women with obesity, meal replacement programme (total for first 26 weeks, partial for the ensuing 26 weeks) with OPTIFAST (OP) resulted in significantly greater weight loss compared with a low‐calorie food‐based (FB) dietary plan, both as part of a comprehensive lifestyle intervention [OP (n = 135)/FB (n = 138) week 26: −12.4%/−6.0%, p <.001; week 52: −10.5%/−5.5%, p <.001]. Here, we examined effects on ASCVD risk factors and 10‐year ASCVD risk. Materials and Methods: Participants with body mass index 30‐55 kg/m2 and age 18‐70 years, and not on anti‐obesity medications, were recruited. The effects on systolic and diastolic blood pressure (SBP, DBP), lipid parameters and 10‐year ASCVD risk were analysed as changes over time using linear mixed models. Subgroup analyses were conducted for changes in SBP, DBP and ASCVD risk by categories of age (<40, 40‐59, ≥60 years), baseline SBP (

Background: Low cardiorespiratory fitness (CRF), high body mass index, and excess visceral adiposity are each associated with impairment in left ventricular (LV) peak circumferential strain (Ecc), an intermediate phenotype that precedes the development of clinical heart failure (HF). However, the association of regional fat distribution and CRF with Ecc independent of each other and other potential confounders is not known. Methods: Participants from the Dallas Heart Study Phase 2 who underwent dual energy X-ray absorptiometry assessment of regional fat distribution, CRF assessment by submaximal treadmill test, and Ecc quantification by tissue-tagged cardiovascular magnetic resonance were included in the analysis. The cross-sectional associations of measures of regional adiposity, namely visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and lower-body fat (LBF) with Ecc after adjustment for CRF and other potential confounders (independent variables) were assessed using multivariable linear regression analysis. Results: The study included 1089 participants (55% female, 39% black). In the unadjusted analysis, higher VAT was associated with greater impairment in Ecc. After adjustment for baseline risk factors, CRF, parameters of LV structure and function, and other fat depots such as SAT and LBF, higher VAT remained associated with greater impairment in Ecc (β: 0.19, P = 0.002). SAT and LBF were not significantly associated with Ecc, however, CRF remained associated with Ecc in the fully adjusted model including all fat depots (β: - 0.15, P < 0.001). Conclusions: VAT and CRF are each independently associated with impairment in Ecc, suggesting that higher VAT burden and low CRF mediate pathological cardiac remodeling through distinct mechanisms. [ABSTRACT FROM AUTHOR]

Aims: Patients with obesity and ischaemic heart failure may counter‐intuitively have better outcomes compared with patients with normal body weight due to an 'obesity paradox'. This study sought to determine if body mass index (BMI) impacts the treatment effects or safety outcomes of the treatment of ischaemic heart failure with coronary artery bypass grafting (CABG). Methods and results: We obtained and reviewed the Surgical Treatment of Ischaemic Heart Failure (STICHES) data for 1212 patients. We categorized obesity by the World Health Organization (WHO) classes to define baseline characteristics and test for treatment interactions for the primary and secondary STICHES outcomes by treatment groups. While CABG decreased the risk of death, there was no evidence of treatment interaction by BMI per 5 kg/m2 (P = 0.83) or WHO obesity class. For the overall cohort, there was no interaction by WHO obesity class for the cumulative incidence of death in either the medical therapy or CABG plus medical therapy (P‐interaction = 0.90). There was a non‐significant trend for higher BMI and a lower risk of death [hazard ratio 0.92, 95% confidence interval (CI) 0.85–1.00, P = 0.051]. Increasing body size (per 5 kg/m2) was associated with return to the operating room (odds ratio 2.48, 95% CI 1.45–4.26, P < 0.001) and infectious mediastinitis (odds ratio 2.09, 95% CI 1.10–3.97, P = 0.024) at 30 days but not other 30 day safety outcomes. Conclusions: The benefit of CABG vs. medical therapy for ischaemic heart failure was consistent regardless of BMI or WHO obesity class for death or secondary clinical outcomes. However, higher BMI was associated with some short‐term post‐CABG complications. [ABSTRACT FROM AUTHOR]

The prevalence of obesity has increased globally over the last 2 decades. Although the body mass index has been a convenient and simple index of obesity at the population level, studies have shown that obesity defined by body mass index alone is a remarkably heterogeneous condition with varying cardiovascular and metabolic manifestations across individuals. Adipose tissue is an exquisitely active metabolic organ engaged in cross-talk between various systems; perturbation of adipose tissue results in a pathological response to positive caloric balance in susceptible individuals that directly and indirectly contributes to cardiovascular and metabolic disease. Inadequate subcutaneous adipose tissue expansion in the face of dietary triglycerides leads to visceral and ectopic fat deposition, inflammatory/adipokine dysregulation, and insulin resistance. Conversely, preferential fat storage in the lower body depot may act as a metabolic buffer and protect other tissues from lipotoxicity caused by lipid overflow and ectopic fat. Translational, epidemiological, and clinical studies over the past 30 years have clearly demonstrated a strong link between visceral and ectopic fat and the development of a clinical syndrome characterized by atherogenic dyslipidemia, hyperinsulinemia/glucose intolerance, hypertension, atherosclerosis, and adverse cardiac remodeling/heart failure. This relationship is even more nuanced when clinical entities such as metabolically healthy obesity phenotype and the obesity paradox are considered. Although it is clear that the accumulation of visceral/ectopic fat is a major contributor to cardiovascular and metabolic risk above and beyond the body mass index, implementation of fat distribution assessment into clinical practice remains a challenge. Anthropometric indexes of obesity are easily implemented, but newer imaging-based methods offer improved sensitivity and specificity for measuring specific depots. Lifestyle, pharmacological, and surgical interventions allow a multidisciplinary approach to overweight/obesity that may improve outcomes and align with a public health message to combat the growing epidemic of obesity worldwide and to build healthier lives free of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Purpose: Leptin dysregulation has been postulated to affect cancer risk through its effects on obesity and inflammation. Epidemiological data evaluating this relationship are conflicting and studies in non-white cohorts is lacking. Therefore, we examined the association of leptin with the risk of incident cancer in the multiethnic Dallas Heart Study (DHS). Methods: Participants enrolled in the DHS without prevalent cancer and with baseline leptin measurements were included. Incident cancer cases were identified through a systematic linkage of the DHS and the Texas Cancer Registry. Leptin was evaluated both as a continuous variable and in sex-specific quartiles. Multivariable Cox proportional hazards modeling was performed to examine the association between leptin levels with incident cancer after adjusting for age, sex, race, smoking status, alcohol use, family history of malignancy, body mass index (BMI), diabetes mellitus and C-reactive protein. Results: Among 2,919 participants (median age 44 years; 54% women; 70% nonwhite; median BMI 29.4 kg/m2), 190 (6.5%) developed cancer after median follow- up of 12 years. Median leptin levels were 12.9 (interquartile range [IQR] 5.8–29.5) ng/ml in the incident cancer group vs. 12.3 (IQR 5.4–26.4) ng/ml those without an incident cancer (p = 0.34). Leptin was not associated with cancer incidence in multivariable analysis (unit standard deviation increase in log-transformed leptin, hazard ratio 0.95; 95% confidence interval, 0.77–1.16; p = 0.60). No association was observed in analyses stratified by sex, race/ethnicity, diabetes, or obesity status. Conclusions: In this study of a predominantly minority population, no association between premorbid leptin levels and cancer incidence was demonstrated. Despite preclinical rationale and positive findings in other studies, this association may not replicate across all racial/ethnic populations. [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]

Objectives: The goal of this study was to investigate the association between natriuretic peptides and body fat distribution in a multiethnic cohort. Background: Natriuretic peptides stimulate lipolysis, reduce weight gain, and promote adipocyte browning in animal models, but data are lacking in humans. Methods: A total of 2,619 participants without heart failure in the Dallas Heart Study underwent measurements of 1) B-type natriuretic peptide (BNP) and N-terminal pro–B-type natriuretic peptide (NT-proBNP); and 2) body fat distribution by dual energy x-ray absorptiometry and magnetic resonance imaging. Cross-sectional associations of natriuretic peptides with adiposity phenotypes were examined after adjustment for age, sex, race, comorbidities, and body mass index. Results: Median BNP and NT-proBNP levels in the study cohort (mean age 44 years; 56% women, 48% African Americans, 32% obese) were 3.0 and 28.1 pg/ml, respectively. Natriuretic peptide levels above the median were associated with a more favorable body fat profile and less insulin resistance, including lower visceral fat, liver fat, and homeostasis model assessment of insulin resistance index, and increased lower body fat and higher adiponectin (p < 0.05 for each). In multivariable analyses, NT-proBNP remained inversely associated with visceral fat (beta coefficient = −0.08; p < 0.0001) and liver fat (beta coefficient = −0.14; p < 0.0001) and positively associated with lower body fat (beta coefficient = 0.07; p < 0.0001) independent of age, sex, race, and obesity status; findings were similar with BNP. Adjustment for body composition, homeostasis model assessment of insulin resistance index, circulating androgens, and adipocytokines did not attenuate the associations. Conclusions: Higher natriuretic peptide levels were independently associated with a favorable adiposity profile, characterized by decreased visceral and liver fat and increased lower body fat, suggesting a link between the heart and adipose tissue distribution mediated through natriuretic peptides. [Copyright &y& Elsevier]

This study examines intercorrelations among waist circumference (WC), intraperitoneal fat (IPF), and subcutaneous abdominal fat (SAF) in ethnically diverseDallasHeart Study consisting of 1538 women and 1212men (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 withWC according to ethnicity and gender were noted for TAF (R2 = 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 withWC. For allWC 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)) andHOMA2-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. [ABSTRACT FROM AUTHOR]

Background: Obesity and diabetes are associated with a higher risk of heart failure (HF). The interrelationships between different measures of adiposity-overall obesity, central obesity, fat mass (FM)-and diabetes status for HF risk are not well-established.Methods: Participant-level data from the ARIC study (Atherosclerosis Risk in Communities; visit 5) and the CHS (Cardiovascular Health Study; visit 1) cohorts were obtained from the National Heart, Lung, and Blood Institute Biologic Specimen and Data Repository Information Coordinating Center, harmonized, and pooled for the present analysis, excluding individuals with prevalent HF. FM was estimated in all participants using established anthropometric prediction equations additionally validated using the bioelectrical impedance-based FM in the ARIC subgroup. Incident HF events on follow-up were captured across both cohorts using similar adjudication methods. Multivariable-adjusted Fine-Gray models were created to evaluate the associations of body mass index (BMI), waist circumference (WC), and FM with risk of HF in the overall cohort as well as among those with versus without diabetes at baseline. The population attributable risk of overall obesity (BMI≥30 kg/m2), abdominal obesity (WC>88 and 102 cm in women and men, respectively), and high FM (above sex-specific median) for incident HF was evaluated among participants with and without diabetes.Results: The study included 10 387 participants (52.9% ARIC; 25.1% diabetes; median age, 74 years). The correlation between predicted and bioelectrical impedance-based FM was high (R2=0.90; n=5038). During a 5-year follow-up, 447 participants developed HF (4.3%). Higher levels of each adiposity measure were significantly associated with higher HF risk (hazard ratio [95% CI] per 1 SD higher BMI=1.15 [1.05, 1.27], WC=1.22 [1.10, 1.36]; FM=1.13 [1.02, 1.25]). A significant interaction was noted between diabetes status and measures of BMI (P interaction=0.04) and WC (P interaction=0.004) for the risk of HF. In stratified analysis, higher measures of each adiposity parameter were significantly associated with higher HF risk in individuals with diabetes (hazard ratio [95% CI] per 1 SD higher BMI=1.29 [1.14-1.47]; WC=1.48 [1.29-1.70]; FM=1.25 [1.09-1.43]) but not those without diabetes, including participants with prediabetes and euglycemia. The population attributable risk percentage of overall obesity, abdominal obesity, and high FM for incident HF was higher among participants with diabetes (12.8%, 29.9%, and 13.7%, respectively) versus those without diabetes (≤1% for each).Conclusions: Higher BMI, WC, and FM are strongly associated with greater risk of HF among older adults, particularly among those with prevalent diabetes. [ABSTRACT FROM AUTHOR]

Obesity contributes to reduced life expectancy because of its link with type 2 diabetes and cardiovascular disease. Yet, targeting this poorly diagnosed, ill-defined, and underaddressed modifiable risk factor remains a challenge. In this review, we emphasize that the tendency among health care professionals to amalgam all forms of obesity altogether as a single entity may contribute to such difficulties and discrepancies. Obesity is a heterogeneous condition both in terms of causes and health consequences. Attention should be given to 2 prevalent subgroups of individuals: 1) patients who are overweight or moderately obese with excess visceral adipose tissue; and 2) patients with severe obesity, the latter group having distinct additional health issues related to their large body fat mass. The challenge of tackling high-cardiovascular-risk forms of obesity through a combination of personalized clinical approaches and population-based solutions is compounded by the current obesogenic environment and economy. [ABSTRACT FROM AUTHOR]

Aim: To investigate the reliability of multicompartmental volumetric mesenchymal segmentations on MRI and their correlations with anthropomorphic and clinical parameters.Materials and Methods: A consecutive series of middle-age (35-50 year old) female volunteers with variable body mass index (BMI) and MRI scans performed as a part of the Dallas Heart Study were included. A semi-automatic segmentation tool was used to partition different mesenchymal tissues- fat, muscle, and bone on MRI of pelvis. Total volumes of each compartment were calculated and compared between overweight/obese (BMI> = 25 kg/m2) and non-obese (BMI < 25 kg/m2) groups, and with physical performance measurements, i.e. mean activity counts per minute (MVPA) and cardiorespiratory fitness (CRF) estimated by submaximal treadmill test (TT). Kruskal Wallis, Mann-Whitney U test, intraclass correlation coefficient (ICC) and Spearman correlations were used. P value <0.05 was considered statistically significant.Results: There were statistically significant positive correlations between fat volume and BMI (p < 0.0001), muscle volume and height (p = 0.03), and bone volume and height (p < 0.0001). Significant inverse correlations were found between bone volume and BMI (p = 0.002). Fair to good interobserver reliability was seen with muscle and fat volumes (ICC = 0.43-0.64) and excellent reliability was seen with bone volumes (ICC = 0.78-0.79). Statistically significant inverse correlations were found between MVPA and age (p = 0.01), and TT with BMI and weight (p = 0.01, 0.03).Conclusion: Multi-compartment mesenchymal tissue volume quantification on pelvic MRI is reliable in females. Inverse correlation of bone volume with BMI has potential implications for future risk of fracture. [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]

Background: GlycA, an integrated glycosylation protein of five acute phase reactants, is a novel inflammatory biomarker associated with both obesity and cardiovascular disease (CVD). We assessed the hypothesis that visceral adipose tissue (VAT) associates with GlycA and this association may partially explain the pathophysiological link between VAT and CVD. Methods: Baseline measurements of risk factors, body mass index (BMI), waist circumference (WC), and VAT were obtained from 2352 adults in the Dallas Heart Study, a multi-ethnic population-based cohort. GlycA was derived from NMR spectral features. Linear regression was used to assess associations between adiposity variables and GlycA. Cox proportional hazards models were used to assess the associations of VAT and GlycA with first or subsequent CVD event over a median of 11.4 years among those with obesity (BMI >=30). Results: Median age was 43, 56% women and 47% blacks. VAT, BMI and WC were each associated with GlycA in separate models adjusted for traditional risk factors (standardized beta estimates of 0.26, 0.27, and 0.27, respectively; all p < 0.0001). VAT remained directly associated with GlycA when additionally adjusting for BMI or WC. In adjusted models for first and recurrent CV events, the significant direct association between VAT and CV events (HR 1.22, 95% CI 1.04 to 1.44; p=0.01) was partially attenuated when adjusted for GlycA (HR 1.19, 95% CI 1.00 to 1.40; p=0.05). In contrast, VAT remained associated with CV events when adjusted for high sensitivity C-reactive protein. GlycA remained strongly associated with CV events despite adjustment for VAT (HR 1.30, 95% CI 1.13 to 1.49; p=0.0002; Table). Conclusions: Direct imaging assessment of VAT is associated with GlycA, a novel marker of inflammation. The link between VAT and CVD may be partly explained by inflammation reflected by GlycA. These findings suggest that GlycA may be a potentially useful surrogate marker for the adverse CVD risk associated with VAT. [ABSTRACT FROM AUTHOR]