Search

Background: Racial differences in cardiovascular disease (CVD) are likely related to differences in clinical and social factors. The relative contributions of these factors to Black-White differences in premature CVD have not been investigated. Methods: In Black and White adults aged 18 to 30 years at baseline in the CARDIA study (Coronary Artery Risk Development in Young Adults), the associations of clinical, lifestyle, depression, socioeconomic, and neighborhood factors across young adulthood with racial differences in incident premature CVD were evaluated in sex-stratified, multivariable-adjusted Cox proportional hazards models using multiply imputed data assuming missing at random. Percent reduction in the β estimate (log-hazard ratio [HR]) for race quantified the contribution of each factor group to racial differences in incident CVD. Results: Among 2785 Black and 2327 White participants followed for a median 33.9 years (25th–75th percentile, 33.7–34.0), Black (versus White) adults had a higher risk of incident premature CVD (Black women: HR, 2.44 [95% CI, 1.71–3.49], Black men: HR, 1.59 [1.20–2.10] adjusted for age and center). Racial differences were not statistically significant after full adjustment (Black women: HR, 0.91 [0.55–1.52], Black men: HR 1.02 [0.70–1.49]). In women, the largest magnitude percent reduction in the β estimate for race occurred with adjustment for clinical (87%), neighborhood (32%), and socioeconomic (23%) factors. In men, the largest magnitude percent reduction in the β estimate for race occurred with an adjustment for clinical (64%), socioeconomic (50%), and lifestyle (34%) factors. Conclusions: In CARDIA, the significantly higher risk for premature CVD in Black versus White adults was statistically explained by adjustment for antecedent multilevel factors. The largest contributions to racial differences were from clinical and neighborhood factors in women, and clinical and socioeconomic factors in men.

Chronic exposure to stress is associated with metabolic syndrome (MetS), but the mechanism is unclear. We investigated the associations between chronic burden, sleep, and MetS in the Coronary Artery Risk Development in Young Adults Study.Chronic burden was self-reported (2000-2001) according to experiences with stressors for longer than 6 months. Wrist actigraphy-measured sleep duration and sleep efficiency were collected for 6 days; sleep duration, sleep quality, and daytime sleepiness were self-reported (2003-2004). MetS was measured during the clinic visit, from 2005 to 2006. Multivariable logistic and Cox proportional hazard models were fit to determine the associations of interest. Mediation by sleep was assessed using the product of coefficients approach.Among participants ( n = 606), the average (standard deviation) age was 40 (3.6) years, 58% were female, and 43% were Black. The prevalences of chronic burden, short sleep (≤6 hours), and MetS were 35%, 43% and 20.5%, respectively. High versus low chronic burden was associated with shorter self-reported sleep duration and higher daytime sleepiness. Chronic burden was associated with 1.85 higher odds (95% confidence interval = 1.11-3.09) of MetS. Sleep characteristics were not associated with MetS. There was no evidence that sleep mediated the chronic burden-MetS relation.Burden of chronic stress may be an emerging novel risk factor for both poor sleep and MetS.

OBJECTIVES: Suicide is the second leading cause of death in youth. We tested whether having a mentoring relationship associated with lower risks for suicidality, particularly among youth at higher risk due to cyberbullying. METHODS: This study pooled the 2017 Youth Risk Behavior Survey (YRBS) data from 5 jurisdictions that asked students if there was at least one teacher or other adult in their school that they could talk with, if they have a problem (mentorship). Students self-reported cyberbullying exposure and suicidality in the past 12 months. Odds of suicidal ideation, planning, and attempts were estimated using multivariable weighted logistic regression in overall and sex-stratified stepwise models. Interactions between mentorship and cyberbullying were also tested. RESULTS: Of the 25,527 student respondents, 87% reported having a mentoring relationship. Mentoring relationships were associated with lower odds of suicidal ideation (aOR, 0.44; 95% CI, 0.33-0.57), planning (aOR, 0.59; 95% CI, 0.41-0.85), and suicide attempts (aOR, 0.42; 95% CI, 0.31-0.56). Stratified analyses showed a significant interaction between cyberbullying and mentorship with suicidal attempts among males, and a near significant association between cyberbullying and mentorship with suicidal thoughts among females. Compared to male students with no cyberbullying and no mentorship, odds of attempting suicide were lower for males with no cyberbullying and mentorship (aOR, 0.55, 95% CI, 0.32-0.92), higher for males with cyberbullying and no mentorship (aOR, 7.78, 95% CI:3.47-17.47), but not significantly different for males with cyberbullying and mentoring relationships (aOR, 1.49, 95% CI, 0.86-2.48). Similarly, compared with females with no cyberbullying and no mentorship, odds of having suicidal thoughts were lower for females with no cyberbullying and mentorship (aOR, 0.40, 95% CI, 0.28-0.57), and higher for females with cyberbullying and no mentorship (aOR, 2.54, 95% CI:1.59-4.07). CONCLUSIONS: School-based mentoring may mitigate risk of suicidality among adolescents and limit the toxic effects of cyberbullying.

BACKGROUND: Neighborhood-level characteristics, such as poverty, have been associated with risk factors for heart failure (HF), including hypertension and diabetes mellitus. However, the independent association between neighborhood poverty and incident HF remains understudied. OBJECTIVE: To evaluate the association between neighborhood poverty and incident HF using a “real-world” clinical cohort. DESIGN: Retrospective cohort study of electronic health records from a large healthcare network. Individuals’ residential addresses were geocoded at the census-tract level and categorized by poverty tertiles based on American Community Survey data (2007–2011). PARTICIPANTS: Patients from Northwestern Medicine who were 30–80 years, free of cardiovascular disease at index visit (January 1, 2005–December 1, 2013), and followed for at least 5 years. MAIN MEASURES: The association of neighborhood-level poverty tertile (low, intermediate, and high) and incident HF was analyzed using generalized linear mixed effect models adjusting for demographics (age, sex, race/ethnicity) and HF risk factors (body mass index, diabetes mellitus, hypertension, smoking status). KEY RESULTS: Of 28,858 patients included, 75% were non-Hispanic (NH) White, 43% were men, 15% lived in a high-poverty neighborhood, and 522 (1.8%) were diagnosed with incident HF. High-poverty neighborhoods were associated with a 1.80 (1.35, 2.39) times higher risk of incident HF compared with low-poverty neighborhoods after adjustment for demographics and HF risk factors. CONCLUSIONS: In a large healthcare network, incident HF was associated with neighborhood poverty independent of demographic and clinical risk factors. Neighborhood-level interventions may be needed to complement individual-level strategies to prevent and curb the growing burden of HF. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11606-021-06785-7.

Background We investigated associations of childhood abuse with 4 cardiovascular disease risk factors in adulthood, and whether exposure to nurturing and household organization in childhood mitigated these associations. Methods and Results The CARDIA (Coronary Artery Risk Development in Young Adults) study (baseline examination, 1985–1986) was used to examine associations of childhood exposures (measured retrospectively at the year 15 examination) with incident obesity, type 2 diabetes, hypertension, and hyperlipidemia (assessed from baseline to year 30). Race‐ and sex‐stratified Cox proportional hazards models were used to examine associations of exposure to childhood abuse with incident cardiovascular disease risk factors. Interaction terms between exposure to abuse and exposure to nurturing relationship and household organization were included to test for effect modifications. Exposure to occasional/frequent abuse (versus no abuse) was associated with incident type 2 diabetes among White men (hazard ratio [HR], 1.81; 95% CI, 1.06–3.08). Exposure to low versus no abuse was associated with incident hyperlipidemia among White men (HR, 1.35; 95% CI, 1.09–1.67) and White women (HR, 1.26; 95% CI, 1.01–1.56). Risks of incident hyperlipidemia were higher for White women who experienced abuse and lived in dysfunctional households (HR, 3.61; 95% CI, 1.62–8.05) or households with low levels of organization (HR, 2.05; 95% CI, 1.25–3.36) compared with White women who experienced abuse but lived in well‐organized households (HR, 0.66; 95% CI, 0.41–1.06). Similar patterns were seen for Black men who lived in dysfunctional households (HR, 3.62; 95% CI, 1.29–10.12) or households with low organization (HR, 2.01; 95% CI, 1.08–3.72). Conclusions We identified race‐ and sex‐specific associations of childhood exposures with incident cardiovascular disease risk factors. The associations of household organization and dysfunction with cardiovascular disease risks merits further investigation.

OBJECTIVES Few researchers have evaluated whether school racial segregation, a key manifestation of structural racism, affects child health, despite its potential impacts on school quality, social networks, and stress from discrimination. We investigated whether school racial segregation affects Black children’s health and health behaviors. METHODS We estimated the association of school segregation with child health, leveraging a natural experiment in which school districts in recent years experienced increased school segregation. School segregation was operationalized as the Black-White dissimilarity index. We used ordinary least squares models as well as quasi-experimental instrumental variables analysis, which can reduce bias from unobserved confounders. Data from the Child Development Supplement of the Panel Study of Income Dynamics (1997–2014, n = 1248 Black children) were linked with district-level school segregation measures. Multivariable regressions were adjusted for individual-, neighborhood-, and district-level covariates. We also performed subgroup analyses by child sex and age. RESULTS In instrumental variables models, a one standard deviation increase in school segregation was associated with increased behavioral problems (2.53 points on a 27-point scale; 95% CI, 0.26 to 4.80), probability of having ever drunk alcohol (0.23; 95% CI, 0.049 to 0.42), and drinking at least monthly (0.20; 95% CI, 0.053 to 0.35). School segregation was more strongly associated with drinking behaviors among girls. CONCLUSIONS School segregation was associated with worse outcomes on several measures of well-being among Black children, which may contribute to health inequities across the life span. These results highlight the need to promote school racial integration and support Black youth attending segregated schools.

AIMS: To assess whether associations between alcohol availability and consumption, drinking to drunkenness, and negative drinking consequences vary among individuals with elevated depressive symptoms. METHODS: 10,482 current drinkers in 2005–2015 National Alcohol Surveys (50.0% female; 74.4% White, 8.7% Black, 11.1% Hispanic). Elevated depressive symptoms was defined as having symptoms suggestive of major depressive disorder (above CES-D8/PHQ-2 cut-offs) versus no/sub-threshold symptoms (below cut-offs). Inverse probability of treatment weighted and covariate adjusted Poisson models with robust standard errors estimated associations of ZIP-code bar density and off-premise outlet density (locations/1,000 residents), elevated depressive symptoms, and their interaction with past-year volume consumed, monthly drinking to drunkenness, and negative drinking consequences. Models were then stratified by sex and race and ethnicity. RESULTS: Overall, 13.7% of respondents had elevated depressive symptoms. Regarding density, the only statistically significant association observed was between off-premise density and volume consumed (rate ratio = 1.3, 95% confidence interval = 1.0, 1.7). Elevated depressive symptoms were associated with higher volume consumed, prevalence of drinking to drunkenness, and prevalence of negative consequences when controlling for off-premise density or bar density. However, there was no evidence of interaction between symptoms and density in the full sample nor among subgroups. CONCLUSION: This study suggests that, while elevated depressive symptoms do not alter associations between alcohol availability and alcohol use and problems, they remain associated with these outcomes among past-year drinkers in a U.S. general population sample even when accounting for differential availability. Addressing depressive symptoms should be considered along with other policies to reduce population-level drinking and alcohol problems.

Current U.S. dietary guidelines recommend a daily potassium intake of 3400 mg/day for men and 2600 mg/day for women. Sub-optimal access to nutrient-rich foods may limit potassium intake and increase cardiometabolic risk. We examined the association of neighborhood characteristics related to food availability with potassium intake in the Hispanic Community Health Study/Study of Latinos (HCHS/SOL). 13,835 participants completed a 24-h dietary recall assessment and had complete covariates. Self-reported potassium intake was calibrated with an objective 24-h urinary potassium biomarker, using equations developed in the SOL Nutrition &amp, Physical Activity Assessment Study (SOLNAS, N = 440). Neighborhood population density, median household income, Hispanic/Latino diversity, and a retail food environment index by census tract were obtained. Linear regression assessed associations with 24-h potassium intake, adjusting for individual-level and neighborhood confounders. Mean 24-h potassium was 2629 mg/day based on the SOLNAS biomarker and 2702 mg/day using multiple imputation and HCHS/SOL biomarker calibration. Compared with the lowest quartile of neighborhood population density, living in the highest quartile was associated with a 26% lower potassium intake in SOLNAS (adjusted fold-change 0.74, 95% CI 0.59–0.94) and a 39% lower intake in HCHS/SOL (adjusted fold-change 0.61 95% CI 0.45–0.84). Results were only partially explained by the retail food environment. The mechanisms by which population density affects potassium intake should be further studied.

Optimism is associated with better health outcomes with hypothesized effects due in part to optimism’s association with restorative health processes. Limited work has examined whether optimism is associated with better quality sleep, a major restorative process. We test the hypothesis that greater optimism is associated with more favorable sleep quality and duration. Main analyses included adults aged 32–51 who participated in the Coronary Artery Risk Development in Young Adults (CARDIA) study (n=3,548) during the fifth (Year 15: 2000–2001) and sixth (Year 20: 2005–2006) follow-up visits. Optimism was assessed using the revised Life-Orientation Test. Self-report measures of sleep quality and duration were obtained twice 5 years apart. A subset of CARDIA participants (2003–2005) additionally provided actigraphic data and completed the Pittsburgh Sleep Quality Index (PSQI) and Epworth Sleepiness Scale (ESS). Multivariate regression analyses were used to examine associations of optimism and sleep indicators. In cross-sectional analyses of 3,548 participants, each standard deviation (SD) higher optimism score resulted in 78% higher odds of self-reporting very good sleep quality. Prospectively, a 1-SD higher optimism score was related to higher odds of reporting persistently good sleep quality across 5-years relative to those with persistently poor sleep [OR=1.31; 95%CI:1.10,1.56]. In participant with supplementary data, each SD higher optimism score was marginally associated with 22% greater odds of favorable sleep quality [OR=1.22; 95%CI:1.00,1.49] as measured by the PSQI, with possible mediation by depressive symptoms. Optimism was unrelated to objective actigraphic sleep data. Findings support a positive cross-sectional and prospective association between optimism and self-reported sleep behavior.

We investigated cross-sectional and longitudinal associations of neighborhood environment characteristics with accelerometer-measured sedentary time (SED), light-intensity physical activity (LPA), and moderate-to-vigorous intensity physical activity (MVPA). Participants were 2,120 men and women in the year 20 (2005–2006) and year 30 CARDIA exams (2015–2016). Year 20 neighborhood characteristics included neighborhood cohesion, resources for physical activity, poverty, and racial residential segregation. Physical activity was measured by accelerometer at years 20 and 30. Multivariable linear regression models examined associations of standardized neighborhood measures at year 20 with SED, LPA, and MVPA assessed that year, and with 10-year changes in SED, LPA, and MVPA. Cross-sectionally, a one standard deviation (SD) increase in cohesion was associated with 4.06 less SED min/day (95% CI: −7.98, − 0.15), and 4.46 more LPA min/day (95% CI: 0.88, 8.03). Each one SD increase in resources was associated with 1.19 more MVPA min/day (95% CI: 0.06, 2.31). A one SD increase in poverty was associated with 11.18 less SED min/day (95% CI: −21.16, −1.18) and 10.60 more LPA min/day (95% CI: 1.79, 19.41) among black men. No neighborhood characteristic was associated with 10-year changes in physical activity in the full sample; however, a one SD increase in cohesion was associated with a 10-year decrease of 25.44 SED min/day (95% CI: −46.73, −4.14) and an increase of 19.0 LPA min/day (95% CI: 1.89, 36.10) in black men. Characteristics of the neighborhood environment are associated with accelerometer-measured physical activity. Differences were observed by race and sex, with more robust findings observed in black men.

Background Assessment of the social determinants of post‐hospital cardiac care is needed. We examined the association and predictive ability of neighborhood‐level determinants (area deprivation index, ADI), readmission risk, and mortality for heart failure, myocardial ischemia, and atrial fibrillation. Methods and Results Using a retrospective (January 1, 2011–December 31, 2018) analysis of a large healthcare system, we assess the predictive ability of ADI on 30‐day and 1‐year readmission and mortality following hospitalization. Cox proportional hazards models analyzed time‐to‐event. Log rank analyses determined survival. C‐statistic and net reclassification index determined the model’s discriminative power. Covariates included age, sex, race, comorbidity, number of medications, length of stay, and insurance. The cohort (n=27 694) had a median follow‐up of 46.5 months. There were 14 469 (52.2%) men and 25 219 White (91.1%) patients. Patients in the highest ADI quintile (versus lowest) were more likely to be admitted within 1 year of index heart failure admission (hazard ratio [HR], 1.25; 95% CI, 1.03‒1.51). Patients with myocardial ischemia in the highest ADI quintile were twice as likely to be readmitted at 1 year (HR, 2.04; 95% CI, 1.44‒2.91]). Patients with atrial fibrillation living in areas with highest ADI were less likely to be admitted within 1 year (HR, 0.79; 95% CI, 0.65‒0.95). As ADI increased, risk of readmission increased, and risk reclassification was improved with ADI in the models. Patients in the highest ADI quintile were 25% more likely to die within a year (HR, 1.25 1.08‒1.44). Conclusions Residence in socioeconomically disadvantaged communities predicts rehospitalization and mortality. Measuring neighborhood deprivation can identify individuals at risk following cardiac hospitalization.

Background Black Americans have a higher risk of hypertension compared with White Americans. Perceived discrimination is a plausible explanation for these health disparities. Few studies have examined the impact of perceived discrimination on the incidence of hypertension among a racially diverse sample. Our study examined associations of everyday and lifetime discrimination with incidence of hypertension and whether these associations varied by sex, discrimination attribution, and racial residential segregation. Methods and Results The study included 3297 Black, Hispanic, Chinese, and White participants aged 45 to 84 years from the Multi‐Ethnic Study of Atherosclerosis who were without hypertension at exam 1 (2000–2002) and who completed at least 1 of 5 follow‐up exams (2002–2018). Cox proportional hazards regression was used to estimate associations of perceived discrimination with incident hypertension. Over the follow‐up period, 49% (n=1625) of participants developed hypertension. After adjustment for age, sex, socioeconomic status, hypertension risk factors, and study site, Black participants reporting any lifetime discrimination (compared with none) were more likely to develop hypertension (hazard ratio [HR], 1.35; 95% CI, 1.07–1.69). In fully adjusted models, everyday discrimination (high versus low) was associated with a lower risk for hypertension among Hispanic participants (HR, 0.73; 95% CI, 0.55–0.98). Statistically significant interactions of perceived discrimination (everyday and lifetime) with sex, discrimination attribution, and racial residential segregation were not observed. Conclusions This study suggests that lifetime, but not everyday discrimination is associated with incident hypertension in Black Americans.

BackgroundLife expectancy in the United States has recently declined, in part attributable to premature cardiometabolic mortality. We characterized national trends in premature cardiometabolic mortality, overall, and by race‐sex groups.Methods and ResultsUsing death certificates from the Centers for Disease Control and Prevention's Wide‐Ranging Online Data for Epidemiologic Research, we quantified premature deaths (ConclusionsOver one‐fifth of cardiometabolic deaths occurred at

Background Childhood adversity and trauma have been shown to be associated with poorer cardiovascular disease ( CVD ) outcomes in adulthood. However, longitudinal studies of this association are rare. Methods and Results Our study used the CARDIA (Coronary Artery Risk Development in Young Adults) Study, a longitudinal cohort that has followed participants from recruitment in 1985–1986 through 2018, to determine how childhood psychosocial environment relates to CVD incidence and all‐cause mortality in middle age. Participants (n=3646) completed the Childhood Family Environment ( CFE ) questionnaire at the year 15 (2000–2001) CARDIA examination and were grouped by high, moderate, or low relative CFE adversity scores. We used sequential multivariable regression models to estimate hazard ratios of incident ( CVD ) and all‐cause mortality. Participants were 25.1±3.6 years old, 47% black, and 56% female at baseline and 198 participants developed CVD (17.9 per 10 000 person‐years) during follow‐up. CVD incidence was >50% higher for those in the high CFE adversity group compared with those in the low CFE adversity group. In fully adjusted models, CVD hazard ratios (95% CI) for participants who reported high and moderate CFE adversity versus those reporting low CFE adversity were 1.40 (0.98–2.11) and 1.25 (0.89–1.75), respectively. The adjusted hazard ratios for all‐cause mortality was 1.68 (1.17–2.41) for those with high CFE adversity scores and 1.55 (1.11–2.17) for those with moderate CFE adversity scores. Conclusions Adverse CFE was associated with CVD incidence and all‐cause mortality later in life, even after controlling for CVD risk factors in young adulthood.

Purpose There are limited data on the relationship between neighborhood level factors and their association with lung health independent of individual socioeconomic status. We sought to determine whether baseline neighborhood level socioeconomic deprivation in young adults is associated with greater 20-year decline in lung function and higher risk of future lung disease, independent of baseline individual income, education, and smoking status. Methods This multicenter population-based cohort study included 2689 participants in Coronary Artery Risk Development in Young Adults (CARDIA) for whom neighborhood deprivation was determined at year 10 (baseline for study) and who had complete lung function measurements at years 10 and 30. Baseline neighborhood deprivation was defined using 1990 Census blocks as a combination of 4 factors involving median household income, poverty level, and educational achievement. The outcomes were decline in lung function over 20 years (year 10 to 30) and odds of emphysema (year 25). Results In multivariable regression models, greater baseline neighborhood deprivation was associated with greater decline in lung function (−2.34 mL/year excess annual decline in forced expiratory volume in 1 second (FEV1) in the highest versus lowest deprivation quartile (P = .014)). Furthermore, baseline neighborhood deprivation was independently associated with greater odds of emphysema (odds ratio [OR] 2.99, 95% confidence interval [CI] 1.42-6.30). Conclusions Residence in neighborhoods with greater socioeconomic deprivation in young adulthood, independent of individual income and smoking, is associated with greater 20-year decline in forced expiratory volume in 1 second and higher risk of future emphysema.

INTRODUCTION: There are known racial differences in cardiovascular health behaviors, including smoking, physical activity, and diet quality. A better understanding of these differences may help identify intervention targets for reducing cardiovascular disease disparities. This study examined whether socioeconomic, psychosocial, and neighborhood environmental factors, in isolation or together, mediate racial differences in health behaviors. METHODS: Participants were 3,081 men and women from the Coronary Artery Risk Development in Young Adults study who were enrolled in 1985–1986 (Year 0) and completed a follow-up examination in 2015–2016 (Year 30). A health behavior score was created at Years 0, 7, 20, and 30 using smoking, physical activity, and diet assessed that year. The race difference in health behavior score was estimated using linear regression in serial cross-sectional analyses. Mediation analyses computed the proportion of the race and health behavior score association attributable to socioeconomic, psychosocial, and neighborhood factors. RESULTS: Data analysis conducted in 2016–2017 found that blacks had significantly lower health behavior scores than whites across 30 years of follow-up. Individual socioeconomic factors mediated 48.9%–70.1% of the association between race and health behavior score, psychosocial factors 20.3%–30.0%, and neighborhood factors 22.1%–41.4% (p

BACKGROUND High neighborhood crime and low perceptions of safety may influence blood pressure (BP) through chronic stress. Few studies have examined these associations using longitudinal data. METHODS We used longitudinal data from 528 participants of the Multi-Ethnic Study of Atherosclerosis (aged 45–84, nonhypertensive at baseline) who lived in Chicago, Illinois. We examined associations of changes in individual-level perceived safety, aggregated neighborhood-level perceived safety, and past-year rates of police-recorded crime in a 1, ½, or ¼ mile buffer per 1,000 population with changes in systolic and diastolic BPs using fixed-effects linear regression. BP was measured five times between 2000 and 2012 and was adjusted for antihypertensive medication use (+10 mm Hg added to systolic and +5 mm Hg added to diastolic BP for participants on medication). Models were adjusted for time-varying sociodemographic and health-related characteristics and neighborhood socioeconomic status. We assessed differences by sex. RESULTS A standard deviation increase in individual-level perceived safety was associated with a 1.54 mm Hg reduction in systolic BP overall (95% confidence interval [CI]: 0.25, 2.83), and with a 1.24 mm Hg reduction in diastolic BP among women only (95% CI: 0.37, 2.12) in adjusted models. Increased neighborhood-level safety was not associated with BP change. An increase in police-recorded crime was associated with a reduction in systolic and diastolic BPs among women only, but results were sensitive to neighborhood buffer size. CONCLUSIONS Results suggest individual perception of neighborhood safety may be particularly salient for systolic BP reduction relative to more objective neighborhood exposures.

Risk factors can drive socioeconomic inequalities in cardiovascular disease (CVD) through differential exposure and differential vulnerability. In this paper, we show how econometric decomposition directly enables simultaneous, policy-oriented assessment of these 2 mechanisms. We specifically estimate contributions of neighborhood environment and proximal risk factors to socioeconomic inequality in CVD incidence via these mechanisms. We followed 5,608 participants in the Multi-Ethnic Study of Atherosclerosis (2000-2012) to their first CVD event (median length of follow-up, 12.2 years). We used a summary measure of baseline socioeconomic position (SEP). Covariates included baseline demographics, neighborhood characteristics, and psychosocial, behavioral, and biomedical risk factors. Using Poisson models, we decomposed the difference (inequality) in incidence rates between low- and high-SEP groups into contributions of 1) differences in covariate means (differential exposure) and 2) differences in CVD risk associated with covariates (differential vulnerability). Notwithstanding large uncertainty in neighborhood estimates, our analysis suggested that differential exposure to poorer neighborhood socioeconomic conditions, adverse social environment, diabetes, and hypertension accounted for most of the inequality. Psychosocial and behavioral contributions were negligible. Further, neighborhood SEP, female sex, and white race were more strongly associated with CVD among low-SEP (vs. high-SEP) participants. These differentials in vulnerability also accounted for nontrivial portions of the inequality and could have important implications for intervention.

Racial disparities in cardiovascular health (CVH) continue to remain a public health concern in the United States. We use unique population-based data from the Multi-Ethnic Study of Atherosclerosis cohort to explore the black-white differences in optimal CVH. Utilizing geographically weighted regression methods, we assess the spatial heterogeneity in black-white differences in optimal CVH and the impact of both individual- and neighborhood-level risk factors. We found evidence of significant spatial heterogeneity in black-white differences that varied within and between the five sites. Initial models showed decreased odds of optimal CVH for blacks that ranged from 60% to 70% reduced odds - with noticeable variation of these decreased odds within each site. Adjusting for risk factors resulted in reductions in the black-white differences in optimal CVH. Further understanding of the reasons for spatial heterogeneities in black-white differences in nationally representative cohorts may provide important clues regarding the drivers of these differences.

Importance Patterns of hypertension risk development over the adult lifespan and lifetime risks for hypertension under the American Heart Association and American College of Cardiology (AHA/ACC) 2017 thresholds for hypertension (≥130/80 mm Hg) are unknown. Objective To quantify and compare lifetime risks for hypertension in white and African American men and women under the AHA/ACC 2017 and the Seventh Joint National Commission (JNC7) hypertension thresholds. Design, setting, and participants We used individual-level pooled data from 3 contemporary cohorts in the Cardiovascular Lifetime Risk Pooling Project: the Framingham Offspring Study, the Coronary Artery Risk Development in Young Adults study, and Atherosclerosis Risk in Communities study. These community-based cohorts included white and African American men and women with blood pressure assessment at multiple cohort examinations. Main outcomes and measures Cumulative lifetime risk for hypertension from ages 20 through 85 years, adjusted for competing risk of death and baseline hypertension prevalence. Incident hypertension under the AHA/ACC threshold was defined by a single-occasion blood pressure measurement of 130/80 mm Hg or more or self-reported use of antihypertensive medications. Incident hypertension under the JNC7 threshold was defined by a single-occasion blood pressure measurement of 140/90 mm Hg or more or the use of antihypertensive medications. Results A total of 13 160 participants contributed 227 600 person-years of follow-up; the data set included individual-level data on 6313 participants at baseline (median age, 25 years), plus person-year data from participants in the Atherosclerosis Risk in Communities and Framingham Offspring studies who enrolled at older ages. Baseline prevalence of hypertension under the AHA/ACC 2017 threshold in participants entering the data set between 20 and 30 years of age was 30.7% in white men (n = 549 of 1790), 23.1% in African American men (n = 245 of 1063), 10.2% in white women (n = 210 of 2070), and 12.3% in African American women (n = 171 of 1390). White men had lifetime risk of hypertension of 83.8% (95% CI, 82.5%-85.0%); African American men, 86.1% (95% CI, 84.1%-88.1%); white women, 69.3% (95% CI, 67.8%-70.7%); and African American women, 85.7% (95% CI, 84.0%-87.5%). These were greater than corresponding lifetime risks under the JNC7 threshold for hypertension (white men, 60.5% [95% CI, 58.9%-62.1%]; African American men, 74.7% [95% CI, 71.9%-77.5%]; white women, 53.9% [95% CI, 52.5%-55.4%]; and African American women, 77.3% [95% CI, 75.0%-79.5%]). Conclusions and relevance Under the AHA/ACC 2017 blood pressure threshold for hypertension, lifetime risks for hypertension exceeded 75% for African American men and women and white men. Furthermore, prevalence of blood pressure of 130/80 mm Hg or more is very high in young adulthood, suggesting that efforts to prevent development of hypertension should be focused early in the life course.

Background While prior studies have linked the neighborhood environment and development of subclinical atherosclerosis, it is unknown whether living in neighborhoods with greater availability of “unhealthy” food outlets (fast‐food chain restaurants and convenience stores) is associated with risk of developing coronary artery calcification ( CAC ). Methods and Results We included 2706 CARDIA study (Coronary Artery Risk Development in Young Adults) participants who underwent CAC measurement during follow‐up years 15 (2000–2001), 20 (2005–2006), and 25 (2010–2011). Neighborhood features examined included percentage of all food outlets that were convenience stores and fast‐food chain restaurants within a 3‐km Euclidean buffer distance from each participant's residence. Econometric fixed effects models, which by design control for all time‐invariant covariates, were used to model the longitudinal association between simultaneous within‐person change in percentage food outlet and change in CAC . At baseline (year 15), 9.7% of participants had prevalent CAC . During 10 years of follow‐up, 21.1% of participants developed CAC . Each 1‐SD increase in percentage of convenience stores was associated with a 1.34 higher odds of developing CAC (95% CI : 1.04, 1.72) after adjusting for individual‐ and neighborhood‐level covariates; however, there was no significant association between increased percentage of fast‐food chain restaurants and developing CAC (odds ratio=1.15; 95% CI : 0.96, 1.38). There were no significant associations between increases in either food outlet percentage and progression of CAC . Conclusions Our findings suggest that increases in the relative availability of convenience stores in participants' neighborhoods is related to the development of CAC over time.

Epidemiological studies have highlighted the disparate impact of coronavirus disease 2019 (COVID-19) on racial and ethnic minority and socioeconomically disadvantaged populations, but data at the neighborhood-level is sparse. The objective of this study was to investigate the disparate impact of COVID-19 on disadvantaged neighborhoods and racial/ethnic minorities in Chicago, Illinois. Using data from the Cook County Medical Examiner, we conducted a neighborhood-level analysis of COVID-19 decedents in Chicago and quantified age-standardized years of potential life lost (YPLL) due to COVID-19 among demographic subgroups and neighborhoods with geospatial clustering of high and low rates of COVID-19 mortality. We show that age-standardized YPLL was markedly higher among the non-Hispanic (NH) Black (559 years per 100,000 population) and the Hispanic (811) compared with NH white decedents (312). We demonstrate that geomapping using residential address data at the individual-level identifies hot-spots of COVID-19 mortality in neighborhoods on the Northeast, West, and South areas of Chicago that reflect a legacy of residential segregation and persistence of inequality in education, income, and access to healthcare. Our results may contribute to ongoing public health and community-engaged efforts to prevent the spread of infection and mitigate the disproportionate loss of life among these communities due to COVID-19 as well as highlight the urgent need to broadly target neighborhood disadvantage as a cause of pervasive racial inequalities in life and health.

Importance Despite recent advances in therapies for heart failure (HF), deaths from HF are increasing, with persistent disparities between Black and White adults. Recent national trends in the prevalence of HF need to be clarified to appropriately allocate resources and develop effective preventive interventions. Objectives To examine the prevalence of ambulatory HF overall and by race/ethnicity and age and the temporal changes in HF prevalence between 2001 and 2016. Design, Setting, and Participants This cross-sectional study of nationally representative data collected biennially through the National Health and Nutrition Examination Survey (NHANES) from January 1, 2001, to December 31, 2016, assessed nonpregnant adults 35 years and older who self-identified as non-Hispanic Black, non-Hispanic White, or Mexican American. Data analysis was performed from November 16, 2019, to April 12, 2020. Exposures Survey period, race/ethnicity, and age group. Main Outcomes and Measures Age-standardized prevalence was calculated within 4-year survey periods (2001-2004, 2005-2008, 2009-2012, and 2013-2016) based on self-report of ambulatory HF overall and by race/ethnicity and age group (35-64 and ≥65 years). Weighted multivariable logistic regression was used to examine trends in ambulatory HF prevalence over time by race/ethnicity and age group. Results A total of 26 097 participants (mean [SD] age, 55.9 [10.7] years; 13 192 [52%] female; 6519 [12%] non-Hispanic Black; and 4906 [7%] Mexican American) were studied. Overall age-standardized prevalence (per 100 000 population) of ambulatory HF was 3184 (95% CI, 2641-3728) from 2001 to 2005 and 3045 (95% CI, 2651-3438) from 2013 to 2016. The prevalence of ambulatory HF was highest among non-Hispanic Black adults: from 2013 to 2016, HF prevalence (per 100 000 population) was 5017 (95% CI, 3755-6279) among non-Hispanic Black adults, 2746 (95% CI, 2313-3179) among non-Hispanic White adults, and 2508 (95% CI, 1154-3862) among Mexican American adults. Differences between White and Black adults in HF prevalence were also present in younger and middle-aged adults (eg, 35-64 years of age in 2013-2016: 3864 [95% CI, 2369-5359] for non-Hispanic Black adults vs 1297 [95% CI, 878-1716] for non-Hispanic White adults). Conclusions and Relevance This study found that a high burden of ambulatory HF persisted between 2001 and 2016 in the US. Disparities were most prominent by age group. Alongside prevention and aggressive management of risk factors, targeted efforts aimed at mitigating racial disparities are needed.

IMPORTANCE: Neighborhood-level residential segregation is implicated as a determinant for poor health outcomes in black individuals, but it is unclear whether this association extends to cognitive aging, especially in midlife. OBJECTIVE: To examine the association between cumulative exposure to residential segregation during 25 years of young adulthood among black individuals and cognitive performance in midlife. DESIGN, SETTING, AND PARTICIPANTS: The ongoing prospective cohort Coronary Artery Risk Development in Young Adults (CARDIA) Study recruited 5115 black and white participants aged 18 to 30 years from 4 field centers at the University of Alabama, Birmingham; University of Minnesota, Minneapolis; Northwestern University, Chicago, Illinois; and Kaiser Permanente, Oakland, California. Data were acquired from February 1985 to May 2011. Among the surviving CARDIA cohort, 3671 (71.8%) attended examination year 25 of the study in 2010, when cognition was measured, and 3008 (81.9%) of those completed the cognitive assessments. To account for time-varying confounding and differential censoring, marginal structural models using inverse probability weighting were applied. Data were analyzed from April 16 to July 20, 2019. MAIN OUTCOMES AND MEASURES: Racial residential segregation was measured using the Getis-Ord G(i)* statistic, and the mean cumulative exposure to segregation was calculated across 6 follow-up visits from baseline to year 25 of the study, then categorized into high, medium, and low segregation. Cognitive function was measured at year 25 of the study, using the Digit Symbol Substitution Test (DSST), Stroop color test (reverse coded), and Rey Auditory Verbal Learning Test. To facilitate comparison of estimates, z scores were calculated for all cognitive tests. RESULTS: A total of 1568 black participants with available cognition data were included in the analysis. At baseline, participants had a mean (SD) age of 25 (4) years and consisted of 936 women (59.7%). Greater cumulative exposure to segregated neighborhoods was associated with a worse DSST z score (for high segregation, β = −0.37 [95% CI, −0.61 to −0.13]; for medium segregation, β = −0.25 [95% CI, −0.51 to 0.0002]) relative to exposure to low segregation. CONCLUSIONS AND RELEVANCE: In this cohort study, exposure to residential segregation throughout young adulthood was associated with worse processing speed among black participants as early as in midlife. This association may potentially explain black-white disparities in dementia risk at older age.

Although racial residential segregation and interpersonal racial discrimination are associated with cardiovascular disease, few studies have examined their link with diabetes risk or management. We used longitudinal data from 2,175 black participants in the Coronary Artery Risk Development in Young Adults (CARDIA) Study to examine associations of racial residential segregation (G(i)* statistic) and experiences of racial discrimination with diabetes incidence and management. Multivariable Cox models estimated associations for incident diabetes and GEE logistic regression estimated associations with diabetes management (meeting targets for HbA1c, systolic blood pressure, and LDL cholesterol). Neither segregation nor discrimination were associated with diabetes incidence or management.

Large and persistent obesity disparities exist in the US by socioeconomic status (SES) and race/ethnicity, and weight loss interventions have traditionally been less effective in these populations. Thus, a better understanding is needed of the behavioral, economic, and geographic factors that influence obesity risk factors such as eating behaviors. We used a discrete choice experiment to evaluate the impact of different meal attributes on meal choice and to test whether the relative importance of these attributes varied by SES and race/ethnicity. Study participants (n = 228) were given a series of 10 choice tasks and asked to choose among 4 meals, each rated based on the following attributes: taste; healthfulness; preparation time; travel time to food outlet for meal/ingredients; and price. SES was measured using education and self-reported difficulty paying for basics. Race/ethnicity was categorized as Hispanic/Latina, non-Hispanic black, non-Hispanic white, and non-Hispanic other. Data were analyzed using mixed logit regression models with interaction terms to determine whether meal attributes influenced meal choices differentially by SES and race/ethnicity. Healthfulness and taste were the most important attributes for all participants. Price was a more important attribute among those in the lowest SES group compared with those in the higher SES groups. Travel was the least important attribute for low SES participants, and it was not significantly related to meal choice in these groups. Discrete choice experiments as illustrated here may help pinpoint the most salient targets for interventions to improve eating behaviors and reduce obesity disparities. Specifically, our findings suggest interventions should incorporate strategies to target the pricing of healthy and unhealthy food options.

BackgroundRacial residential segregation has been linked to adverse health outcomes, but associations may operate through multiple pathways. Prior studies have not examined associations of neighbourhood-level racial segregation with an index of cardiometabolic risk (CMR) and whether associations differ by race/ethnicity.MethodsWe used data from the Multi-Ethnic Study of Atherosclerosis to estimate cross-sectional and longitudinal associations of baseline neighbourhood-level racial residential segregation with a composite measure of CMR. Participants included 5015 non-Hispanic black, non-Hispanic white and Hispanic participants aged 45–84 years old over 12 years of follow-up (2000–2012). We used linear mixed effects models to estimate race-stratified associations of own-group segregation with CMR at baseline and with the rate of annual change in CMR. Models were adjusted for sociodemographics, medication use and individual-level and neighbourhood-level socioeconomic status (SES).ResultsIn models adjusted for sociodemographics and medication use, high baseline segregation was associated with higher baseline CMR among blacks and Hispanics but lower baseline CMR among whites. Individual and neighbourhood-level SES fully explained observed associations between segregation and CMR for whites and Hispanics. However, associations of segregation with CMR among blacks remained (high vs low segregation: mean difference 0.17 SD units, 95% CI 0.02 to 0.32; medium vs low segregation: mean difference 0.18 SD units, 95% CI 0.03 to 0.33). Baseline segregation was not associated with change in CMR index scores over time.ConclusionAssociations of own-group racial residential segregation with CMR varied by race/ethnicity. After accounting for SES, living in a more segregated neighbourhood was associated with greater risk among black participants only.

Background: Smoke-free legislation has been associated with lower rates of cardiovascular disease hospital admissions in ecological studies. However, prior studies lacked detailed information on individual-level factors (eg, sociodemographic and clinical characteristics) that could potentially confound associations. Our objective was to estimate associations of smoke-free policies with incident cardiovascular disease in a longitudinal cohort after controlling for sociodemographics, cardiovascular disease risk factors, and policy covariates. Methods: Longitudinal data from 3783 black and white adults in the CARDIA study (Coronary Artery Risk Development in Young Adults; 1995–2015) were linked to state, county, and local 100% smoke-free policies in bars, restaurants, and nonhospitality workplaces by Census tract. Extended Cox regression estimated hazard ratios (HRs) of incident cardiovascular disease associated with time-dependent smoke-free policy exposures. Models were adjusted for sociodemographic characteristics, cardiovascular disease risk factors, state cigarette tax, participant-reported presence of a smoking ban at their workplace, field center, and metropolitan statistical area poverty. Results: During a median follow-up of 20 years (68 332 total person-years), 172 participants had an incident cardiovascular disease event (2.5 per 1000 person-years). Over the follow-up period, 80% of participants lived in areas with smoke-free policies in restaurants, 67% in bars, and 65% in nonhospitality workplaces. In fully adjusted models, participants living in an area with a restaurant, bar, or workplace smoke-free policy had a lower risk of incident cardiovascular disease compared with those in areas without smoke-free policies (HR, 0.75, 95% confidence interval, 0.49–1.15; HR, 0.76, 95% confidence interval, 0.47–1.24; HR, 0.54, 95% confidence interval, 0.34–0.86, respectively; HR, 0.58, 95% confidence interval, 0.33–1.00 for living in an area with all 3 types of policies compared with none). The estimated preventive fraction was 25% for restaurant policies, 24% for bar policies, and 46% for workplace policies. Conclusions: Consistent with prior ecological studies, these individual-based data add to the evidence that 100% smoke-free policies are associated with lower risk of cardiovascular disease among middle-aged adults.

Introduction Few studies have used longitudinal cohort data to examine associations of cigarette prices with smoking cessation or whether price sensitivity varies by income or education. This study examines these associations in a multicenter US cohort and explores whether associations vary by education and income. Methods Longitudinal data from baseline daily cigarette smokers aged 18-30 years in the Coronary Artery Risk Development in Young Adults study were linked to inflation-adjusted cigarette carton prices from the Council for Community and Economic Research Cost of Living Index based on residential address at baseline and in years 7, 10, and 15 (1985-2001). Multivariable Cox models estimated hazard ratios (HRs) of first (any) smoking cessation and sustained smoking cessation (no relapse) associated with each $1 increase in time-dependent cigarette price over 15 years of follow-up. Models were adjusted for sociodemographic, health-related, and policy covariates. We assessed effect modification by education and household income. Results Among 1489 participants, a $1.00 higher cigarette carton price was associated with a 16% higher likelihood of first smoking cessation (HR = 1.16, 95% CI = 1.11 to 1.21) and an 8% higher likelihood of sustained smoking cessation (HR = 1.08, 95% CI = 1.02 to 1.14). Associations were strongest among participants with lower income for first cessation, and among those with higher income for sustained cessation. Associations were strongest for participants with less than a high school degree for both outcomes. Conclusions Results suggest higher cigarette prices promote smoking cessation among young to middle-aged adults, and that price sensitivity may differ by socioeconomic status. Implications Few studies have examined longitudinal associations of cigarette prices with smoking cessation, and findings are mixed on whether price sensitivity varies by education or income. In a cohort of US adult daily smokers, cigarette prices were associated with greater likelihood of both a first cessation and sustained cessation. Price associations with first cessation were stronger among low-income smokers, but associations with sustained cessation were stronger among high-income smokers. Results suggest that although higher cigarette prices may promote short-term smoking cessation among smokers at all income levels, additional supports may be needed to facilitate sustained smoking cessation among low-income smokers.

Background Social factors may enhance health effects of air pollution, yet empirical support is inconsistent. The interaction of social and environmental factors may only be evident with long-term exposures and outcomes that reflect long-term disease development. Methods We used cardiac magnetic resonance imaging data from the Multi-Ethnic Study of Atherosclerosis to assess left-ventricular mass index (LVMI) and left-ventricular ejection fraction (LVEF). We assigned residential concentrations of fine particulate matter (PM2.5), oxides of nitrogen, and nitrogen dioxide in the year 2000 to each participant in 2000 using prediction models. We examined modifying roles of four measures of adversity: race/ethnicity, racial/ethnic residential segregation, and socioeconomic status and psychosocial adversity as composite indices on the association between air pollution and LVMI or LVEF. Results Compared with whites, blacks showed a stronger adjusted association between air pollution and LVMI. For example, for each 5 µg/m greater PM2.5 level, whites showed a 1.0 g/m greater LVMI (95% confidence interval = -1.3, 3.1), while blacks showed an additional 4.0 g/m greater LVMI (95% confidence interval = 0.3, 8.2). Results were similar for oxides of nitrogen and nitrogen dioxide with regard to black race and LVMI. However, we found no evidence of a modifying role of other social factors or ethnic groups. Furthermore, we found no evidence of a modifying role for any social factors or racial/ethnic groups on the association between air pollution and LVEF. Conclusions Our results suggest that racial group membership may modify the association between air pollution and cardiovascular disease.

Perceived discrimination is positively related to cardiovascular disease (CVD) risk factors; its relationship with incident CVD is unknown. Using data from the Multi-Ethnic Study of Atherosclerosis, a population-based multiethnic cohort study of 6,508 adults aged 45-84 years who were initially free of clinical CVD, we examined lifetime discrimination (experiences of unfair treatment in 6 life domains) and everyday discrimination (frequency of day-to-day occurrences of perceived unfair treatment) in relation to incident CVD. During a median 10.1 years of follow-up (2000-2011), 604 incident events occurred. Persons reporting lifetime discrimination in ≥2 domains (versus none) had increased CVD risk, after adjustment for race/ethnicity and sociodemographic factors, behaviors, and traditional CVD risk factors (hazard ratio (HR) = 1.36, 95% confidence interval (CI): 1.09, 1.70) and after control for chronic stress and depressive symptoms (HR = 1.28, 95% CI: 1.01, 1.60). Reported discrimination in 1 domain was unrelated to CVD (HR = 1.05, 95% CI: 0.86, 1.30). There were no differences by race/ethnicity, age, or sex. In contrast, everyday discrimination interacted with sex (P = 0.03). Stratified models showed increased risk only among men (for each 1-standard deviation increase in score, adjusted HR = 1.14, 95% CI: 1.03, 1.27); controlling for chronic stress and depressive symptoms slightly reduced this association (HR = 1.11, 95% CI: 0.99, 1.25). This study suggests that perceived discrimination is adversely related to CVD risk in middle-aged and older adults.

Despite 50 years since the passage of the Fair Housing Act of 1968, the majority of black Americans continue to live in highly segregated communities. Differing exposure to obesogenic environments in segregated neighborhoods may contribute to racial disparities in obesity prevalence.We used prospective data from the Coronary Artery Risk Development in Young Adults (CARDIA) study to examine associations between levels of neighborhood-level racial residential segregation and incident obesity in black men and women. Obesity, determined by measured anthropometry, and residential segregation, measured using the local Gi*statistic, were recorded at baseline and follow-up at years 7, 10, 15, 20, and 25. We used marginal structural survival models to account for time-dependent confounding and for loss to follow-up.Black women living in highly segregated neighborhoods at the prior exam were 30% more likely to become obese during the follow-up period as compared with women living in neighborhoods with low levels of segregation after adjustment for sociodemographic and cardiovascular risk covariates (hazard ratio = 1.3 [95% confidence interval = 1.0, 1.7]). Cumulatively high exposure to segregation averaged across time points was associated with 50% higher hazard of obesity (hazard ratio = 1.5 [95% confidence interval = 1.0, 2.3]) among women. We observed few differences in obesity incidence among men by segregation levels.Fewer health-promoting resources, stressful neighborhood context, and social norms that are less stigmatizing of obesity may contribute to these findings, but more research on specific pathways leading from segregation to obesity is needed to understand differing patterns between men and women.

Previous analyses utilizing birth certificate data have shown environmental factors such as racial residential segregation may contribute to disparities in adverse pregnancy outcomes. However, birth certificate data are ill equipped to reliably differentiate among small for gestational age, spontaneous preterm birth, and medically indicated preterm birth.We sought to utilize data from electronic medical records to determine whether residential segregation among Black women is associated with an increased risk of adverse pregnancy outcomes.The study population was composed of 4770 non-Hispanic Black women who delivered during the years 2009 through 2013 at a single urban medical center. Addresses were geocoded at the level of census tract, and this tract was used to determine the degree of residential segregation for an individual's neighborhood. Residential segregation was measured using the Gi* statistic, a z-score that measures the extent to which the neighborhood racial composition deviates from the composition of the larger surrounding area. The Gi* statistic z-scores were categorized as follows: low (z0), medium (z = 0-1.96), and high (z 1.96). Adverse pregnancy outcomes included overall preterm birth, spontaneous preterm birth, medically indicated preterm birth, and small for gestational age. Hierarchical logistic regression models accounting for clustering by census tract and repeated births among mothers were used to estimate odds ratios of adverse pregnancy outcomes associated with segregation.In high segregation areas, the prevalence of overall preterm birth was significantly higher than that in low segregation areas (15.5% vs 10.7%, respectively; P.001). Likewise, the prevalence of spontaneous preterm birth and medically indicated preterm birth were higher in high (9.5% and 6.0%) vs low (6.2% and 4.6%) segregation neighborhoods (P .001 and P = .046, respectively). The associations of high segregation with overall preterm birth (odds ratio, 1.31; 95% confidence interval, 1.02-1.69) and spontaneous preterm birth (odds ratio, 1.37; 95% confidence interval, 1.02-1.85) remained significant with adjustment for neighborhood poverty, insurance status, parity, and maternal medical conditions.Among non-Hispanic Black women in an urban area, high levels of segregation were independently associated with the higher odds of spontaneous preterm birth. These findings highlight one aspect of social determinants (ie, segregation) through which adverse pregnancy outcomes may be influenced and points to a potential target for intervention.

We sought to determine whether sustained poverty is associated with change in body mass index (BMI, calculated as weight (kg)/height (m)(2)) among 4,762 black and white adults from the Coronary Artery Risk Development in Young Adults study. Household income in the prior year and current BMI were measured at 7 visits between 1990 and 2015. Sustained poverty was the proportion of visits during which household income was below 200% of the federal poverty level (range, 0%–100%). Sustained poverty and BMI were time-updated. Mean age in 1990 was 30 years. In adjusted linear mixed-effects models, every 10% increase in sustained poverty was significantly associated with faster BMI growth among white men (0.004/year, 95% CI: 0.001, 0.008) and white women (0.003/year, 95% CI: 0.000, 0.006), and slower BMI growth among black men (−0.008/year, 95% CI: −0.010, −0.005) and black women (−0.003/year, 95% CI: −0.006, 0.000). In other words, being always versus never in poverty from 1990 to 2015 was predicted to result in greater BMI gain by 1.00 unit and 0.75 units among white men and women and less BMI gain by 2.0 units and 0.75 units among black men and women, respectively. Sustained poverty was a predictor of changes in BMI with differential associations according to race.

BACKGROUND The association of Cardiovascular Health (CVH; defined by the American Heart Association by assigning points for health-related behavioral and clinical factors) with endothelial and erectile dysfunction has not been reported, although endothelial and erectile dysfunction have been associated with components of CVH. METHODS Data were collected in 1,136 men in the Multi-Ethnic Study of Atherosclerosis at baseline and erectile dysfunction status (measured by survey or medication use) at exam 5. CVH was determined with 7 health metrics. Endothelial function was measured with brachial artery flow-mediated dilation (FMD). Poisson regression was used to determine associations between CVH and erectile dysfunction across categories of CVH (low, moderate, and high). RESULTS Age and proportion of Black or Latino participants decreased while proportion of Chinese-American participants increased with higher CVH category. FMD was higher in men without erectile dysfunction and higher in men with high vs. low CVH. Erectile dysfunction prevalence was lower with better CVH; 58% in men with low CVH, 41% with moderate CVH, and 33% with high CVH (P < 0.001). CVH was associated with erectile dysfunction; prevalence ratio = 0.75 (95% confidence interval (CI) = 0.66, 0.84) with moderate CVH and 0.68 (95% CI = 0.49, 0.94) with high CVH (vs. men with low CVH) and 0.93 (95% CI = 0.91, 0.96) for every 1-point higher CVH score in a fully adjusted model, including FMD, age, education, depression score, use of antidepressant or beta-blocker medications, chronic disease, heavy drinking, and race. CONCLUSION CVH is associated with future erectile dysfunction, even after adjustment for baseline FMD. Maintaining high CVH may improve quality of life for men.

Experiences of discrimination are associated with increased risk of adverse health outcomes; however, it is unknown whether discrimination is related to incident type 2 diabetes mellitus (diabetes). We investigated the associations of major experiences of discrimination (unfair treatment in 6 situations) and everyday discrimination (frequency of day-to-day experiences of unfair treatment) with incident diabetes among 5,310 participants from the Multi-Ethnic Study of Atherosclerosis, enrolled in 2000-2002. Using Cox proportional hazards models, we estimated hazard ratios and confidence intervals, adjusting for demographic factors, depressive symptoms, stress, smoking, alcohol, physical activity, diet, waist circumference, and body mass index. Over a median follow-up of 9.4 years, 654 diabetes cases were accrued. Major experiences of discrimination were associated with greater risk of incident diabetes when modeled continuously (for each additional experience of discrimination, hazard ratio = 1.09, 95% confidence interval: 1.01, 1.17) or categorically (for ≥2 experiences vs. 0, hazard ratio = 1.34, 95% confidence interval: 1.08, 1.66). Similar patterns were observed when evaluating discrimination attributed to race/ethnicity or to a combination of other sources. Everyday discrimination was not associated with incident diabetes. In conclusion, major experiences of discrimination were associated with increased risk of incident diabetes, independent of obesity or behavioral and psychosocial factors. Future research is needed to explore the mechanisms of the discrimination-diabetes relationship.

Objectives. We described the associations of ambient air pollution exposure with race/ethnicity and racial residential segregation. Methods. We studied 5921 White, Black, Hispanic, and Chinese adults across 6 US cities between 2000 and 2002. Household-level fine particulate matter (PM2.5) and nitrogen oxides (NOX) were estimated for 2000. Neighborhood racial composition and residential segregation were estimated using US census tract data for 2000. Results. Participants in neighborhoods with more than 60% Hispanic populations were exposed to 8% higher PM2.5 and 31% higher NOX concentrations compared with those in neighborhoods with less than 25% Hispanic populations. Participants in neighborhoods with more than 60% White populations were exposed to 5% lower PM2.5 and 18% lower NOX concentrations compared with those in neighborhoods with less than 25% of the population identifying as White. Neighborhoods with Whites underrepresented or with Hispanics overrepresented were exposed to higher PM2.5 and NOX concentrations. No differences were observed for other racial/ethnic groups. Conclusions. Living in majority White neighborhoods was associated with lower air pollution exposures, and living in majority Hispanic neighborhoods was associated with higher air pollution exposures. This new information highlighted the importance of measuring neighborhood-level segregation in the environmental justice literature.

Background Several individual-level stressors have been linked to incident coronary heart disease (CHD), but less attention has focused on the influence of neighbourhood-level sources of stress. In this study we examined prospective associations of individual-level and neighbourhood-level stressors with incident CHD. Methods Multi-Ethnic Study of Atherosclerosis participants aged 45–84 years at baseline (2000–2002) with complete data were included in the analyses (n=6678 for individual-level and n=6105 for neighbourhood-level stressors). CHD was defined as non-fatal myocardial infarction, resuscitated cardiac arrest or CHD death. Median follow-up was 10.2 years. Multivariable Cox proportional hazards models were fitted to estimate associations of individual-level and neighbourhood-level stressors (categorised into approximate tertiles) with incident CHD. Results Higher reported individual-level stressors were associated with higher incident CHD. Participants in the high individual-level stressor category had 65% higher risk of incident CHD (95% CI 1.23 to 2.22) than those in the low category after adjusting for sociodemographics (P for trend=0.002). This association weakened but remained significant with further adjustment for behavioural and biological risk factors. There was a non-linear relationship between neighbourhood-level stressors and incident CHD (P for quadratic term=0.01). Participants in the medium category had 49% higher CHD risk (95% CI 1.06 to 2.10) compared with those in the low category; those in the high category had only 27% higher CHD risk (95% CI 0.83 to 1.95). These associations persisted with adjustment for risk factors and individual-level stressors. Conclusions Individual-level and neighbourhood-level stressors were independently associated with incident CHD, though the nature of the relationships differed.

Background and Purpose— This study investigated chronic stress, depressive symptoms, anger, and hostility in relation to incident stroke and transient ischemic attacks in middle-aged and older adults. Methods— Data were from the Multi-Ethnic Study of Atherosclerosis (MESA), a population-based cohort study of 6749 adults, aged 45 to 84 years and free of clinical cardiovascular disease at baseline, conducted at 6 US sites. Chronic stress, depressive symptoms, trait anger, and hostility were assessed with standard questionnaires. The primary outcome was clinically adjudicated incident stroke or transient ischemic attacks during a median follow-up of 8.5 years. Results— One hundred ninety-five incident events (147 strokes; 48 transient ischemic attacks) occurred during follow-up. A gradient of increasing risk was observed for depressive symptoms, chronic stress, and hostility (all P for trend ≤0.02) but not for trait anger ( P >0.10). Hazard ratios (HRs) and 95% confidence intervals indicated significantly elevated risk for the highest-scoring relative to the lowest-scoring group for depressive symptoms (HR, 1.86; 95% confidence interval, 1.16–2.96), chronic stress (HR, 1.59; 95% confidence interval, 1.11–2.27), and hostility (HR, 2.22; 95% confidence interval, 1.29–3.81) adjusting for age, demographics, and site. HRs were attenuated but remained significant in risk factor–adjusted models. Associations were similar in models limited to stroke and in secondary analyses using time-varying variables. Conclusions— Higher levels of stress, hostility, and depressive symptoms are associated with significantly increased risk of incident stroke or transient ischemic attacks in middle-aged and older adults. Associations are not explained by known stroke risk factors.

Few studies have examined longitudinal associations between close social relationships and weight change. Using data from 3,074 participants in the Coronary Artery Risk Development in Young Adults Study who were examined in 2000, 2005, and 2010 (at ages 33-45 years in 2000), we estimated separate logistic regression random-effects models to assess whether patterns of exposure to supportive and negative relationships were associated with 10% or greater increases in body mass index (BMI) (weight (kg)/height (m)(2)) and waist circumference. Linear regression random-effects modeling was used to examine associations of social relationships with mean changes in BMI and waist circumference. Participants with persistently high supportive relationships were significantly less likely to increase their BMI values and waist circumference by 10% or greater compared with those with persistently low supportive relationships after adjustment for sociodemographic characteristics, baseline BMI/waist circumference, depressive symptoms, and health behaviors. Persistently high negative relationships were associated with higher likelihood of 10% or greater increases in waist circumference (odds ratio = 1.62, 95% confidence interval: 1.15, 2.29) and marginally higher BMI increases (odds ratio = 1.50, 95% confidence interval: 1.00, 2.24) compared with participants with persistently low negative relationships. Increasingly negative relationships were associated with increases in waist circumference only. These findings suggest that supportive relationships may minimize weight gain, and that adverse relationships may contribute to weight gain, particularly via central fat accumulation.

Quantifying the impact of different modifiable behavioral and biological risk factors on socioeconomic disparities in coronary heart disease (CHD) may help inform targeted, population-specific strategies to reduce the unequal distribution of the disease. Previous studies have used analytic approaches that limit our ability to disentangle the relative contributions of these risk factors to CHD disparities. The goal of this study was to assess mediation of the effect of low education on incident CHD by multiple risk factors simultaneously. Analyses are based on 15,067 participants of the Dutch Monitoring Project on Risk Factors for Chronic Diseases aged 20-65 years examined 1994-1997 and followed for events until January 1, 2008. Path analysis was used to quantify and test mediation of the low education-CHD association by behavioral (current cigarette smoking, heavy alcohol use, poor diet, and physical inactivity) and biological (obesity, hypertension, diabetes, and hypercholesterolemia) risk factors. Behavioral and biological risk factors accounted for 56.6 % (95 % CI 42.6-70.8 %) of the low education-incident CHD association. Smoking was the strongest mediator, accounting for 27.3 % (95 % CI 17.7-37.4 %) of the association, followed by obesity (10.2 %; 95 % CI 4.5-16.1 %), physical inactivity (6.3 %; 95 % CI 2.7-10.0 %), and hypertension (5.3 %; 95 % CI: 2.8-8.0 %). In summary, in a Dutch cohort, the majority of the relationship between low education and incident CHD was mediated by traditional behavioral and biological risk factors. Addressing barriers to smoking cessation, blood pressure and weight management, and physical activity may be the most effective approaches to eliminating socioeconomic inequalities in CHD.

Background Endothelial dysfunction may represent an important link between chronic stress and cardiovascular disease (CVD) risk. However, few studies have examined the impact of chronic stress on endothelial dysfunction. The purpose of this study was to examine whether chronic stress was associated with flow-mediated dilation (FMD) and 2 biomarkers of endothelial dysfunction (intercellular adhesion molecule-1 (ICAM-1) and E-selectin) in a multiethnic sample of adults (ages 45-84 years). Methods Data come from the baseline examination of Multi-Ethnic Study of Atherosclerosis participants. Chronic stress was assessed based on self-report of the presence and severity of ongoing problems in 5 domains. FMD was obtained using high-resolution ultrasound; biomarkers were assayed in different subsets of participants. Results Higher chronic stress was associated with lower absolute FMD (mm FMD) in models adjusted for demographic and socioeconomic characteristics (0.169mm in high-stress participants vs. 0.178 and 0.179mm in medium and low-stress participants; P for trend = 0.04). This association remained unchanged with further adjustment for behavioral and biological CVD risk factors. Higher stress was related to higher ICAM-1 in models adjusted for sociodemographic characteristics and biological risk factors (P for trend = 0.005), but this association attenuated with adjustment for cigarette smoking (P for trend = 0.07). Chronic stress was not associated with E-selectin. Conclusions Our findings suggest chronic stress is related to endothelial dysfunction, possibly in part through other stress-associated CVD risk factors such as cigarette smoking.

Background Racial disparities in hypertension prevalence in the United States are established. Given our understanding of racial and ethnic disparities in sleep characteristics and demonstrated associations between sleep characteristics and hypertension, we tested whether sleep characteristics mediated racial disparities in hypertension. Methods Analyses were performed in the Chicago Area Sleep Study, a population-based cohort study of 154 Blacks, 128 Whites, 103 Hispanics, and 109 Asians without obstructive sleep apnea. Participants underwent 7 days of wrist actigraphy monitoring. Algorithms were used to determine sleep duration and sleep maintenance (the percent of sleep in the sleep period). Hypertension was determined as systolic blood pressure >140mm Hg or diastolic blood pressure >90mm Hg or the use of antihypertensive medications. We estimated sample prevalence ratios for hypertension before and after adjustment for sleep characteristics and also conducted mediation analysis. Results The sample prevalence of hypertension was highest in Blacks (36%), followed by Hispanics (14%), Asians (8%), and Whites (5%). The sample prevalence ratio for hypertension for Blacks vs. Whites was 5.52 (95% confidence interval (CI): 2.36, 13.23) after adjusting for age, sex, and education. Adjustment for sleep duration had no influence on the effect estimate, but adjustment for sleep maintenance attenuated the sample prevalence ratio to 4.55 (95% CI: 1.91, 11.14). Sleep maintenance mediated 11.4% of the difference in hypertension prevalence between Blacks and Whites in this sample. Conclusions Sleep maintenance mediated a small but significant portion of the disparity in hypertension between Blacks and Whites. Future research should investigate the mechanisms underlying these findings.

Objective To examine associations of lifetime and everyday discrimination with inflammation independent of sociodemographic characteristics. Method Cross-sectional associations of self-reported experiences of everyday discrimination and lifetime discrimination with interleukin-6 (IL-6) and C-reactive protein (CRP) were examined by gender in a multiethnic sample of 3,099 men and 3,468 women aged 45-84 years. Everyday discrimination, lifetime discrimination due to any attribution, and lifetime discrimination attributed to race/ethnicity were based on self-report, and IL-6 and CRP were assayed from blood samples. Results Among women, higher levels of all 3 discrimination measures were significantly associated with higher IL-6 in models adjusted for sociodemographic characteristics, recent infection, anti-inflammatory medication use, and hormone replacement therapy use. All associations were attenuated with adjustment for body mass index (BMI). For men, everyday discrimination was inversely associated with IL-6 in all adjusted models. Lifetime discrimination was not related to IL-6 among men. Discrimination was unassociated with CRP in all models for both men and women. Conclusions The association between discrimination and inflammation varied by gender and marker of inflammation. These findings highlight the complex relationship between discrimination and cardiovascular disease (CVD) risk and point to areas in need of further research. (PsycINFO Database Record

Recent guidelines highlight the importance of improving cardiovascular health in the general population in addition to disease prevention among high risk individuals. We investigated factors associated with ethnic and nativity-related differences in the prevalence of low cardiovascular risk (optimal levels of all major cardiovascular risk factors).We used logistic regression to estimate differences in likelihood of being low risk (not currently smoking; no diabetes; untreated total cholesterol200mg/dL; untreated blood pressure120/80; and body mass index25 kg/m(2)) among 8693 foreign- and U.S.-born Mexican-American and non-Hispanic White 2003-2008 U.S. National Health and Nutrition Examination Survey participants before and after adjustment for socioeconomic, lifestyle, and acculturation-related factors.Foreign-born Mexican-Americans were more likely to be low risk than non-Hispanic Whites after adjustment for all covariates (Odds Ratio [OR]: 1.53; 95% Confidence Interval [CI]: 1.00, 2.34). In contrast, U.S.-born Mexican-Americans were less likely to be low risk compared to Whites (OR: 0.60; 95% CI: 0.43, 0.84). Differences between foreign-born and U.S.-born Mexican-Americans were largely attenuated after adjustment for acculturation indicators.Our findings support the healthy migrant hypothesis and suggest that acculturation-related factors may be important drivers of ethnic and nativity-related differences in low cardiovascular risk.

Few studies have examined geographic variation in hypertension disparities, but studies of other health outcomes indicate that racial residential segregation may help to explain these variations. The authors used data from 8,071 black and white participants in the National Health and Nutrition Examination Survey (1999-2006) who were aged 25 years or older to investigate whether black-white hypertension disparities varied by level of metropolitan-level racial residential segregation and whether this was explained by race differences in neighborhood poverty. Racial segregation was measured by using the black isolation index. After adjustment for demographics and individual-level socioeconomic position, blacks had 2.74 times higher odds of hypertension than whites (95% confidence interval (CI): 2.32, 3.25). However, race differences were significantly smaller in low- than in high-segregation areas (P(interaction) = 0.006). Race differences in neighborhood poverty did not explain this heterogeneity, but poverty further modified race disparities: Race differences were largest in segregated, low-poverty areas (odds ratio = 4.14, 95% CI: 3.18, 5.38) and smallest in nonsegregated, high-poverty areas (odds ratio = 1.24, 95% CI: 0.77, 2.01). These findings suggest that racial disparities in hypertension are not invariant and are modified by contextual levels of racial segregation and neighborhood poverty, highlighting the role of environmental factors in the genesis of disparities.

We sought to understand the link between low socioeconomic position (SEP) and cardiovascular disease (CVD) by examining the association between SEP, health-related coping behaviors, and C-reactive protein (CRP), an inflammatory marker and independent risk factor for CVD, in a U.S. sample of adults.We used a multiple mediation model to evaluate how these behaviors work in concert to influence CRP levels and whether these relationships were moderated by gender and race/ethnicity.CRP levels were divided into two categories: elevated CRP (3.1-10.0 mg/L) and normal CRP (or =3.0 mg/L).Both poverty and low educational attainment were associated with elevated CRP, and these associations were primarily explained through higher levels of smoking and lower levels of exercise. In the education model, poor diet also emerged as a significant mediator. These behaviors accounted for 87.9% of the total effect of education on CRP and 55.8% the total effect of poverty on CRP. We also found significant moderation of these mediated effects by gender and race/ethnicity.These findings demonstrate the influence of socioeconomically patterned environmental constraints on individual-level health behaviors. Specifically, reducing socioeconomic inequalities may have positive effects on CVD disparities through reducing cigarette smoking and increasing vigorous exercise.

BACKGROUND Many studies have examined differences in hypertension across race/ethnic groups but few have evaluated differences within groups. METHODS We investigated within-group geographic variations in hypertension prevalence among 3,322 black and white participants of the Multi-Ethnic Study of Atherosclerosis (MESA). Place of birth and place of residence were included in multivariate Poisson regression analyses. RESULTS Blacks born in southern states were 1.11 (95% confidence interval (CI): 1.02, 1.23) times more likely to be hypertensive than non-southern states after adjusting for age and sex. Findings were similar, though not statistically significant, for whites (prevalence ratio (PR): 1.15, 95% CI: 0.98, 1.35). Blacks and whites living in Forsyth (blacks, PR: 1.23, 95% CI: 1.07, 1.42; whites, PR: 1.32, 95% CI: 1.09, 1.60) and Baltimore (blacks, PR: 1.14, 95% CI: 1.00, 1.31; whites, PR: 1.24, 95% CI: 1.05, 1.47) were also significantly more likely to be hypertensive than those living in Chicago after adjusting for age and sex. Among blacks, those living in New York were also significantly more likely to be hypertensive. Geographic heterogeneity was partially explained by socioeconomic indicators, neighborhood characteristics or hypertension risk factors. There was also evidence of substantial heterogeneity in black-white differences depending on which geographic groups were compared (ranging from 82 to 13% higher prevalence in blacks compared with whites). CONCLUSIONS A better understanding of geographic heterogeneity may inform interventions to reduce racial/ethnic disparities.

Despite cross-sectional evidence linking racial residential segregation to hypertension prevalence among non-Hispanic blacks, it remains unclear how changes in exposure to neighborhood segregation may be associated with changes in blood pressure.To examine the association of changes in neighborhood-level racial residential segregation with changes in systolic and diastolic blood pressure over a 25-year period.This observational study examined longitudinal data of 2280 black participants of the Coronary Artery Risk Development in Young Adults (CARDIA) study, a prospective investigation of adults aged 18 to 30 years who underwent baseline examinations in field centers in 4 US locations from March 25, 1985, to June 7, 1986, and then were re-examined for the next 25 years. Racial residential segregation was assessed using the Getis-Ord Gi* statistic, a measure of SD between the neighborhood's racial composition (ie, percentage of black residents) and the surrounding area's racial composition. Segregation was categorized as high (Gi*1.96), medium (Gi* 0-1.96), and low (Gi*0). Fixed-effects linear regression modeling was used to estimate the associations of within-person change in exposure to segregation and within-person change in blood pressure while tightly controlling for time-invariant confounders. Data analyses were performed between August 4, 2016, and February 9, 2017.Within-person changes in systolic and diastolic blood pressure across 6 examinations over 25 years.Of the 2280 participants at baseline, 974 (42.7%) were men and 1306 (57.3%) were women. Of these, 1861 (81.6%) were living in a high-segregation neighborhood; 278 (12.2%), a medium-segregation neighborhood; and 141 (6.2%), a low-segregation neighborhood. Systolic blood pressure increased by a mean of 0.16 (95% CI, 0.06-0.26) mm Hg with each 1-SD increase in segregation score after adjusting for interactions of time with age, sex, and field center. Of the 1861 participants (81.6%) who lived in high-segregation neighborhoods at baseline, reductions in exposure to segregation were associated with reductions in systolic blood pressure. Mean differences in systolic blood pressure were -1.33 (95% CI, -2.26 to -0.40) mm Hg when comparing high-segregation with medium-segregation neighborhoods and -1.19 (95% CI, -2.08 to -0.31) mm Hg when comparing high-segregation with low-segregation neighborhoods after adjustment for time and interactions of time with baseline age, sex, and field center. Changes in segregation were not associated with changes in diastolic blood pressure.Decreases in exposure to racial residential segregation are associated with reductions in systolic blood pressure. This study adds to the small but growing body of evidence that policies that reduce segregation may have meaningful health benefits.