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Cardiovascular diseases, community-based participatory research, obesity, social determinants of health, syndemic Obesity, diabetes, and cardiovascular disease (CVD) prevalence remains stagnant or is rising across populations and geographic regions. Keywords: cardiovascular diseases; community-based participatory research; obesity; social determinants of health; syndemic EN cardiovascular diseases community-based participatory research obesity social determinants of health syndemic 105 107 3 01/06/23 20230110 NES 230110 We are experiencing converging pandemics. [Extracted from the article]

The article focuses on the epidemic of overweight and obesity, affecting over 70 present of the U.S. adult population, and discusses the cardiovascular benefits of pharmacologic tools, specifically glucagon-like peptide-1 (GLP-1) receptor agonists, with the SELECT trial demonstrating a 20 present reduction in the risk of cardiovascular events in patients with preexisting atherosclerotic cardiovascular disease.

The global obesity epidemic is well established, with increases in obesity prevalence for most countries since the 1980s. Obesity contributes directly to incident cardiovascular risk factors, including dyslipidemia, type 2 diabetes, hypertension, and sleep disorders. Obesity also leads to the development of cardiovascular disease and cardiovascular disease mortality independently of other cardiovascular risk factors. More recent data highlight abdominal obesity, as determined by waist circumference, as a cardiovascular disease risk marker that is independent of body mass index. There have also been significant advances in imaging modalities for characterizing body composition, including visceral adiposity. Studies that quantify fat depots, including ectopic fat, support excess visceral adiposity as an independent indicator of poor cardiovascular outcomes. Lifestyle modification and subsequent weight loss improve both metabolic syndrome and associated systemic inflammation and endothelial dysfunction. However, clinical trials of medical weight loss have not demonstrated a reduction in coronary artery disease rates. In contrast, prospective studies comparing patients undergoing bariatric surgery with nonsurgical patients with obesity have shown reduced coronary artery disease risk with surgery. In this statement, we summarize the impact of obesity on the diagnosis, clinical management, and outcomes of atherosclerotic cardiovascular disease, heart failure, and arrhythmias, especially sudden cardiac death and atrial fibrillation. In particular, we examine the influence of obesity on noninvasive and invasive diagnostic procedures for coronary artery disease. Moreover, we review the impact of obesity on cardiac function and outcomes related to heart failure with reduced and preserved ejection fraction. Finally, we describe the effects of lifestyle and surgical weight loss interventions on outcomes related to coronary artery disease, heart failure, and atrial fibrillation. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic has highlighted structural inequalities and racism promoting health disparities among communities of color. Taking cardiovascular disease as an example, we provide a framework for multidisciplinary efforts leveraging translational and epidemiologic approaches to decode the biological impacts of inequalities and racism and develop targeted interventions that promote health equity. [ABSTRACT FROM AUTHOR]

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While essential for health and wellness, the various dimensions of sleep health are generally not equitably distributed across the population, and reasons for racial/ethnic sleep disparities are not fully understood. In this review, we describe racial/ethnic sleep disparities and subsequent implications for health from prior and recently conducted epidemiological and clinical studies as well as the potential sleep interventions presented at the 2018 Research Conference on Sleep and the Health of Women at the National Institutes of Health. Given the clear connection between sleep and poor health outcomes such as cardiovascular disease, we concluded that future studies are needed to focus on sleep health in general, sleep disorders such as insomnia and obstructive sleep apnea in particular, and disparities in both sleep health and sleep disorders among women using an intersectional framework. Future research should also integrate sleep into interventional research focused on women's health as these results could address health disparities by informing, for example, future mobile health (mHealth) interventions prioritizing women beyond the clinical setting. [ABSTRACT FROM AUTHOR]

Using data from the Multi-Ethnic Study of Atherosclerosis (MESA), we evaluated associations of neighborhood crime and safety with changes in adiposity (body mass index (BMI) and waist circumference). MESA is a longitudinal study of cardiovascular disease among adults aged 45-84 years at baseline in 2000-2002, from 6 US sites, with follow-up for MESA participants until 2012. Data for this study were limited to Chicago, Illinois, participants in the MESA Neighborhood Ancillary Study, for whom police-recorded crime data were available, and who had complete baseline data (n = 673). We estimated associations of individual-level safety, aggregated neighborhood-level safety, and police-recorded crime with baseline levels and trajectories of BMI and waist circumference over time using linear mixed modeling with random effects. We also estimated how changes in these factors related to changes in BMI and waist circumference using econometric fixed-effects models. At baseline, greater individual-level safety was associated with more adiposity. Increasing individual- and neighborhood-level safety over time were associated with decreasing BMI over the 10-year period, with a more pronounced effect observed in women for individual-level safety and men for neighborhood-level safety. Police-recorded crime was not associated with adiposity. Neighborhood-level safety likely influences adiposity change and subsequent cardiovascular risk in multiethnic populations. [ABSTRACT FROM AUTHOR]

A scientific statetement from nonprofit organization American Heart Association, describing the limitations of current simple measures, such as the use of body mass index and waist-hip ratio with standard thresholds to identify overweight and obesity, as applied to racial and ethnic minorities, is presented. The statement intents to provide practical guidance for clinicians, emphasizing simple anthropometric measures alone or in combination with other measures of overall cardiovascular risk.

Introduction Despite a proposed connection between neighborhood environment and obesity, few longitudinal studies have examined the relationship between change in neighborhood socioeconomic deprivation, as defined by moving between neighborhoods, and change in body weight. The purpose of this study is to examine the longitudinal relationship between moving to more socioeconomically deprived neighborhoods and weight gain as a cardiovascular risk factor. Methods Weight (kilograms) was measured in the Dallas Heart Study (DHS), a multiethnic cohort aged 18–65 years, at baseline (2000–2002) and 7-year follow-up (2007–2009, N=1,835). Data were analyzed in 2013–2014. Geocoded addresses were linked to Dallas County, TX, census block groups. A block group-level neighborhood deprivation index (NDI) was created. Multilevel difference-in-difference models with random effects and a Heckman correction factor (HCF) determined weight change relative to NDI change. Results Forty-nine percent of the DHS population moved (263 to higher NDI, 586 to lower NDI, 47 within same NDI), with blacks more likely to move than whites or Hispanics ( p <0.01), but similar baseline BMI and waist circumference were observed in movers versus non-movers ( p >0.05). Adjusting for HCF, sex, race, and time-varying covariates, those who moved to areas of higher NDI gained more weight compared to those remaining in the same or moving to a lower NDI (0.64 kg per 1-unit NDI increase, 95% CI=0.09, 1.19). Impact of NDI change on weight gain increased with time ( p =0.03). Conclusions Moving to more–socioeconomically deprived neighborhoods was associated with weight gain among DHS participants. [ABSTRACT FROM AUTHOR]

ObjectiveThe Dietary Approaches to Stop Hypertension (DASH) dietary pattern has been shown to reduce cardiometabolic risk. Little is understood about the relationship between objective diet quality and perceived diet quality (PDQ), a potential psychosocial barrier to appropriate dietary intake. We compared PDQ and diet quality measured by a nutrient-based DASH index score in the USA.DesignCross-sectional study. Participants in the 2005–2006 National Health and Nutrition Examination Survey (NHANES) rated diet quality on a 5-point Likert scale and PDQ scores were generated (low, medium, high). A single 24 h dietary recall was used to estimate DASH index scores (range 0–9 points) by assigning 0, 0·5 or 1 point (optimal) for nine target nutrients: total fat, saturated fat, protein, cholesterol, fibre, Ca, Mg, K and Na.SettingNationally representative sample of the US population.SubjectsAdults aged ≥19 years in 2005–2006 NHANES (n 4419).ResultsParticipants with high PDQ (33 %) had higher DASH index scores (mean 3·0 (sd 0·07)) than those with low PDQ (mean 2·5 (sd 0·06), P < 0·001), but average scores did not align with targets for intermediate or optimal DASH accordance. Adults with high PDQ reported higher total fat, saturated fat and Na intakes compared with optimal DASH nutrient goals. Differences between those with high v. low PDQ were similar for Whites and Blacks, but there was no difference between PDQ groups for Mexican Americans.ConclusionsAmong Whites and Blacks, but not Mexican Americans, high PDQ may be associated with higher diet quality, but not necessarily a diet meeting DASH nutrient goals. This disconnect between PDQ and actual diet quality may serve as a target in obesity prevention. [ABSTRACT FROM AUTHOR]

Background: Housing instability is a key social determinant of health and has been linked to adverse short- and long-term health. Eviction reflects a severe form of housing instability and disproportionately affects minority and women residents in the USA; however, its relationship with mortality has not previously been described. Objective: To evaluate the independent association of county-level eviction rates with all-cause mortality in the USA after adjustment for county demographic, socioeconomic, and health-related characteristics. Design: Cross-sectional. Participants: Six hundred eighty-six US counties with available 2016 county-level eviction and mortality data. Exposure: 2016 US county-level eviction rate. Outcome: 2016 US county-level age-adjusted all-cause mortality. Key Results: Among 686 counties (66.1 million residents, 50.5% [49.7–51.2] women, 2% [0.5–11.1] Black race) with available eviction and mortality data in 2016, we observed a significant and graded relationship between county-level eviction rate and all-cause mortality. Counties in the highest eviction tertile demonstrated a greater proportion of residents of Black race and women and a higher prevalence of poverty and comorbid health conditions. After adjustment for county-level sociodemographic traits and prevalent comorbid health conditions, age-adjusted all-cause mortality was highest among counties in the highest eviction tertile (Tertile 3 vs 1 (per 100,000 people) 33.57: 95% CI: 10.5–56.6 p=.004). Consistent results were observed in continuous analysis of eviction, with all-cause mortality increasing by 9.32 deaths per 100,000 people (4.77, 13.89, p<.0001) for every 1% increase in eviction rates. Significant interaction in the relationship between eviction and all-cause mortality was observed by the proportion of Black and women residents. Conclusions: In this cross-sectional analysis, county-level eviction rates were significantly associated with all-cause mortality with the strongest effects observed among counties with the highest proportion of Black and women residents. State and federal protections from evictions may help to reduce the health consequences of housing instability and address disparities in health outcomes. [ABSTRACT FROM AUTHOR]

Objective The aim of this study is to examine a relationship between neighborhood-level socioeconomic deprivation and weight change in a multi-ethnic cohort from Dallas County, Texas and whether behavioral/psychosocial factors attenuate the relationship. Methods Non-movers (those in the same neighborhood throughout the study period) aged 18-65 (N=939) in Dallas Heart Study (DHS) underwent weight measurements between 2000 and 2009 (median 7-year follow-up). Geocoded home addresses defined block groups; a neighborhood deprivation index (NDI) was created (higher NDI=greater deprivation). Multi-level modeling determined weight change relative to NDI. Model fit improvement was examined with adding physical activity and neighborhood environment perceptions (higher score=more unfavorable perceptions) as covariates. A significant interaction between residence length and NDI was found (p-interaction=0.04); results were stratified by median residence length (11years). Results Adjusting for age, sex, race/ethnicity, smoking, and education/income, those who lived in neighborhood > 11years gained 1.0kg per one-unit increment of NDI (p=0.03), or 6kg for those in highest NDI tertile compared with those in the lowest tertile. Physical activity improved model fit; NDI remained associated with weight gain after adjustment for physical activity and neighborhood environment perceptions. There was no significant relationship between NDI and weight change for those in their neighborhood ↜ 11years. Conclusions Living in more socioeconomically deprived neighborhoods over a longer time period was associated with weight gain in DHS. [ABSTRACT FROM AUTHOR]

Prior reports have associated increased circulating levels of matrix metalloproteinase-9 (MMP-9), an endopeptidase active in the extracellular matrix, with the formation and rupture of aortic aneurysms, raising the possibility that MMP-9 may be a useful diagnostic or therapeutic target for aortic pathology. However, associations between MMP-9 and pathological abdominal aortic phenotypes in the general population have not been reported. In the Dallas Heart Study, a population-based sample of Dallas County residents (n = 2304), we measured MMP-9 and performed magnetic resonance imaging (MRI) of the abdominal aorta, measuring aortic compliance, plaque, wall thickness and luminal diameter. After adjustment for traditional cardiac risk factors and body size, higher MMP-9 quartiles were independently associated with higher aortic wall thickness and larger luminal diameter (p < 0.0001 for each), but not abdominal aortic plaque (p = 0.08), coronary artery calcium (p = 0.20) or the aortic luminal diameter/aortic wall thickness ratio (p = 0.37), supporting the hypothesis that therapies targeting MMP-9 may affect the abdominal aortic wall and modify aortic pathology. [ABSTRACT FROM AUTHOR]

BACKGROUND: Quantifying the economic burden of cardiovascular disease and stroke over the coming decades may inform policy, health system, and community-level interventions for prevention and treatment. METHODS: We used nationally representative health, economic, and demographic data to project health care costs attributable to key cardiovascular risk factors (hypertension, diabetes, hypercholesterolemia) and conditions (coronary heart disease, stroke, heart failure, atrial fibrillation) through 2050. The human capital approach was used to estimate productivity losses from morbidity and premature mortality due to cardiovascular conditions. RESULTS: One in 3 US adults received care for a cardiovascular risk factor or condition in 2020. Annual inflation-adjusted (2022 US dollars) health care costs of cardiovascular risk factors are projected to triple between 2020 and 2050, from $400 billion to $1344 billion. For cardiovascular conditions, annual health care costs are projected to almost quadruple, from $393 billion to $1490 billion, and productivity losses are projected to increase by 54%, from $234 billion to $361 billion. Stroke is projected to account for the largest absolute increase in costs. Large relative increases among the Asian American population (497%) and Hispanic American population (489%) reflect the projected increases in the size of these populations. CONCLUSIONS: The economic burden of cardiovascular risk factors and overt cardiovascular disease in the United States is projected to increase substantially in the coming decades. Development and deployment of cost-effective programs and policies to promote cardiovascular health are urgently needed to rein in costs and to equitably enhance population health. [ABSTRACT FROM AUTHOR]

Background: Cooking interventions have increased in popularity in recent years. Evaluation by meta-analyses and systematic reviews show consistent changes in dietary quality reports and cooking confidence, but not of cardiovascular (CVD) biomarkers. Interventions evaluating or reporting behavioral mechanisms as an explanatory factor for these outcomes has been sparse. Moreover, evaluations of cooking interventions among communities with health disparities or food access limitations have received little attention in the literature. Methods: This study will occur over two phases. Phase 1 will assess acceptability among the target population of African-American adults living within an urban food desert. Phase 2 will consist of a 6-week cooking intervention delivered at a community kitchen setting. Pre and post intervention visits for clinical examinations and biomarker collection will be conducted, as well as dietary and cooking skill assessments. Primary outcomes include cooking behavior and feasibility measures. Secondary outcomes are related to dietary quality, psychosocial factors, CVD biomarkers, and food environment measures. Discussion: This study seeks to demonstrate feasibility of a community-based cooking intervention and to provide necessary information to plan future interventions that identify cooking behavior as an outcome of participation in cooking interventions among African-American adults, especially in relation to dietary and biomarker outcomes. Trial registration: This study was registered at ClinicalTrials.gov (NCT04305431) on March 12, 2020. [ABSTRACT FROM AUTHOR]

Background: Heart failure (HF) and kidney disease frequently co-occur, increasing mortality risk. The cardiorenal syndrome results from damage to either the heart or kidney impacting the other organ. The epidemiology of cardiorenal syndrome among the general population is incompletely characterized and despite shared risk factors with HF, differences in mortality risk across key demographics have not been well described. Thus, the primary goal of this study was to analyze annual trends in cardiorenal-related mortality, evaluate if these trends differed by age, sex, and race or ethnicity, and describe these trends against a backdrop of HF mortality. Methods and findings: The Centers for Disease Control and Prevention Wide-ranging ONline Data for Epidemiologic Research database was used to examine cardiorenal- and HF-related mortality in the US between 2011and 2020. International Classification of Diseases, 10 Revision codes were used to classify cardiorenal-related deaths (I13.x) and HF-related deaths (I11.0, I13.0, I13.2, and I50.x), among decedents aged 15 years or older. Decedents were further stratified by age group, sex, race, or ethnicity. Crude and age-adjusted mortality rates (AAMR) per 100,000 persons were calculated. A total of 97,135 cardiorenal-related deaths and 3,453,655 HF-related deaths occurred. Cardiorenal-related mortality (AAMR, 3.26; 95% CI: 3.23–3.28) was significantly lower than HF-related mortality (AAMR, 115.7; 95% CI: 115.6–115.8). The annual percent change (APC) was greater and increased over time for cardiorenal-related mortality (2011–2015: APC, 7.1%; 95% CI: 0.7–13.9%; 2015–2020: APC, 19.7%, 95% CI: 16.3–23.2%), whereas HF-related mortality also increased over that time period, but at a consistently lower rate (2011–2020: APC, 2.4%; 95% CI: 1.7–3.1%). Mortality was highest among older and male decedents for both causes. Cardiorenal-related deaths were more common in non-Hispanic or Latino Blacks compared to Whites, but similar rates were observed for HF-related mortality. A larger proportion of cardiorenal-related deaths, compared to HF-related deaths, listed cardiorenal syndrome as the underlying cause of death (67.0% vs. 1.2%). Conclusions: HF-related deaths substantially outnumber cardiorenal-related deaths; however, cardiorenal-related deaths are increasing at an alarming rate with the highest burden among non-Hispanic or Latino Blacks. Continued surveillance of cardiorenal-related mortality trends is critical and future studies that contain detailed biomarker and social determinants of health information are needed to identify mechanisms underlying differences in mortality trends. [ABSTRACT FROM AUTHOR]

Background: Prior studies showed that neighborhood deprivation increases the risk of lethal prostate cancer. However, the role of neighborhood gentrification in prostate cancer development and outcome remains poorly understood. We examined the relationships of gentrification with prostate cancer and serum proteomedefined inflammation and immune function in a diverse cohort. Methods: The case–control study included 769 cases [405 African American (AA), 364 European American (EA) men] and 1023 controls (479 AA and 544 EA), with 219 all-cause and 59 prostate cancer-specific deaths among cases. Geocodes were linked to a neighborhood gentrification index (NGI) derived from US Census data. Cox and logistic regression, and MANOVA, were used to determine associations between NGI, as continuous or quintiles (Q), and outcomes. Results: Adjusting for individual socioeconomic status (SES), continuous NGI was positively associated with prostate cancer among all men (odds ratio [OR] 1.07, 95% confidence interval [CI] 1.01–1.14). AA and low-income men experienced the highest odds of prostate cancer when residing in tracts with moderate gentrification, whereas EA men experienced reduced odds of regional/metastatic cancer with increased gentrification in SES-adjusted analyses. Continuous NGI also associated with mortality among men presenting with localized disease and low-income men in SES-adjusted Cox regression analyses. NGI was not associated with serum proteome-defined chemotaxis, inflammation, and tumor immunity suppression. Conclusions: Findings show that neighborhood gentrification associates with prostate cancer and mortality in this diverse population albeit associations were heterogenous within subgroups. The observations suggest that changing neighborhood socioeconomic environments may affect prostate cancer risk and outcome, likely through multifactorial mechanisms. [ABSTRACT FROM AUTHOR]

Background: Research has suggested that artificial light at night (LAN) may disrupt circadian rhythms, sleep, and contribute to the development of obesity. However, almost all previous studies are cross-sectional, thus, there is a need for prospective investigations of the association between LAN and obesity risk. The goal of our current study was to examine the association between baseline LAN and the development of obesity over follow-up in a large cohort of American adults.Methods: The study included a sample of 239,781 men and women (aged 50-71) from the NIH-AARP Diet and Health Study who were not obese at baseline (1995-1996). We used multiple logistic regression to examine whether LAN at baseline was associated with the odds of developing obesity at follow-up (2004-2006). Outdoor LAN exposure was estimated from satellite imagery and obesity was measured based on self-reported weight and height.Results: We found that higher outdoor LAN at baseline was associated with higher odds of developing obesity over 10 years. Compared with the lowest quintile of LAN, the highest quintile was associated with 12% and 19% higher odds of developing obesity at follow-up in men (OR (95% CI) = 1.12 (1.00, 1.250)) and women (1.19 (1.04, 1.36)), respectively.Conclusions: Our findings suggest that high LAN exposure could predict a higher risk of developing obesity in middle-to-older aged American adults. [ABSTRACT FROM AUTHOR]

Background: A growing body of research has demonstrated that individuals who live in neighborhoods with more severe socioeconomic deprivation may have higher risks for colorectal cancer (CRC). However, previous studies have examined neighborhood socioeconomic status (SES) at only 1 point in time, and it is unclear whether changes in neighborhood SES also can influence the risks of CRC.Methods: Cox regression analysis was used to examine different trajectories of change in neighborhood SES over 10 years in relation to the incidence of CRC among 266,804 participants (ages 51-70 years) in the National Institutes of Health-AARP Diet and Health Study. Eligible participants reported living in the same neighborhood at baseline (1995-1996) and from 2004 to 2006 according to a follow-up questionnaire. Changes in neighborhood SES were measured between 1990 and 2000 by SES indices derived from Census data. Neighborhoods were grouped into 4 categories based on median SES indices in 1990 and 2000 (low-low, low-high, high-low, and high-high).Results: Compared with residents whose neighborhoods were in the higher SES group at both time points (reference category), those whose neighborhoods were consistently in the low SES group had a 7% higher risk of developing CRC (hazard ratio, 1.07; 95% confidence interval, 1.00-1.14). Moreover, the risk of CRC was 15% higher (hazard ratio, 1.15; 95% confidence interval, 1.02-1.28) for those living in neighborhoods with decreasing SES (high-low) over time.Conclusions: The current findings suggest that exposure to consistently low SES neighborhoods and/or a decrease in neighborhood SES over a period of time may be associated with higher risks of CRC. [ABSTRACT FROM AUTHOR]

Low neighborhood socioeconomic status has been linked to adverse health outcomes. However, it is unclear whether changing the neighborhood may influence health. We examined 10-year change in neighborhood socioeconomic deprivation in relation to mortality rate among 288,555 participants aged 51–70 years who enrolled in the National Institutes of Health-AARP Diet and Health Study in 1995–1996 (baseline) and did not move during the study. Changes in neighborhood socioeconomic deprivation between 1990 and 2000 were measured by US Census data at the census tract level. All-cause, cardiovascular disease, and cancer deaths were ascertained through annual linkage to the Social Security Administration Death Master File between 2000 and 2011. Overall, our results suggested that improvement in neighborhood socioeconomic status was associated with a lower mortality rate, while deterioration was associated with a higher mortality rate. More specially, a 30-percentile-point reduction in neighborhood deprivation among more deprived neighborhoods was associated with 11% and 19% reductions in the total mortality rate among men and women, respectively. On the other hand, a 30-point increase in neighborhood deprivation in less deprived neighborhoods was associated with an 11% increase in the mortality rate among men. Our findings support a longitudinal association between changing neighborhood conditions and mortality. [ABSTRACT FROM AUTHOR]

The article comments on the study by Rana and colleagues which examines diabetes as a coronary heart disease (CHD) equivalent or CHD risk factor. The author says that delineating diabetes as CHD risk factor is important to improving the accuracy of cardiovascular risk prediction and in developing risk reduction strategies. The result of the study is also discussed.

BACKGROUND: The association of historical redlining policies, a marker of structural racism, with contemporary heart failure (HF) risk among White and Black individuals is not well established. METHODS: We aimed to evaluate the association of redlining with the risk of HF among White and Black Medicare beneficiaries. Zip code–level redlining was determined by the proportion of historically redlined areas using the Mapping Inequality Project within each zip code. The association between higher zip code redlining proportion (quartile 4 versus quartiles 1–3) and HF risk were assessed separately among White and Black Medicare beneficiaries using generalized linear mixed models adjusted for potential confounders, including measures of the zip code–level Social Deprivation Index. RESULTS: A total of 2 388 955 Medicare beneficiaries (Black n=801 452; White n=1 587 503; mean age, 71 years; men, 44.6%) were included. Among Black beneficiaries, living in zip codes with higher redlining proportion (quartile 4 versus quartiles 1–3) was associated with increased risk of HF after adjusting for age, sex, and comorbidities (risk ratio, 1.08 [95% CI, 1.04–1.12]; P <0.001). This association remained significant after further adjustment for area-level Social Deprivation Index (risk ratio, 1.04 [95% CI, 1.002–1.08]; P =0.04). A significant interaction was observed between redlining proportion and Social Deprivation Index (P interaction<0.01) such that higher redlining proportion was significantly associated with HF risk only among socioeconomically distressed regions (above the median Social Deprivation Index). Among White beneficiaries, redlining was associated with a lower risk of HF after adjustment for age, sex, and comorbidities (risk ratio, 0.94 [95% CI, 0.89–0.99]; P =0.02). CONCLUSIONS: Historical redlining is associated with an increased risk of HF among Black patients. Contemporary zip code–level social determinants of health modify the relationship between redlining and HF risk, with the strongest relationship between redlining and HF observed in the most socioeconomically disadvantaged communities. [ABSTRACT FROM AUTHOR]

While it is well known from numerous epidemiologic investigations that social determinants (socioeconomic, environmental, and psychosocial factors exposed to over the life-course) can dramatically impact cardiovascular health, the molecular mechanisms by which social determinants lead to poor cardiometabolic outcomes are not well understood. This review comprehensively summarizes a variety of current topics surrounding the biological effects of adverse social determinants (i.e., the biology of adversity), linking translational and laboratory studies with epidemiologic findings. With a strong focus on the biological effects of chronic stress, we highlight an array of studies on molecular and immunological signaling in the context of social determinants of health (SDoH). The main topics covered include biomarkers of sympathetic nervous system and hypothalamic-pituitary-adrenal axis activation, and the role of inflammation in the biology of adversity focusing on glucocorticoid resistance and key inflammatory cytokines linked to psychosocial and environmental stressors (PSES). We then further discuss the effect of SDoH on immune cell distribution and characterization by subset, receptor expression, and function. Lastly, we describe epigenetic regulation of the chronic stress response and effects of SDoH on telomere length and aging. Ultimately, we highlight critical knowledge gaps for future research as we strive to develop more targeted interventions that account for SDoH to improve cardiometabolic health for at-risk, vulnerable populations. [ABSTRACT FROM AUTHOR]

In the United States, African Americans (AAs) have greater risk for Class III obesity and cardiovascular disease (CVD). Previous reports suggest that AAs have a different immune cell profile when compared to Caucasians. The immune cell profile of AAs was characterized by flow cytometry using two experimental setups: ex vivo (N = 40) and in vitro (N = 10). For ex vivo experiments, PBMC were treated with participant serum to understand how lipid contents may contribute to monocyte phenotypic differences. For in vitro experiments, monocytes were low-density lipoprotein (LDL)- or vehicle-treated for four hours and subsequently analyzed by flow cytometry and RT-qPCR. When PBMCs were treated with participant sera, subsequent multivariable regression analysis revealed that serum triglycerides and LDL levels were associated with monocyte subset differences. In vitro LDL treatment of monocytes induced a phenotypic switch in monocytes away from classical monocytes accompanied by subset-specific chemokine receptor CCR2 and CCR5 expression changes. These observed changes are partially translation-dependent as determined by co-incubation with cycloheximide. LDL treatment of monocytes induces a change in monocyte subsets and increases CCR2/CCR5 expression in a subset-specific manner. Understanding the molecular mechanisms could prove to have CVD-related therapeutic benefits, especially in high-risk populations with hyperlipidemia and increased risk for CVD. LDL associated changes on monocyte subsets and CCR2/5 expression. [Display omitted] • Little is known about the impact of LDL cholesterol on monocytes in African Americans. • LDL cholesterol is associated with monocyte phenotypes in African Americans. • LDL promotes monocyte subsets and monocyte chemokine receptor expression in a subset-specific way in vitro. • LDL-induced changes are partly mediated by translation in a subset-specific manner. [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]

There are approximately 38 million people globally living with Human immunodeficiency virus 1 (HIV-1) and given the tremendous success of combination antiretroviral therapy (cART) this has dramatically reduced mortality and morbidity with prevention benefits. However, HIV-1 persists during cART within the human body and re-appears upon cART interruption. This HIV-1 reservoir remains a barrier to cure with cellular sites of viral persistence not fully understood. In this study we provide evidence corroborating a recently published article in STM demonstrating the role of platelets as a novel cellular disseminator of HIV-1 particles in the setting of viral suppression. Using classical transmission electron microscopy with and without immunogold labeling, we visualize HIV-1 in both platelets and monocytes in cART suppressed HIV donors. Our study suggests that due to the close proximity of platelets and monocytes an alternative life cycle of HIV-1 cycling within monocytes and platelets without the need of active replication under cART occurs. Our findings are supported by the lack of detectable HIV-1 particles in platelets derived from HIV uninfected donors or the 'Berlin' patient suggesting that platelets may serve as an underappreciated hidden bearer for HIV-1 and should be considered in HIV remission studies and trials. [ABSTRACT FROM AUTHOR]

Amygdalar 18F-fluorodeoxyglucose (FDG) uptake represents chronic stress-related neural activity and associates with coronary artery disease by coronary computed tomography angiography (CCTA). Allostatic load score is a multidimensional measure related to chronic physiological stress which incorporates cardiovascular, metabolic and inflammatory indices. To better understand the relationship between chronic stress-related neural activity, physiological dysregulation and coronary artery disease, we studied the association between amygdalar FDG uptake, allostatic load score and subclinical non-calcified coronary artery burden (NCB) in psoriasis. Consecutive psoriasis patients (n = 275 at baseline and n = 205 at one-year follow-up) underwent CCTA for assessment of NCB (QAngio, Medis). Amygdalar FDG uptake and allostatic load score were determined using established methods. Psoriasis patients were middle-aged, predominantly male and white, with low cardiovascular risk by Framingham risk score and moderate-severe psoriasis severity. Allostatic load score associated with psoriasis severity (β = 0.17, p = 0.01), GlycA (a systemic marker of inflammation, β = 0.49, p < 0.001), amygdalar activity (β = 0.30, p < 0.001), and NCB (β = 0.39; p < 0.001). Moreover, NCB associated with amygdalar activity in participants with high allostatic load score (β = 0.27; p < 0.001) but not in those with low allostatic load score (β = 0.07; p = 0.34). Finally, in patients with an improvement in allostatic load score at one year, there was an 8% reduction in amygdalar FDG uptake (p < 0.001) and a 6% reduction in NCB (p = 0.02). In psoriasis, allostatic load score represents physiological dysregulation and may capture pathways by which chronic stress-related neural activity associates with coronary artery disease, emphasizing the need to further study stress-induced physiological dysregulation in inflammatory disease states. Image 1 • Allostatic load score represents physiological stress mechanisms. • Allostatic load associates with increases in psoriasis severity and systemic inflammation. • Neural stress activity relates to allostatic load score. • Allostatic load score relates to subclinical atherosclerosis at baseline and over time. [ABSTRACT FROM AUTHOR]

Background: Little is known about the associations between perceived neighborhood social environment (PNSE) and depressive symptoms among African Americans. Furthermore, the role of physical activity (PA) as a mediator of this association has not been investigated. The two-fold objectives of this study, therefore, were (1) to examine the associations between PNSE and depressive symptoms among African Americans, and (2) to test the degree to which these associations were mediated by total PA. Methods: We used baseline data from the Jackson Heart Study (JHS), a single-site, prospective, community-based study of African-American adults (n = 2209) recruited from Jackson, Mississippi. PNSE variables included scores for neighborhood violence (i.e., higher score = more violence), problems (higher score = more problems), and social cohesion (higher score = more cohesion). Depressive symptoms were measured by the 20-item Center for Epidemiological Studies Depression (CES-D) score. First, multilevel modeling, controlling for census tract clustering effects, was used to estimate associations between each PNSE variable and CES-D score, adjusting for covariates, including demographic, health-related, and population density. Second, validated, self-reported total PA, based on active living, sport, and home indices, was tested as the mediator. Multivariable linear regressions with bootstrap-generated 95% bias-corrected confidence intervals (BC CIs) were estimated to test for significant unstandardized indirect effects, controlling for all covariates. Results: Our participants were 64.2% female with a mean age of 52.6 (SD = 12.2) and a mean CES-D score of 10.8 (SD = 8.1). In the fully-adjusted model, neighborhood violence and problems were positively related to depressive symptoms (B = 3.59, 95%CI = 0.93, 6.26, and B = 3.06, 95%CI = 1.19, 4.93, respectively). Neighborhood violence and problems were also indirectly related to depressive symptoms via total PA (B = 0.26, 95%BC CI = 0.05, 0.55; and B = 0.15, 95%BC CI = 0.02, 0.34, respectively). Social cohesion was neither directly nor indirectly related to depressive symptoms. Conclusions: We found that higher levels of perceived neighborhood problems and violence were directly and positively associated with depressive symptoms. These associations may be explained in part by lower total PA levels. Future interventions to reduce depressive symptoms attributed to neighborhood features should consider emphasizing built environment features that facilitate PA increases in conjunction with community efforts to reduce neighborhood violence and problems. [ABSTRACT FROM AUTHOR]

Supplemental Digital Content is available in the text. Background: A malignant subphenotype of left ventricular hypertrophy (LVH) has been described, in which minimal elevations in cardiac biomarkers identify individuals with LVH at high risk for developing heart failure (HF). We tested the hypothesis that a higher prevalence of malignant LVH among blacks may contribute to racial disparities in HF risk. Methods: Participants (n=15 710) without prevalent cardiovascular disease were pooled from 3 population-based cohort studies, the ARIC Study (Atherosclerosis Risk in Communities), the DHS (Dallas Heart Study), and the MESA (Multi-Ethnic Study of Atherosclerosis). Participants were classified into 3 groups: those without ECG-LVH, those with ECG-LVH and normal biomarkers (hs-cTnT (high sensitivity cardiac troponin-T) <6 ng/L and NT-proBNP (N-terminal pro-B-type natriuretic peptide) <100 pg/mL), and those with ECG-LVH and abnormal levels of either biomarker (malignant LVH). The outcome was incident HF. Results: Over the 10-year follow-up period, HF occurred in 512 (3.3%) participants, with 5.2% in black men, 3.8% in white men, 3.2% in black women, and 2.2% in white women. The prevalence of malignant LVH was 3-fold higher among black men and women versus white men and women. Compared with participants without LVH, the adjusted hazard ratio for HF was 2.8 (95% CI, 2.1–3.5) in those with malignant LVH and 0.9 (95% CI, 0.6–1.5) in those with LVH and normal biomarkers, with similar findings in each race/sex subgroup. Mediation analyses indicated that 33% of excess hazard for HF among black men and 11% of the excess hazard among black women was explained by the higher prevalence of malignant LVH in blacks. Of black men who developed HF, 30.8% had malignant LVH at baseline, with a corresponding population attributable fraction of 0.21. The proportion of HF cases occurring among those with malignant LVH, and the corresponding population attributable fraction, were intermediate and similar among black women and white men and lowest among white women. Conclusions: A higher prevalence of malignant LVH may in part explain the higher risk of HF among blacks versus whites. Strategies to prevent development or attenuate risk associated with malignant LVH should be investigated as a strategy to lower HF risk and mitigate racial disparities. [ABSTRACT FROM AUTHOR]

Neighborhood environment perception (NEP) has been associated with health outcomes. However, little is known about how NEP relates to routine healthcare utilization. This study investigated the relationship between NEP and independent subfactors with healthcare utilization behavior, as measured by self-reported (1) usual source of healthcare and (2) time since last routine healthcare check-up. We used cross-sectional data from the Dallas Heart Study, which features a diverse, probability-based sample of Dallas County residents ages 18 to 65. We used logistic regression modeling to examine the association of self-reported NEP and routine healthcare utilization. NEP was assessed via a questionnaire exploring residents' neighborhood perceptions, including violence, the physical environment, and social cohesion. Routine healthcare utilization was assessed via self-reported responses regarding usual source of care and time since last routine healthcare check-up. The analytic sample (N = 1706) was 58% black, 27% white, 15% Hispanic, 42% male, and had a mean age of 51 (SD = 10.3). Analysis of NEP by tertile demonstrated that younger age, lower income, and lower education were associated with unfavorable overall NEP (p trend <0.05 for each). After adjustment for potential confounders, including neighborhood deprivation, health insurance, disease burden and psychosocial factors, we found that individuals with more unfavorable perception of their physical environment were more likely to report lack of a usual source of care (p = 0.013). Individuals with more unfavorable perception of the neighborhood physical environment or greater neighborhood violence reported longer time periods since last routine visit (p = 0.001, p = 0.034 respectively). There was no relationship between perceived social cohesion and healthcare utilization. Using a multi-ethnic cohort, we found that NEP significantly associates with report of a usual source of care and time since last routine check-up. Our findings suggest that public health professionals should prioritize improving NEP since it may act as barrier to routine preventive healthcare and ideal health outcomes. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular disease (CVD) is the leading cause of death in the world. Given the role of immune cells in atherosclerosis development and progression, effective methods for characterizing immune cell populations are needed, particularly among populations disproportionately at risk for CVD.Results: By using a variety of antibodies combined in one staining protocol, we were able to identify granulocyte, lymphocyte, and monocyte sub-populations by CD-antigen expression from 500 µl of whole blood, enabling a more extensive comparison than what is possible with a complete blood count and differential (CBC). The flow cytometry panel was established and tested in a total of 29 healthy men and women. As a proof of principle, these 29 samples were split by their race/ethnicity: African-Americans (AA) (N = 14) and Caucasians (N = 15). We found in accordance with the literature that AA had fewer granulocytes and more lymphocytes when compared to Caucasians, though the proportion of total monocytes was similar in both groups. Several new differences between AA and Caucasians were noted that had not been previously described. For example, AA had a greater proportion of platelet adhesion on non-classical monocytes when compared to Caucasians, a cell-to-cell interaction described as crucially important in CVD. We also examined our flow panel in a clinical population of AA women with known CVD risk factors (N = 20). Several of the flow cytometry parameters that cannot be measured with the CBC displayed correlations with clinical CVD risk markers. For instance, Framingham Risk Score (FRS) calculated for each participant correlated with immune cell platelet aggregates (PA) (e.g. T cell PA β = 0.59, p = 0.03 or non-classical monocyte PA β = 0.54, p = 0.02) after adjustment for body mass index (BMI).Conclusion: A flow cytometry panel identified differences in granulocytes, monocytes, and lymphocytes between AA and Caucasians which may contribute to increased CVD risk in AA. Moreover, this flow panel identifies immune cell sub-populations and platelet aggregates associated with CVD risk. This flow cytometry panel may serve as an effective method for phenotyping immune cell populations involved in the development and progression of CVD. [ABSTRACT FROM AUTHOR]

Little is known about the spatial clustering of neighborhood deprivation across the United States (US). Using data from the 2010 US Census Bureau, we created a neighborhood deprivation index (NDI: higher NDI indicates higher deprivation/ lower neighborhood socioeconomic status) for each county within the US County level scores were loaded into ArcGIS 10.5.1 where they were mapped and analyzed using Moran's I and Anselin Local Moran's I. Ultimately, NDI varies spatially across the US. The highest NDI scores were found in the Southeastern and Southwestern US states, and inland regions of Southern California. This information is critical for public health initiative development as planners may need to tailor the scale of their efforts based on the higher NDI neighborhoods of the county or geographic region with potentially greater chronic disease burden. [ABSTRACT FROM AUTHOR]

Neighborhood socioeconomic deprivation is associated with increased cardiovascular risk factors, including inflammation. Inflammation plays an important role in modifying the cardioprotective function of high-density lipoprotein (HDL). Moreover, recent studies suggest that very high HDL is associated with adverse cardiovascular disease (CVD) outcomes. Thus, we sought to explore the relationships between neighborhood socioeconomic deprivation as a marker of chronic stress, inflammation, proprotein convertase subtilisin/kexin type 9 (PCSK9) (a core component of the HDL proteome), HDL characterisitcs, and biological aging as a predictor of CVD and all-cause mortality. Sixty African American subjects were recruited to the NIH Clinical Center as part of a community-based participatory research-designed observational study. Neighborhood deprivation index (NDI), a marker of neighborhood socioeconomic deprivation, was measured using US Census data. HDL characteristics (cholesterol, particle number, size, subspecies) were determined from NMR lipoprotein profiling, and plasma cytokines (IL-1β, IL-6, IL-8, TNFα, IFNγ) were measured using an ELISA-based multiplex technique. Epigenetic clock biomarkers of aging were measured using DNA methylation data obtained from participants' buffy coat samples. We used linear regression modeling adjusted for atherosclerotic cardiovascular disease (ASCVD) risk score, body mass index (BMI), and lipid-lowering medication use to investigate relationships of interest. NDI directly associated with large HDL particle count (H7P) and IFNγ and trended toward significance with HDL-C and PCSK9. IFNγ and PCSK9 then directly associated with H7P. H7P also directly associated with higher DNA methylation phenotypic age (PhenoAge). We highlight associations between neighborhood socioeconomic deprivation, IFNγ, PCSK9, HDL subspecies, and epigenetic biomarkers of aging. Taken together, our findings suggest indirect pathways linking neighborhood deprivation-related stress and inflammation to HDL and immune epigenetic changes. Moreover, these results add to recent work showing the pathogenicity of high HDL levels and underscore the need to understand how chronic stress-related inflammation and lipoprotein subspecies relate to CVD risk across diverse populations. [Display omitted] • Neighborhood socioeconomic deprivation associates with IFNγ, PCSK9, and H7P. • IFNγ and PCSK9 associate with H7P. • H7P associates with DNAm PhenoAge. • Chronic stress-related inflammation may modify the cardioprotective capacity of HDL. [ABSTRACT FROM AUTHOR]

The digital divide related to consumer information technologies (CITs) has diminished, thus increasing the potential to use CITs to overcome barriers of access to health interventions as well as to deliver interventions situated in the context of daily lives. However, the evidence base regarding the use and impact of CIT-enabled interventions in health disparity populations lags behind that for the general population. Literature and case examples are summarized to demonstrate the use of mHealth, telehealth, and social media as behavioral intervention platforms in health disparity populations, identify challenges to achieving their use, describe strategies for overcoming the challenges, and recommend future directions. The evidence base is emerging. However, challenges in design, implementation, and evaluation must be addressed for the promise to be fulfilled. Future directions include (1) improved design methods, (2) enhanced research reporting, (3) advancement of multilevel interventions, (4) rigorous evaluation, (5) efforts to address privacy concerns, and (6) inclusive design and implementation decisions. [ABSTRACT FROM AUTHOR]

Persistent skin inflammation and impaired resolution are the main contributors to psoriasis and associated cardiometabolic complications. Omega-3 polyunsaturated fatty acids (PUFAs), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), are known to exert beneficial effects on inflammatory response and lipid function. However, a specific role of omega-3 PUFAs in psoriasis and accompanied pathologies are still a matter of debate. Here, we carried out a direct comparison between EPA and DHA 12 weeks diet intervention treatment of psoriasis-like skin inflammation in the K14-Rac1V12 mouse model. By utilizing sensitive techniques, we targeted EPA- and DHA-derived specialized pro-resolving lipid mediators and identified tightly connected signaling pathways by RNA sequencing. Treatment with experimental diets significantly decreased circulating pro-inflammatory cytokines and bioactive lipid mediators, altered psoriasis macrophage phenotypes and genes of lipid oxidation. The superficial role of these changes was related to DHA treatment and included increased levels of resolvin D5, protectin DX and maresin 2 in the skin. EPA treated mice had less pronounced effects but demonstrated a decreased skin accumulation of prostaglandin E 2 and thromboxane B 2. These results indicate that modulating psoriasis skin inflammation with the omega-3 PUFAs may have clinical significance and DHA treatment might be considered over EPA in this specific disease. [Display omitted] [ABSTRACT FROM AUTHOR]

Meta-analyses are becoming increasingly popular, especially in the fields of cardiovascular disease prevention and treatment. They are often considered to be a reliable source of evidence for making healthcare decisions. Unfortunately, problems among meta-analyses such as the misapplication and misinterpretation of statistical methods and tests are long-standing and widespread. The purposes of this statement are to review key steps in the development of a metaanalysis and to provide recommendations that will be useful for carrying out meta-analyses and for readers and journal editors, who must interpret the findings and gauge methodological quality. To make the statement practical and accessible, detailed descriptions of statistical methods have been omitted. Based on a survey of cardiovascular metaanalyses, published literature on methodology, expert consultation, and consensus among the writing group, key recommendations are provided. Recommendations reinforce several current practices, including protocol registration; comprehensive search strategies; methods for data extraction and abstraction; methods for identifying, measuring, and dealing with heterogeneity; and statistical methods for pooling results. Other practices should be discontinued, including the use of levels of evidence and evidence hierarchies to gauge the value and impact of different study designs (including meta-analyses) and the use of structured tools to assess the quality of studies to be included in a metaanalysis. We also recommend choosing a pooling model for conventional meta-analyses (fixed effect or random effects) on the basis of clinical and methodological similarities among studies to be included, rather than the results of a test for statistical heterogeneity. [ABSTRACT FROM AUTHOR]

Background: Little is known about the association between cardiovascular (CV) health and health insurance status. We hypothesized that U.S. adults without health insurance coverage would have a lower likelihood of ideal cardiovascular health. Methods and Results: Using National Health and Nutrition Examination Survey (NHANES) data from 2007–2010, we examined the relationship between health insurance status and ideal CV health in U.S. adults aged ≥19 years and <65 (N = 3304). Ideal CV health was defined by the American Heart Association (AHA) as the absence of clinically manifested CV disease and the simultaneous presence of 6–7 “ideal” CV health factors and behaviors. Logistic regression modeling was used to determine the relationship between health insurance status and the odds of ideal CV health. Of the U.S. adult population, 5.4% attained ideal CV health, and 23.5% were without health insurance coverage. Those without health insurance coverage were more likely to be young (p<0.0001), male (p<0.0001), non-white (p<0.0001), with less than a high school degree (p<0.0001), have a poverty-to-income ratio less than 1 (p<0.0001) and unemployed (p<0.0001) compared to those with coverage. Lack of health insurance coverage was associated with a lower likelihood of ideal CV health; however, this relationship was attenuated by socioeconomic status. Conclusions: U.S. adults without health insurance coverage are less likely to have ideal CV health. Population-based strategies and interventions directed at the community-level may be one way to improve overall CV health and reach this at-risk group. [ABSTRACT FROM AUTHOR]

In the past 15 years, a major research enterprise has emerged that is aimed at understanding associations between geographic and contextual features of the environment (especially the built environment) and elements of human energy balance, including diet, weight and physical activity. Here we highlight aspects of this research area with a particular focus on research and opportunities in the United States as an example. We address four main areas: (1) the importance of valid and comparable data concerning behaviour across geographies; (2) the ongoing need to identify and explore new environmental variables; (3) the challenge of identifying the causally relevant context; and (4) the pressing need for stronger study designs and analytical methods. Additionally, we discuss existing sources of geo-referenced health data which might be exploited by interdisciplinary research teams, personnel challenges and some aspects of funding for geospatial research by the US National Institutes of Health in the past decade, including funding for international collaboration and training opportunities. [ABSTRACT FROM PUBLISHER]

R4593 --> 676.7 --> Obesity and related chronic diseases (i.e. cardiovascular disease (CVD) and cancer) disproportionately affect African Americans (AA), shortening life expectancy and impacting quality of life. Life‐long exposure to adverse social determinants of health (SDoH) have been linked to obesity, warranting intensified research to further elucidate the 'biology of adversity' or the biologic consequences of adverse social conditions. Evidence suggests that exposure to chronic psychological and environmental stressors as SDoH leads to immune cell dysfunction, particularly for Natural Killer (NK) cells. Therefore, we examined changes in NK cell function in AA women, a group at high risk of Class III obesity (BMI ≥40 kg/m2). We have previously shown that NK cell degranulation is impaired in AA women with Class III obesity accompanied by a decrease in IFNg and TNFa, a loss in function driven by plasma LDL levels (b=‐0.35, p=0.03). A similar phenotype of dysfunctional NK cells could be achieved by overnight LDL treatment (50mg/dl) of healthy donor NK cells. To further determine the underlying signaling pathways, we employed proteomics of control and LDL treated NK cells. Here we identified 18 statistically significant regulated proteins (p<0.05), and 23 proteins approaching significance (p<0.07). Signaling pathway analysis revealed endolysosomal function, actin cytoskeleton regulation, and regulation of innate immune responses as significant pathways. Several proteins associated with autophagy and ubiquitination were also identified. This is of particular importance as LDL treatment of various cell types has been related to damaging lysosomes and a subsequent potential induction of lysophagy. Therefore, we investigated the impact of LDL on NK cell autophagy through western blot analysis of LC3 and p62 and found that enhanced autophagy is present in LDL treated NK cells. By employing the proteasome inhibitor MG‐132, we also found that the LDL‐induced increase in autophagy appears to be dependent on the activation of the 20S proteasome and subsequent ubiquitination of lysosomal proteins which results in depletion of functional lysosomes through lysophagy and is accompanied by NK cell function loss. In summary, we show a novel pathway potentially explaining obesity‐related NK cell function loss as a result of adverse SDoH in a population at highest risk for obesity‐related diseases like CVD and cancer. In the future, more research is needed to further understand the 'biology of adversity' and identifying targets for tailored interventions, ultimately reducing health inequities in chronic disease outcomes. [ABSTRACT FROM AUTHOR]

R4809 --> 510.5 --> Social determinants of health (SDoH) include socioeconomic, environmental, and psychological factors that impact health. Low neighborhood socioeconomic status (nSES) is a SDoH that associates with cardiovascular mortality in longitudinal studies. While nSES as a chronic stress contributes to adverse health outcomes, the molecular mechanisms and pathogenesis are poorly understood. Previously, we found that residing in lower nSES areas may alter monocyte expression of C‐C chemokine receptor type 2 (CCR2), a regulator of monocyte recruitment during atherogenesis. To explore the effects of nSES as a chronic stress on monocyte CCR2 expression, we treated monocytes in vitro for 4 hours with catecholamines (epinephrine [Epi], norepinephrine [NE], or dopamine [DA]) used as stress biomarkers. Only DA increased CCR2 expression in a dose‐dependent manner (p<0.01), especially on non‐classical monocytes (NCM). In our current study, we investigated DA receptor signaling to learn which pathways may contribute to increases in CCR2 expression. Dopamine acts on five known receptors, the D1‐like receptors (D1 and D5) and D2‐like receptors (D2, D3, and D4). First, we performed flow cytometry on untreated monocytes and found D2 receptors were most abundant on the surface of all monocyte subsets (ie., classical monocytes [CM], intermediate monocytes [IM], and NCM as determined by CD14/CD16 expression). Furthermore, spearman correlation between D2‐like receptor surface expression and surface CCR2 expression in NCM suggested D2‐like receptor signaling (R2=0.79, p=0.04). Because the D2‐like receptor response is known to decrease cAMP levels compared to a D1‐like receptor response, a cAMP assay was performed on monocytes with DA treatment. Indicative of D2‐signaling, cAMP levels were found to be lower in DA‐treated monocytes compared to untreated controls (ctr 29.78pmol/ml vs DA 22.97 pmol/ml; p=0.038). We then investigated downstream mechanisms following DA signaling that could result in increased CCR2 expression. Filamin A (FlnA), a prominent actin‐cross‐linking protein, is known to regulate CCR2 recycling. We examined the expression of FlnA by flow cytometry and RT‐qPCR on flow sorted monocytes with and without DA treatment. There was a significant decrease in FlnA expression in NCM (p < 0.05), indicating a slowing of CCR2 recycling. Expression of an associated scaffold protein mRNA, b‐arrestin 1, was decreased by 66% in NCM (p= 0.008). Overall, we provide a novel immunological mechanism, driven by DA signaling and CCR2, for how nSES may contribute to atherogenesis. Future studies should investigate the importance of DA in CVD development and progression in populations disproportionately experiencing chronic stress due to SDoH. [ABSTRACT FROM AUTHOR]

Lifetime risk estimation for cardiovascular disease (CVD) has been proposed as a useful strategy to improve risk communication in the primary prevention setting. However, the perception of lifetime risk for CVD is unknown. We included 2,998 subjects from the Dallas Heart Study. Lifetime risk for developing CVD was classified as high (≥39%) versus low (<39%) according to risk factor burden as described in our previously published algorithm. Perception of lifetime risk for myocardial infarction was assessed by way of a 5-point scale. Baseline characteristics were compared across levels of perceived lifetime risk. Multivariable logistic regression analyses were performed to determine the association of participant characteristics with level of perceived lifetime risk for CVD and with correctness of perceptions. Of the 2,998 participants, 64.8% (n = 1,942) were classified as having high predicted lifetime risk for CVD. There was significant discordance between perceived and predicted lifetime risk. After multivariable adjustment, family history of premature myocardial infarction, high self-reported stress, and low perceived health were all strongly associated with high perceived lifetime risk (odds ratio [OR] 2.37, 95% confidence interval [CI] 1.72 to 3.27; OR 2.17, 95% CI 1.66 to 2.83; and OR 2.71, 95% CI 2.09 to 3.53; respectively). However, the association between traditional CVD risk factors and high perceived lifetime risk was more modest. In conclusion, misperception of lifetime risk for CVD is common and frequently reflects the influence of factors other than traditional risk factor levels. These findings highlight the importance of effectively communicating the significance of traditional risk factors in determining the lifetime risk for CVD. [ABSTRACT FROM AUTHOR]

PURPOSE: Previous studies suggest that African Americans (AA) have lower levels of cardiorespiratory fitness (CRF) than their Caucasian (C) counterparts. However, the association between CRF and race/ethnicity in the context of higher socioeconomic status (SES) has not been explored. METHODS: We evaluated 589 AA (309 men and 203 women) and 33,015 C (19,399 men and 8753 women) enrolled in the Cooper Center Longitudinal Study. Education years and access to a preventive health care examination were used as a proxy for higher SES. Data were collected from a questionnaire, maximal treadmill exercise stress test, and other clinical measures. The outcome variable was CRF, which was stratified into low fit (quintile 1 of CRF) and fit (quintiles 2-5). Multivariable regression was used to compare adjusted mean CRF between groups. P values were adjusted for unbalanced sample size and unequal variance between groups. RESULTS: The mean education years were similar for AA and C men at 16 yr; however, AA women had more years of education than C (15.8 vs 15.2 yr, P = 0.0062). AA men and women had a significantly higher prevalence of being unfit compared with their C counterparts (men 26.7% vs 12.6%, P < 0.0001; women 21.3% vs 8.4%, P < 0.0001). The adjusted mean estimated maximal METs were 10.9 vs 11.7 and 8.8 vs 9.8 for AA and C men and women, respectively. Fully adjusted odds ratios revealed that AA men had more than twice the risk of being unfit compared with C men. A trend persisted for AA women to have a lower MET value than their counterparts. CONCLUSIONS: Despite comparable higher SES, lower CRF existed among AA men versus C men. These results suggest that CRF may not be mediated strictly by environmental factors related to SES. [ABSTRACT FROM AUTHOR]

Importance: Younger individuals are experiencing a greater cumulative exposure to excess adiposity over their lifetime. However, few studies have determined the consequences of long-term obesity.Objective: To examine whether the duration of overall and abdominal obesity was associated with the presence and 10-year progression of coronary artery calcification (CAC), a subclinical predictor of coronary heart disease.Design, Setting, and Participants: Prospective study of 3275 white and black adults aged 18 to 30 years at baseline in 1985-1986 who did not initially have overall obesity (body mass index [BMI] ≥30) or abdominal obesity (men: waist circumference [WC] >102 cm; women: >88 cm) in the multicenter, community-based Coronary Artery Risk Development in Young Adults (CARDIA) study. Participants completed computed tomography scanning for the presence of CAC during the 15-, 20-, or 25-year follow-up examinations. Duration of overall and abdominal obesity was calculated using repeat measurements of BMI and WC, respectively, performed 2, 5, 7, 10, 15, 20, and 25 years after baseline.Main Outcomes and Measures: Presence of CAC was measured by computed tomography at the year 15 (2000-2001), year 20 (2005-2006), or year 25 (2010-2011) follow-up examinations. Ten-year progression of CAC (2000-2001 to 2010-2011) was defined as incident CAC in 2010-2011 or an increase in CAC score of 20 Agatston units or greater.Results: During follow-up, 40.4% and 41.0% developed overall and abdominal obesity, respectively. Rates of CAC per 1000 person-years were higher for those who experienced more than 20 years vs 0 years of overall obesity (16.0 vs 11.0, respectively) and abdominal obesity (16.7 vs 11.0). Approximately 25.2% and 27.7% of those with more than 20 years of overall and abdominal obesity, respectively, experienced progression of CAC vs 20.2% and 19.5% of those with 0 years. After adjustment for BMI or WC and potential confounders, the hazard ratios for CAC for each additional year of overall or abdominal obesity were 1.02 (95% CI, 1.01-1.03) and 1.03 (95% CI, 1.02-1.05), respectively. The adjusted odds ratios for CAC progression were 1.04 (95% CI, 1.01-1.06) and 1.04 (95% CI, 1.01-1.07), respectively. Associations were attenuated but largely persisted following additional adjustment for potential intermediate metabolic factors during follow-up.Conclusions and Relevance: Longer duration of overall and abdominal obesity was associated with subclinical coronary heart disease and its progression through midlife independent of the degree of adiposity. Preventing or at least delaying the onset of obesity in young adulthood may lower the risk of developing atherosclerosis through middle age. [ABSTRACT FROM AUTHOR]

IMPORTANCE: Younger individuals are experiencing a greater cumulative exposure to excess adiposity over their lifetime. However, few studies have determined the consequences of long-term obesity. OBJECTIVE: To examine whether the duration of overall and abdominal obesity was associated with the presence and 10-year progression of coronary artery calcification (CAC), a subclinical predictor of coronary heart disease. DESIGN, SETTING, AND PARTICIPANTS: Prospective study of 3275 white and black adults aged 18 to 30 years at baseline in 1985-1986 who did not initially have overall obesity (body mass index [BMI] >30) or abdominal obesity (men; waist circumference [WC] >102 cm; women; >88 cm) in the multicenter, community-based Coronary Artery Risk Development in Young Adults (CARDIA) study. Participants completed computed tomography scanning for the presence of CAC during the 15-, 20-, or 25-year follow-up examinations. Duration of overall and abdominal obesity was calculated using repeat measurements of BMI and WC, respectively, performed 2,5,7,10,15,20, and 25 years after baseline. MAIN OUTCOMES AND MEASURES: Presence of CAC was measured by computed tomography at the year 15 (2000-2001), year 20 (2005-2006), or year 25 (2010-2011) follow-up examinations. Ten-year progression of CAC (2000-2001 to 2010-2011) was defined as incident CAC in 2010-2011 or an increase in CAC score of 20 Agatston units or greater. RESULTS: During follow-up, 40.4% and 41.0% developed overall and abdominal obesity, respectively. Rates of CAC per 1000 person-years were higher for those who experienced more than 20 years vs 0 years of overall obesity (16.0 vs 11.0, respectively) and abdominal obesity (16.7 vs 11.0). Approximately 25.2% and 27.7% of those with more than 20 years of overall and abdominal obesity, respectively, experienced progression of CAC vs 20.2% and 19.5% of those with 0 years. After adjustment for BMI or WC and potential confounders, the hazard ratios for CAC for each additional year of overall or abdominal obesity were 1.02 (95% CI, 1.01-1.03) and 1.03 (95% CI, 1.02-1.05), respectively. The adjusted odds ratios for CAC progression were 1.04 (95% CI, 1.01-1.06) and 1.04 (95% CI, 1.01-1.07), respectively. Associations were attenuated but largely persisted following additional adjustment for potential intermediate metabolic factors during follow-up. CONCLUSIONS AND RELEVANCE: Longer duration of overall and abdominal obesity was associated with subclinical coronary heart disease and its progression through midlife independent of the degree of adiposity. Preventing or at least delaying the onset of obesity in young adulthood may lower the risk of developing atherosclerosis through middle age. [ABSTRACT FROM AUTHOR]

The article discusses the long term outcome of bariatric surgery. It reports that sustained weight loss, lower incidences of cardiovascular diseases, diabetes and cancer are some of the benefits from bariatric surgery. The study was conducted in obese controlled Swedish subjects. During a follow up of 20 years following the bariatric procedure, the surgery patients used a 54 mean cumulative hospital days against the 40 days of the control group at a confidence interval (C.I.) of 95 percent. However, the study highlights that the drug costs from the seventh year were lower for patients who underwent the surgery than control patients.

Objectives: The aim of this study was to assess the impact of extreme (class III) obesity (body mass index [BMI] ≥40 kg/m(2)) on care and outcomes in patients with ST-segment elevation myocardial infarction (STEMI).Background: Although its prevalence is increasing rapidly, little is known about the impact of extreme obesity on STEMI presentation, treatments, complication rates, and outcomes.Methods: The relationship between BMI and baseline characteristics, treatment patterns, and risk-adjusted in-hospital outcomes was quantified for 50,149 patients with STEMI from the National Cardiovascular Data Registry (NCDR) ACTION Registry-GWTG.Results: The proportions of patients with STEMI by BMI category were as follows: underweight (BMI <18.5 kg/m(2)) 1.6%, normal weight (18.5 kg/m(2) ≤BMI <25 kg/m(2)) 23.5%, overweight (25 kg/m(2) ≤BMI <30 kg/m(2)) 38.7%, class I obese (30 kg/m(2) ≤BMI <35 kg/m(2)) 22.4%, class II obese (35 kg/m(2) ≤BMI <40 kg/m(2)) 8.7%, and class III obese 5.1%. Extreme obesity was associated with younger age at STEMI presentation (median age 55 years for class III obese vs. 66 years for normal weight); a higher prevalence of diabetes, hypertension, and dyslipidemia; a lower prevalence of smoking; and less extensive coronary artery disease and higher left ventricular ejection fraction. Process-of-care measures were similar across BMI categories, including the extremely obese. Using class I obesity as the referent, risk-adjusted in-hospital mortality rates were significantly higher only for class III obese patients (adjusted odds ratio: 1.64; 95% confidence interval: 1.32 to 2.03).Conclusions: Patients with extreme obesity present with STEMI at younger ages and have less extensive coronary artery disease, better left ventricular systolic function, and similar processes and quality of care. Despite these advantages, extreme obesity remains independently associated with higher in-hospital mortality. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study was to assess the impact of extreme (class III) obesity (body mass index [BMI] ≥40 kg/m2) on care and outcomes in patients with ST-segment elevation myocardial infarction (STEMI). Background: Although its prevalence is increasing rapidly, little is known about the impact of extreme obesity on STEMI presentation, treatments, complication rates, and outcomes. Methods: The relationship between BMI and baseline characteristics, treatment patterns, and risk-adjusted in-hospital outcomes was quantified for 50,149 patients with STEMI from the National Cardiovascular Data Registry (NCDR) ACTION Registry–GWTG. Results: The proportions of patients with STEMI by BMI category were as follows: underweight (BMI <18.5 kg/m2) 1.6%, normal weight (18.5 kg/m2 ≤BMI <25 kg/m2) 23.5%, overweight (25 kg/m2 ≤BMI <30 kg/m2) 38.7%, class I obese (30 kg/m2 ≤BMI <35 kg/m2) 22.4%, class II obese (35 kg/m2 ≤BMI <40 kg/m2) 8.7%, and class III obese 5.1%. Extreme obesity was associated with younger age at STEMI presentation (median age 55 years for class III obese vs. 66 years for normal weight); a higher prevalence of diabetes, hypertension, and dyslipidemia; a lower prevalence of smoking; and less extensive coronary artery disease and higher left ventricular ejection fraction. Process-of-care measures were similar across BMI categories, including the extremely obese. Using class I obesity as the referent, risk-adjusted in-hospital mortality rates were significantly higher only for class III obese patients (adjusted odds ratio: 1.64; 95% confidence interval: 1.32 to 2.03). Conclusions: Patients with extreme obesity present with STEMI at younger ages and have less extensive coronary artery disease, better left ventricular systolic function, and similar processes and quality of care. Despite these advantages, extreme obesity remains independently associated with higher in-hospital mortality. [Copyright &y& Elsevier]

Background: A malignant subphenotype of left ventricular hypertrophy (LVH) has been described, in which minimal elevations in cardiac biomarkers identify individuals with LVH at high risk for developing heart failure (HF). We tested the hypothesis that a higher prevalence of malignant LVH among blacks may contribute to racial disparities in HF risk.Methods: Participants (n=15 710) without prevalent cardiovascular disease were pooled from 3 population-based cohort studies, the ARIC Study (Atherosclerosis Risk in Communities), the DHS (Dallas Heart Study), and the MESA (Multi-Ethnic Study of Atherosclerosis). Participants were classified into 3 groups: those without ECG-LVH, those with ECG-LVH and normal biomarkers (hs-cTnT (high sensitivity cardiac troponin-T) <6 ng/L and NT-proBNP (N-terminal pro-B-type natriuretic peptide) <100 pg/mL), and those with ECG-LVH and abnormal levels of either biomarker (malignant LVH). The outcome was incident HF.Results: Over the 10-year follow-up period, HF occurred in 512 (3.3%) participants, with 5.2% in black men, 3.8% in white men, 3.2% in black women, and 2.2% in white women. The prevalence of malignant LVH was 3-fold higher among black men and women versus white men and women. Compared with participants without LVH, the adjusted hazard ratio for HF was 2.8 (95% CI, 2.1-3.5) in those with malignant LVH and 0.9 (95% CI, 0.6-1.5) in those with LVH and normal biomarkers, with similar findings in each race/sex subgroup. Mediation analyses indicated that 33% of excess hazard for HF among black men and 11% of the excess hazard among black women was explained by the higher prevalence of malignant LVH in blacks. Of black men who developed HF, 30.8% had malignant LVH at baseline, with a corresponding population attributable fraction of 0.21. The proportion of HF cases occurring among those with malignant LVH, and the corresponding population attributable fraction, were intermediate and similar among black women and white men and lowest among white women.Conclusions: A higher prevalence of malignant LVH may in part explain the higher risk of HF among blacks versus whites. Strategies to prevent development or attenuate risk associated with malignant LVH should be investigated as a strategy to lower HF risk and mitigate racial disparities. [ABSTRACT FROM AUTHOR]