Search

Background: Social and psychosocial factors are associated with cardiovascular health (CVH). Our objective was to examine the contributions of individual-level social and psychosocial factors to racial and ethnic differences in population CVH in the NHANES (National Health and Nutrition Examination Surveys) 2011 to 2018, to inform strategies to mitigate CVH inequities. Methods: In NHANES participants ages ≥20 years, Kitagawa-Blinder-Oaxaca decomposition estimated the statistical contribution of individual-level factors (education, income, food security, marital status, health insurance, place of birth, depression) to racial and ethnic differences in population mean CVH score (range, 0–14, accounting for diet, smoking, physical activity, body mass index, blood pressure, cholesterol, blood glucose) among Hispanic, non-Hispanic Asian, or non-Hispanic Black adults compared with non-Hispanic White adults. Results: Among 16 172 participants (representing 255 million US adults), 24% were Hispanic, 12% non-Hispanic Asian, 23% non-Hispanic Black, and 41% non-Hispanic White. Among men, mean (SE) CVH score was 7.45 (2.3) in Hispanic, 8.71 (2.2) in non-Hispanic Asian, 7.48 (2.4) in non-Hispanic Black, and 7.58 (2.3) in non-Hispanic White adults. In Kitagawa-Blinder-Oaxaca decomposition, education explained the largest component of CVH differences among men (if distribution of education were similar to non-Hispanic White participants, CVH score would be 0.36 [0.04] points higher in Hispanic, 0.24 [0.04] points lower in non-Hispanic Asian, and 0.23 [0.03] points higher in non-Hispanic Black participants; P P P Conclusions: Education and place of birth confer the largest statistical contributions to the racial and ethnic differences in mean CVH score among US adults.

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.

Introduction: Racial discrimination is associated with poorer cardiometabolic health. Whether physical activity can buffer these adverse health effects is unknown. We hypothesized that greater discrimination would be associated with poorer cardiometabolic health, but associations would be blunted with higher moderate-to-vigorous physical activity (MVPA). Methods: This was an analysis of 2,129 CARDIA participants. Perceived race discrimination was reported at baseline (2000-2001) and categorized as none, moderate, or high for Black participants and none or any for White participants. Different categorization was used to account for the low percentage of White participants reporting discrimination. Health markers including blood pressure (BP), cholesterol (total, HDL-C, LDL-C), HbA1c, and C-reactive protein were measured at baseline, 5, 10, and 15 years. MVPA was measured using an accelerometer at 5-year follow-up. Race stratified mixed effects linear regression examined the main effect of race specific discrimination with health markers. Moderation by MVPA was examined by its product with discrimination in each model. Main effect estimates were computed using linear predictions at the mean and ± 1 SD of MVPA if the interaction term was p Results: Participants were 58% female, 40% black, and 45.3 ± 3.5 years of age at baseline. Contrary to our hypothesis, race discrimination was not significantly associated with health markers in Black or White participants. Significant interactions are presented in the Figure . Among Black participants, high discrimination was associated with higher HbA1c at higher MVPA (+1 SD) only. Conclusions: Perceived race discrimination was not associated with cardiometabolic health among Black or White participants though associations with HbA1c among Black participants may depend on MVPA levels in an unexpected direction. Future studies should further examine MVPA and additional factors which may be related to the health effects of discrimination among minoritized groups.

ImportanceOnly modest attention has been paid to the contributions of social determinants of health to atrial fibrillation (AF) risk factors, diagnosis, symptoms, management, and outcomes. The diagnosis of AF provides unique challenges exacerbated by the arrhythmia’s often paroxysmal nature and individuals’ disparate access to health care and technologies that facilitate detection. Social determinants of health affect access to care and management decisions for AF, increasing the likelihood of adverse outcomes among individuals who experience systemic disadvantages. Developing effective approaches to address modifiable social determinants of health requires research to eliminate the substantive inequities in health care delivery and outcomes in AF.ObservationsThe National Heart, Lung, and Blood Institute convened an expert panel to identify major knowledge gaps and research opportunities in the field of social determinants of AF. The workshop addressed the following social determinants: (1) socioeconomic status and access to care; (2) health literacy; (3) race, ethnicity, and racism; (4) sex and gender; (5) shared decision-making in systemically disadvantaged populations; and (6) place, including rurality, neighborhood, and community. Many individuals with AF have multiple adverse social determinants, which may cluster in the individual and in systemically disadvantaged places (eg, rural locations, urban neighborhoods). Cumulative disadvantages may accumulate over the life course and contribute to inequities in the diagnosis, management, and outcomes in AF.Conclusions and RelevanceWorkshop participants identified multiple critical research questions and approaches to catalyze social determinants of health research that address the distinctive aspects of AF. The long-term aspiration of this work is to eradicate the substantive inequities in AF diagnosis, management, and outcomes across populations.

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.

Introduction: Black and Hispanic Americans have higher rates for dementia than other racial/ethnic groups. Perceived discrimination has many adverse health effects and may contribute to racial disparities in dementia risk. Our objective was to assess the association between lifetime experiences of discrimination and incident dementia. Methods: We included data for 6509 participants, 45-84 years of age at baseline (2000-2002) enrolled in the Multi-Ethnic Study of Atherosclerosis (MESA). We assessed lifetime experiences of discrimination at baseline in six domains related to: hiring; promotion; police; education; housing; and from neighbors. Incidence of dementia was determined from International Classification of Diseases codes and medication inventory. We used Cox proportional hazards to estimate hazard ratios (HR) for incident dementia over 17 years after accounting for cohort attrition and sociodemographic, clinical, and behavioral factors. We assessed effect modification of the association by race/ethnicity. Results: Of the sample, 42% reported experiencing discrimination in their lifetime. We observed 466 incident cases of dementia and lifetime discrimination was associated with incident dementia (Wald χ 2 p=0.03). Individuals reporting lifetime discrimination in ≥2 domains (compared to none) had greater risk for dementia (HR: 1.40; 95%: 1.08, 1.82) after adjustment for sociodemographic, clinical, and behavioral risk factors ( Table ). Associations did not differ by race/ethnicity (p-interaction >0.1). Conclusion: Our findings demonstrate an association between discrimination and incident dementia and provide justification to advance research on the association of discrimination with race-disparities in dementia risk.

Background: Limited health literacy (HL) is associated with individual cardiovascular risk factors and poor risk factor control. The association of HL to composite indices of cardiovascular health (CVH) has not been documented. Hypothesis: Limited HL is associated with suboptimal achievement of ideal CVH as identified by Life’s Simple 7 (LS7). Methods: Included in this analysis are 3766 participants of the Multi-Ethnic Study of Atherosclerosis who completed four HL questionnaire items via follow-up phone calls (2016-2018). Item scores were summed and dichotomized into adequate (≤10) or limited HL (>10). Clinical measures of BMI, total cholesterol, blood pressure, and fasting blood glucose, along with self-reported smoking status, physical activity, and healthy diet were measured at baseline (2000-2002) and categorized by LS7 achievement criteria (poor, inadequate, ideal). LS7 metrics were incorporated into overall CVH (low, medium, high). Poisson regression with robust variance estimation was used to compute prevalence risk ratios and 95% confidence intervals (PRR[95% CI]) of high/medium CVH as well as intermediate/ideal LS7 comparing limited HL to adequate HL. Results: Participants were on average(SD) 59.4(9.13) years old at baseline, 46.0% male, and 58.0% non-white. Prevalence of limited HL was 15.0%. Compared to adequate HL, participants with limited HL were less likely to have medium CVH (0.90[0.84-0.97]) and high CVH achievement (0.53[0.39-0.73]) after adjusting for age, sex, race/ethnicity and field center ( Table ). These associations attenuated with further adjustment for education and income, to 0.94[0.88-1.02] for medium and 0.68[0.50-0.94] for high CVH. Of individual LS7 metrics, limited HL was significantly associated with high glucose levels. Conclusion: Limited HL was associated with suboptimal overall CVH as well as elevated blood glucose levels independent of education. Clinical trials are needed to assess whether improving health literacy enhances CVH.

Background: Adults who maintain high CVH profiles up to midlife have lower risk of several chronic diseases and better quality of life. However, the relationship between the access to different neighborhood resources in young adulthood and the maintenance of CVH into midlife remain understudied. Methods: We used data from 2,317 CARDIA participants. Measures of the neighborhood food and physical activity environment (Table) were linked to participant addresses collected at the baseline exam (1985-1986), when participants were 18-30 years old. CVH was measured at baseline and the year 30 follow-up exam. We examined associations of neighborhood food and physical activity environments with year 30 CVH scores (moderate vs. high and low vs. high) using multinomial logistic regression. Individual- and neighborhood-level covariates (Table) were adjusted for sequentially. Results: At baseline, 31% of participants had high and 5% had low CVH scores, respectively, whereas 11% had high and 34% had low CVH scores 30 years later. At year 30, compared to those with low CVH scores, participants with high CVH scores had better baseline neighborhood conditions (e.g., mean distance to nearest major park 4767m vs. 7043m, mean count of community and public physical activity facilities 50.70 vs. 43.57, mean percentage of food outlets that are supermarkets 0.75% vs. 0.44%) and were more likely to be female (70.99% vs. 59.21%) and White (86.64% vs. 39.14%). In adjusted models, participants who lived in neighborhoods with a higher percentage of supermarkets and more community and public physical activity facilities were less likely to have low CVH scores compared to high CVH scores (Table). Participants who lived in neighborhoods with a higher percentage of convenience stores and further from a major park were more likely to have low vs. high CVH scores. Conclusion: Improving access to physical activity and healthy food resources in young adulthood may have significant implications in longevity and quality of life in midlife.

Introduction: Adverse family environment (AFE) in childhood may have deleterious health effects; however, whether these exposures relate to health promoting behaviors in adulthood is unknown. We hypothesize that AFE in childhood will be associated with higher sedentary behavior (SED), and lower light- (LPA) and moderate-to-vigorous (MVPA) physical activity in adulthood and that associations will be moderated by social network size or social support. Methods: This was an analysis of 2,127 CARDIA study participants. AFE in childhood was self-reported in year 15 (2000-2001) and categorized as low, moderate, or high adversity using a 7-item questionnaire. Average SED, LPA, and MVPA (min/day) were measured using year 20 (2005-2006) accelerometry data and exercise units/day of MVPA was self-reported. Linear regression models examined associations of AFE in childhood with accelerometer measured SED, LPA, MVPA and self-reported MVPA in adulthood. We further tested for interactions between AFE and adult social network size or social support with each activity outcome and stratified analyses if interactions were p Results: Participants were 57% female and 45.3 ± 3.5 years of age. High AFE (versus low) was only associated with lower SED (ß: -10.72 min/day, p=0.039). Interaction analyses identified a significant social network x AFE interaction with SED and social support x AFE interaction with self-reported MVPA. In stratified analyses, those with small social network and high AFE had lower SED (ß: -17.99 min/day, p=0.015) compared small social network and low AFE. Those with high social support and high AFE had significantly lower self-reported MVPA (ß: -44.74 exercise units/day, p=0.026) compared to high social support and low AFE (Table). Conclusions: In conclusion, high AFE, among those with a small social network, was related to lower SED and among those with high social support, lower self-reported MVPA. These data are hypothesis generating as associations were in unexpected directions.

Background: Neighborhood-level racial residential segregation has been linked to several cardiovascular disease risk factors and outcomes in Black adults, but its impact on subclinical atherosclerosis remains unknown. In addition, although the impact of segregation on health may vary over the life course, most studies have examined segregation exposure at a single point in time. This article takes a life course approach by examining associations of exposure to neighborhood-level racial residential segregation in young adulthood and patterns of exposure from young adulthood to midlife with coronary artery calcification (CAC) incidence. Methods: We used data on 1125 Black CARDIA study (Coronary Artery Risk Development in Young Adults) participants free of CAC. Residential segregation was assessed using the G i * statistic and measured when participants were young adults (18–30 years old, in 1985–1986) and as the pattern from young adulthood to midlife (15 years later). Poisson regression with generalized estimating equations models was used to measure CAC incidence. Results: We found participants living in low segregation neighborhoods in young adulthood had 0.52 (rate ratio [95% CI: 0.28–0.98]) times lower risk of developing CAC compared with high segregation after adjusting for young adulthood sociodemographic characteristics and neighborhood poverty. Associations were attenuated and no longer statistically significant with adjustment for midlife CAC risk factors hypothesized to be on the causal pathway (rate ratio: 0.56 [95% CI: 0.29–1.09]). Findings for patterns of segregation over time suggest participants living in low segregation neighborhoods in young adulthood were less likely to develop CAC than those who started out in medium/high segregation neighborhoods, regardless of where they lived in midlife (rate ratio for increase from low to medium/high: 0.42 [95% CI: 0.19–0.95]; rate ratio for continuously low versus continuously medium/high segregation neighborhoods: 0.75 [95% CI: 0.31–1.83]). Conclusions: We found that participants living in more segregated neighborhoods in young adulthood were more likely to develop CAC due at least in part to differences in CAC risk factor burden accumulated over follow-up.

Background Residential segregation, a geospatial manifestation of structural racism, is a fundamental driver of racial and ethnic health inequities, and longitudinal studies examining segregation’s influence on cardiovascular health are limited. This study investigates the impact of segregation on hypertension in a multiracial and multiethnic cohort and explores whether neighborhood environment modifies this association. Methods and Results Leveraging data from a diverse cohort of adults recruited from 6 sites in the United States with 2 decades of follow‐up, we used race‐ and ethnicity‐stratified Cox models to examine the association between time‐varying segregation with incident hypertension in 1937 adults free of hypertension at baseline. Participants were categorized as residing in segregated and nonsegregated neighborhoods using a spatial‐weighted measure. We used a robust covariance matrix estimator to account for clustering within neighborhoods and assessed effect measure modification by neighborhood social or physical environment. Over an average follow‐up of 7.35 years, 65.5% non‐Hispanic Black, 48.1% Chinese, and 53.7% Hispanic participants developed hypertension. Net of confounders, Black and Hispanic residents in segregated neighborhoods were more likely to develop hypertension relative to residents in nonsegregated neighborhoods (Black residents: hazard ratio [HR], 1.33; 95% CI, 1.09–1.62; Hispanic residents: HR, 1.33; 95% CI, 1.04–1.70). Results were similar but not significant among Chinese residents (HR, 1.20; 95% CI, 0.83–1.73). Among Black residents, neighborhood social environment significantly modified this association such that better social environment was associated with less pronounced impact of segregation on hypertension. Conclusions This study underscores the importance of continued investigations of groups affected by the health consequences of racial residential segregation while taking contextual neighborhood factors, such as social environment, into account.

Introduction: Black adults experience higher rates of cardiovascular disease (CVD) compared with White adults, particularly across young adulthood. To identify intervention targets to reduce disparities, we quantified the contribution of individual- and neighborhood-level determinants across young adulthood to Black-White differences in incidence of premature CVD. Methods: In Black and White adults (baseline age 18-30 years) in the Coronary Artery Risk Development in Young Adults (CARDIA) Study, the associations of clinical, lifestyle, psychosocial, socioeconomic, and neighborhood determinants with racial disparities in incident CVD were evaluated with sex-stratified Cox proportional hazards models adjusted for time-updated risk factors. Percent reduction in the ß estimate (log-hazard ratio [HR]) for race quantified the contribution of each risk factor group, individually and combined, to incident CVD racial disparities. Results: In 1707 Black and 2001 White young adults followed for median 33.9 (IQR 33.7-34.0) years, Black adults had higher risk of incident CVD than White adults (Figure). The fully adjusted model yielded significant attenuation of the disparity: HR 1.22 (0.68-2.21) for Black vs. White women, HR 1.42 (0.91-2.23) for Black vs. White men. In women, clinical risk factors were associated with the largest percent reduction in the ß estimate (83%) for race. In men, socioeconomic, lifestyle and clinical risk factors were each associated with significant percent reductions in ß estimates (45%, 37%, and 28%, respectively). Conclusions: In CARDIA, risk for premature CVD was no longer significantly higher in Black vs. White adults after adjustment for upstream determinants across multiple domains. The largest contribution to racial disparities was from clinical factors in women and socioeconomic factors in men. These findings may inform earlier-life interventions to reduce disparities in premature CVD.

Background: Income volatility is on the rise and presents a growing public health problem. Because in many epidemiological studies income is measured at a single point in time, the association of long-term income volatility with incident cardiovascular disease (CVD) and mortality has not been adequately explored. The goal of this study was to examine associations of income volatility from 1990 to 2005 with incident CVD and all-cause mortality in the subsequent 10 years. Methods: The Coronary Artery Risk Development in Young Adults Study is an ongoing prospective cohort study conducted within urban field centers in Birmingham, AL; Chicago, IL; Minneapolis, MN; and Oakland, CA. We studied 3937 black and white participants 23 to 35 years of age in 1990 (our study baseline). Income volatility was defined as the intraindividual SD of the percent change in income across 5 assessments from 1990 to 2005. An income drop was defined as a decrease of ≥25% from the previous visit and less than the participant’s average income from 1990 to 2005. CVD events (fatal and nonfatal) and all-cause mortality between 2005 and 2015 were adjudicated with the use of medical records and death certificates. CVD included primarily acute events related to heart disease and stroke. Results: A total of 106 CVD events and 164 deaths occurred between 2005 and 2015 (incident rate, 2.76 and 3.66 per 1000 person-years, respectively). From Cox models adjusted for sociodemographic, behavioral, and CVD risk factors, higher income volatility and more income drops were associated with greater CVD risk (high versus low volatility: hazard ratio, 2.07; 95% CI, 1.10–3.90; ≥2 versus 0 income drops: hazard ratio, 2.54; 95% CI, 1.24–5.19) and all-cause mortality (high versus low volatility: hazard ratio, 1.78; 95% CI,1.03–3.09; ≥2 versus 0 income drops: hazard ratio, 1.92; 95% CI, 1.07–3.44). Conclusions: In a cohort of relatively young adults, income volatility and drops during a 15-year period of formative earning years were independently associated with a nearly 2-fold risk of CVD and all-cause mortality.

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.

Introduction: Increasing research demonstrates psychosocial factors are associated with blood pressure control (BPC) among individuals with hypertension. To date, little research has examined multiple psychosocial factors simultaneously to identify distinguishing profiles among individuals with hypertension. The association of psychosocial profiles and BPC remains unknown. Thus, the goal of this study was to characterize the psychosocial profiles of individuals with hypertension and assess whether they are associated with BPC over 14 years. Hypothesis: We hypothesize that discrete psychosocial profiles will emerge, and they will be associated with BPC longitudinally. Methods: We included 2,665 MESA participants (38.57% Black; 55.43% Female) with prevalent hypertension in 2002-2004. Latent Profile Analysis (LPA) was used to identify distinct psychosocial profiles based on a combination of nine psychosocial variables (Table). We used generalized estimating equations to determine associations of the psychosocial profiles with BPC, defined as systolic blood pressure (SBP) < 140 mm Hg and diastolic blood pressure (DBP) < 90 mm Hg. Results: The LPA revealed an optimal model of three psychosocial profile groups (AIC 121,229; entropy = .88) namely “Healthy”, “Depressed Mood” and “Discriminated Against”. There were no significant differences in BPC of both targets (SBP and DBP) combined across the profiles. Examining SBP and DBP separately, participants in the “Depressed Mood” profile group were 60% less likely [95% CI: 0.43, 0.84] to have their DBP < 90 mm Hg as compared to the “Healthy” profile in the unadjusted model, but there was no association with covariate adjustment. Conclusions: Discrete psychosocial profiles exist among individuals with hypertension, but were not associated with BPC after full covariate adjustment.

Introduction: Deeper understanding of the longitudinal associations of social determinants of health (SDOH) at younger ages with cardiovascular health (CVH) in middle age is needed to address persistent health disparities. Methods: We used repeated measures of individual and neighborhood-level SDOH data from CARDIA participants (ppts) to understand how SDOH change from ages 18-44 years. There were 48 diverse SDOH exposures measured. Using a novel, machine learning, sequential pattern mining method (Subgraph Augmented Non-negative Matrix Factorization), we identified clusters of time-dependent SDOH variables occurring in 5% or more of ppts. Clusters were then used as independent variables in logistic regression models to assess associations with CVH at age ≥45 years. CVH status was defined using the AHA’s Simple 7 metrics on diet, physical activity, smoking, BMI, cholesterol, blood pressure, and blood glucose, and summarized by a 14-point score (poor 0-7, moderate 8-11, high 12-14 points). We tested associations of clusters with the outcome of poor CVH at age ≥45 years, and identified the characteristics of significant SDOH clusters. Results: There were 3,522 ppts included (46.3% Black, 55.9% women; mean age 25.3 years at baseline). Mean CVH score (out of 14) was 10.4 ± 1.8 points at baseline and 8.9 ± 2.3 points at age ≥45 years; 483 ppts (13.7%) had high, 2026 (57.5%) had moderate, and 1013 (28.8%) had poor CVH in middle age. The best performing logistic model included 4 SDOH trend clusters (Table). SDOH Clusters 1, 2, and 3 were each associated with significant 50-80% lower odds of having poor CVH in middle age, whereas Cluster 4 was associated with 2.5-fold higher odds of poor CVH. The most informative variables over time comprising each SDOH cluster are also shown in the Table. Conclusions: Specific SDOH clusters through young adulthood are significantly associated with reaching mid-life with poor CVH status. Components of these SDOH clusters may be potential targets for social interventions and policies to improve CVH.

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

Introduction: Social determinants of health (SDOH) affect cardiovascular outcomes. Our objective was to examine the association between neighborhood-level SDOH, and risk of readmission and mortality for atrial fibrillation (AF), heart failure, (HF) and myocardial ischemia (MI). Hypothesis: We hypothesized that neighborhood-level SDOH 1) is associated with readmission and death, 2) would significantly contribute to risk-prediction. Methods: We conducted a retrospective analysis from a regional health center to test the predictive ability of the area deprivation index (ADI) on 30-day and one-year readmission and mortality among patients admitted to hospital. Covariates included age, sex, race, comorbidity, number of medications, length of stay, and insurance. We used Cox proportional hazards and log rank analyses. To evaluate the discriminative power of the prediction models, we used the C-statistic and net reclassification methods after adding ADI into the model. Results: Our cohort of 31,633 adult patients followed was for 49.88 months (interquartile range 47.99). The cohort was 51.4% male and 90.6% white. Almost half (15,543, 49.1%) lived in neighborhoods in the two highest (worst) ADI quintiles. Patients living in areas with highest ADI were 28% less likely to be admitted within one year of index AF admission (HR=0.72, 95% CI [0.59, 0.87]). Patients in the highest ADI quintile were 30% more likely to be admitted within one year of index HF admission (HR=1.30, 95%CI [1.11, 1.52]). For MI, patients in the highest ADI quintile had a one-year risk for readmission that was twice that of those in the lowest quintile (HR=2.08, 95%CI [1.53, 2.81]). As ADI increased, risk of cardiac readmission and all-cause readmission increased at 30 days and one year. Reclassification of readmission risk was significantly improved when including ADI in the models. Patients in the highest ADI quintile were 46% more likely to die within 30 days when compared with those in the lowest quintile (HR=1.46, 95% CI [1.04, 2.06]) and 26% more likely to die within a year (HR=1.26 [1.10, 1.43]). Conclusions: Residence in disadvantaged communities predicts rehospitalization and mortality. ADI can be used to identify vulnerable cardiac patients after discharge.

Introduction: Social determinants of health are multi-dimensional and span various interrelated domains. In order to inform community-engaged clinical and policy efforts, we sought to examine the association between a national social vulnerability index (SVI) and age-adjusted mortality rate (AAMR) of CVD. Hypothesis: Higher county-level SVI or greater vulnerability will be associated with higher AAMR of CVD between 1999-2018 in the United States. Methods: In this serial, cross-sectional analysis, we queried CDC WONDER for age-adjusted mortality rates (AAMRs) per 100,000 population for cardiovascular disease (I00-78) at the county-level between 1999-2018. We quantified the association of county-level SVI and CVD AAMR using Spearman correlation coefficients and examined trends in CVD AAMR stratified by median SVI at the county-level. Finally, we performed geospatial county-level analysis stratified by combined median SVI and CVD AAMR (high/high, high/low, low/high, and low/low). Results: We included data from 2766 counties (representing 95% of counties in the US) with median SVI 0.53 (IQR 0.28, 0.76). Overall SVI and the household and socioeconomic subcomponents were strongly correlated with 2018 CVD AAMR (0.47, 0.50, and 0.56, respectively with p Conclusion: County-level social vulnerability is associated with higher CVD mortality. High SVI and CVD AAMR coexist in more than 1 in 3 US counties and have persisted over the past 2 decades. Identifying counties that are disproportionately vulnerable may inform targeted and community-based strategies to equitably improve cardiovascular health across the country.

Cardiovascular disease disparities are shaped by differences in risk factors across racial and ethnic groups. Housing remains an important social determinant of health. The objective of this statement is to review and summarize research that has examined the associations of housing status with cardiovascular health and overall health. PubMed/Medline, Centers for Disease Control and Prevention data, US Census data, Cochrane Library reviews, and the annual Heart Disease and Stroke Statistics report from the American Heart Association were used to identify empirical research studies that examined associations of housing with cardiovascular health and overall well-being. Health is affected by 4 prominent dimensions of housing: stability, quality and safety, affordability and accessibility, and neighborhood environment. Vulnerable and underserved populations are adversely affected by housing insecurity and homelessness, are at risk for lower-quality and unsafe housing conditions, confront structural barriers that limit access to affordable housing, and are at risk for living in areas with substandard built environment features that are linked to cardiovascular disease. Research linking select pathways to cardiovascular health is relatively strong, but research gaps in other housing pathways and cardiovascular health remain. Efforts to eliminate cardiovascular disease disparities have recently emphasized the importance of social determinants of health. Housing is a prominent social determinant of cardiovascular health and well-being and should be considered in the evaluation of prevention efforts to reduce and eliminate racial/ethnic and socioeconomic disparities.

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.

Introduction: Age of onset for heart disease (HD), cerebrovascular disease (CBD), and diabetes (DM) has shifted earlier, with increases in avoidable cardiometabolic deaths. We quantified total and trends in years of potential life lost (YPLL) before the age of 65 from HD, CBD, and DM, to describe population burden of premature preventable cardiometabolic mortality. Hypothesis: YPLL from premature cardiometabolic deaths in the U.S. have increased and are highest in black adults. Methods: Death certificates from the CDC’s Wide-Ranging Online Database for Epidemiologic Research (WONDER) were used to quantify mean age at death and proportion of deaths that were premature ( Results: Between 1999-2017, 19% of HD deaths, 14% of CBD deaths, and 27% of DM deaths were premature. Overall, premature YPLL from HD decreased between 1999-2011 from 512 to 416 per 100,000 (APC -1.7%/year, 95% CI [-2.0, -1.5]), then remained unchanged from 2011-2017. For CBD, premature YPLL decreased 1.8%/year (-2.2, -1.5) to 70 per 100,000 in 2011, but remained unchanged through 2017. Premature YPLL from DM remained unchanged at 71 per 100,000 from 1999-2011, then increased 2.5%/year (1.8, 3.1) to 81 per 100,000 in 2017. Premature YPLL were higher in black men and women compared with white men and women, respectively (FIGURE). Conclusions: Premature YPLL from cardiometabolic causes plateaued or increased after 2011. Disparities in YPLL have persisted in the past decade with nearly half of cardiometabolic deaths in black men occurring before age 65. Equitable promotion of cardiometabolic health early in the lifespan may reduce population, health system, and financial burden of premature cardiometabolic mortality.

Background: Substantial disparities in risk of heart failure (HF) exist by race, which may be driven by certain social or environmental factors. The relationship between the neighborhood built environment, including food and physical activity facilities, and risk of HF is unclear. The associations of the built environment and subclinical cardiac dysfunction may offer insight into mechanisms that lead to increased HF risk. Methods: In the CARDIA study, we evaluated the associations between measures of the neighborhood built environment and echocardiographic indices of cardiac function at the Year 25 exam (Y25). Built measures were assessed within a 3-km Euclidean distance from participant residence and included: 1) proportion of fast food restaurants or convenience stores relative to total food outlets and 2) number of public or commercial physical activity facilities. Results: Among 2,363 participants (44% male, 51% black) with available data from Y25, higher proportions of fast food restaurants and convenience stores were independently associated with lower left ventricular (LV) diastolic function (lower e’ tissue velocities and higher E/e’) ( Table ). Lower number of public and commercial physical activity facilities were independently associated with lower LV systolic function (LV longitudinal strain) and diastolic function. Conclusions: Food environments with higher proportions of fast food and convenience stores are associated with lower diastolic function, and environments with less physical activity facilities are associated with worse systolic and diastolic function. These findings suggest relationships between the built environment and subclinical HF.

Introduction: Psychosocial factors are associated with the onset of chronic disease, however few studies have examined the association between these factors and cardiovascular disease risk factor (CVDRF) control over time in individuals who already have a chronic disease. Thus, the goal of this study was to evaluate associations of psychosocial factors with a composite measure of CVDRF control. Methods: This study includes 1,018 CARDIA participants (51.6% Black; 41.6% Male) with prevalent hypertension (n = 604), hypercholesterolemia (n = 636), and/or diabetes (n = 210) in 2000-2001 (Year 15 follow-up exam). Latent Profile Analysis (LPA) was used to identify distinct psychosocial profiles based on a combination of personality, social life, and psychological health factors (Table). We used generalized estimating equations to determine associations of the psychosocial profiles with composite control, defined as HbA1c < 7.0%, systolic blood pressure (SBP) < 140 mm Hg, and LDL-cholesterol < 100 mm/dl, all measured in 2005-2016. Results: The LPA revealed an optimal model of three psychosocial profile groups (AIC 87,467.545; entropy = .895) namely “Healthy”, “Depressed Mood” and “Discriminated Against”. There were no significant differences in composite control across the profiles. Looking at HbA1C, SBP, and LDL separately in the unadjusted models, we found participants in the Depressed and Discriminated Against profiles were less likely to meet guidelines for SBP compared to individuals in the Healthy profile. Participants in the Discriminated profile were significantly less likely to meet the guidelines for HbA1C levels compared to the Healthy profile. These associations were attenuated with adjustment for sociodemographic covariates. Conclusions: Psychosocial profiles were associated with CVDRF control in unadjusted models, but not independent of socio-demographic characteristics.

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.

Introduction: As many as 20-50% of persons with chronic kidney disease have mild-to-moderate cognitive impairment or overt dementia. Shared risk factors, such as aging, sex, hypertension, and diabetes have been suggested to play a role in this association. Our objective was to examine the contribution of non-modifiable and modifiable risk factors to this association. Hypothesis: We hypothesize that non-modifiable and modifiable risk factors could explain part, but not all, of the association between worse kidney function with incidence of dementia. Methods: We included 6025 CVD free participants (mean age 62 yrs, 51% women, 38% white). Kidney function was assessed by estimated glomerular filtration rate (eGFR) and albumin-to-creatinine ratio (ACR). Participants were followed for an average of 12±4 yrs for dementia ICD code hospitalization. Multiple Cox regression models, adjusted for baseline non-modifiable (age, sex, race, and APOE4 carriership) and modifiable risk factors (BMI, smoking, SBP, diabetes, cholesterol, alcohol intake, education, physical activity, and healthy diet score) were used to estimate the association of worse kidney function with incidence of dementia hospitalization. Results: During follow-up, 268 (4.4%) participants were hospitalized for dementia. Non-modifiable risk factors vs. modifiable risk factors were associated with greater reduction in HRs from a crude model for association between each SD lower eGFR and risk of dementia (70% vs. 8%). Non-modifiable risk factors explained a higher percentage of the association of doubling ACR with risk of dementia than modifiable risk factors (14% vs. 7%) (Figure). Adjusting for all factors, worse kidney function remained associated with incident dementia. Conclusions: Findings suggest that conventional modifiable and non-modifiable risk factors cannot fully explain higher risk of dementia in relation to worse kidney function. This finding warrants exploring other potential novel vascular and nonvascular mechanisms of this association.

Introduction: Growing evidence suggests that features of the neighborhood environment are associated with moderate to vigorous intensity physical activity (MVPA). Less is known about whether the neighborhood environment is associated with sedentary time (SED) or light-intensity physical activity (LPA), two emerging, independent risk factors for adverse health outcomes. Objective: To investigate the cross-sectional and longitudinal associations of perceived and objective characteristics of the neighborhood environment with accelerometer-measured SED, LPA, and MVPA. Methods: Participants were 2,120 men and women from the Coronary Artery Risk Development in Young Adults (CARDIA) study who took part in the year 20 (2005-2006, aged 38-50 years) and year 30 exams (2015-2016, aged 48-60 years). Characteristics of the neighborhood environment assessed at year 20 included self-reported neighborhood cohesion, self-reported resources for physical activity, and objectively-measured neighborhood poverty and racial residential segregation using geocoded addresses linked to U.S. Census data. Physical activity was measured by accelerometer at year 20 in the full sample, and at year 30 in a sub-sample (n=892). Multivariable linear regression models examined cross-sectional associations of neighborhood measures at year 20 with SED, LPA, and MVPA assessed that year, and with 10-year changes in SED, LPA, and MVPA. Differences by race and sex group were also examined. Results: In cross-sectional analyses, each one standard deviation increase in the neighborhood cohesion score was associated with 4.1 less SED minutes/day (95% CI: -8.0, -0.2, p=0.04), and 4.5 more LPA minutes/day (95% CI: 0.9, 8.0, p=0.01). Each one standard deviation increase in the neighborhood resources score was associated with 1.2 more MVPA minutes/day (95% CI: 0.1, 2.3, p=0.04). A one standard deviation increase in neighborhood poverty was associated with 11.1 less SED minutes/day (95% CI: -21.2, -1.2, p=0.03) and 10.6 more LPA minutes/day (95% CI: 1.8, 19.4, p=0.02), among black men only. None of the neighborhood characteristics were associated with 10-year changes in activity in the full study sample; however, each one standard deviation increase in the neighborhood cohesion score was associated with a 10-year decrease of 25.4 SED minutes/day (95% CI: -46.7, -4.1, p=0.02) and a 10-year increase of 19.0 LPA minutes/day (95% CI: 1.9, 36.1, p=0.03), among black men only. Conclusions: Higher neighborhood cohesion and resources were beneficially associated with accelerometer-measured activity in cross-sectional analyses; however, neighborhood characteristics did not associate with 10-year changes in activity. Differences were observed by race and sex, with more robust findings observed in black men for neighborhood poverty and cohesion.

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.

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.

Background Hispanics are the fastest growing ethnic group in the United States, and little is known about how Hispanic ethnic population density impacts cardiovascular disease ( CVD ) mortality. Methods and Results We examined county‐level deaths for Hispanics and non‐Hispanic whites from 2003 to 2012 using data from the National Center for Health Statistics’ Multiple Cause of Death mortality files. Counties with more than 20 Hispanic deaths (n=715) were included in the analyses. CVD deaths were identified using International Classification of Diseases, Tenth Revision (ICD‐10), I00 to I78, and population estimates were calculated using linear interpolation from 2000 and 2010 census data. Multivariate linear regression was used to examine the association of Hispanic ethnic density with Hispanic and non‐Hispanic white age‐adjusted CVD mortality rates. County‐level age‐adjusted CVD mortality rates were adjusted for county‐level demographic, socioeconomic, and healthcare factors. There were a total of 4 769 040 deaths among Hispanics (n=382 416) and non‐Hispanic whites (n=4 386 624). Overall, cardiovascular age‐adjusted mortality rates were higher among non‐Hispanic whites compared with Hispanics (244.8 versus 189.0 per 100 000). Hispanic density ranged from 1% to 96% in each county. Counties in the highest compared with lowest category of Hispanic density had 60% higher Hispanic mortality (215.3 versus 134.2 per 100 000 population). In linear regression models, after adjusting for county‐level demographic, socioeconomic, and healthcare factors, increasing Hispanic ethnic density remained strongly associated with mortality for Hispanics but not for non‐Hispanic whites. Conclusions CVD mortality is higher in counties with higher Hispanic ethnic density. County‐level characteristics do not fully explain the higher CVD mortality among Hispanics in ethnically concentrated counties.

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: Laws banning smoking in indoor public places have been associated with reductions in second-hand smoke exposure and cardiovascular disease among non-smokers. Second-hand smoke exposure has been associated with hypertension in prior studies. However, it is unknown whether smoke-free policies are associated with changes in blood pressure. Hypothesis: We tested the hypothesis that living in an area with a smoke-free policy banning smoking in restaurants, bars, and/or other workplaces is associated with reductions in systolic and diastolic blood pressure among non-smokers. Methods: Longitudinal data from 2,896 non-smoking participants of the Coronary Artery Risk Development in Young Adults (CARDIA) Study (aged 18-30 at enrollment, 1985-2011, 14,193 person-exam-years) were linked to state, county, and local 100% smoke-free policies in bars, restaurants, and/or non-hospitality workplaces based on participants’ census tract of residence at each exam. Fixed-effects linear regression estimated associations of each type of smoke-free policy (restaurant, bar, workplace) with within-person changes in systolic and diastolic blood pressure (SBP and DBP). Models adjusted for time-varying covariates: exam year (categorical), socio-demographic (education, income, marital status), health-related (body mass index, total physical activity, alcohol use), and policy (state cigarette tax, self-reported ban on smoking in their workplace) covariates, and interactions of baseline covariates (age, sex, race, field center) with exam year to account for differences in blood pressure patterns that were associated with these characteristics (p Results: At baseline, mean SBP was 110.5 mmHg and mean DBP was 69.3 mmHg. By year 25, a majority of participants were exposed to smoke-free policies in restaurants (1,759 of 2,264, 78%), bars (1,536 of 2,264, 68%), and other workplaces (1,518 of 2,264, 67%). Smoke-free policies were associated with within-person reductions in SBP and DBP in fully adjusted models (expressed as average change between exams in mmHg). Mean reductions in SBP were -0.77 (95% CI: -1.51, -0.02) for restaurant policies, -0.73 (95% CI: -1.54, 0.08) for bar policies, and -0.79 (95% CI: -1.51, -0.08) for workplace policies. Mean reductions in DBP were -0.67 (95% CI: -1.27, -0.06) for restaurant policies, -0.54 (95% CI: -1.20, 0.11) for bar policies, and -0.86 (95% CI: -1.44, -0.28) for workplace policies. Conclusions: Smoke-free policies in restaurants and other workplace are associated with within-person reductions in systolic and diastolic blood pressure among non-smokers. These results suggest an additional health benefit of these policies beyond those previously described in the literature.

Introduction: Elevated Fibroblast Growth Factor 23 (FGF23) - an endocrine hormone linked to cardiovascular and kidney disease outcomes - is a compensatory response to high dietary phosphate load or chronic kidney disease. Large quantities of inorganic phosphates additives are found in processed foods, and food insecurity is associated with higher consumption of processed foods. Hypothesis: We hypothesized that developing food insecurity is associated with an increase in FGF23. Methods: We included CARDIA study participants with a stored plasma sample available from at least two consecutive exams at years 20, 25, and 30 (N=3,421). Food insecurity was assessed through a single question about ability to afford quantity and quality of food. FGF23 levels were assessed using a commercial c-terminal ELISA. Due to a strong right skew in FGF23 levels, we divided FGF23 in quartiles and compared the highest quartile to the combined lower three quartiles using logistic regression. Econometric fixed effects models that adjust by design for all time-invariant covariates were used to model the longitudinal association between simultaneous within-person change in food insecurity and FGF23. Due to an interaction between food insecurity and race ( p =0.002), we stratified by race. Results: About 29% of blacks and 14% of whites experienced change in food insecurity during follow-up. Developing food insecurity was associated with a 1.46 greater odds of increasing to the highest quartile of FGF23 (95% CI: 1.02,2.10) among blacks; however, there was no significant longitudinal association among whites (OR=1.05; 95% CI: 0.62,1.77). Conclusions: Using models that tightly control for all time-invariant confounding, we found that developing food insecurity was associated with increases in FGF23 among blacks. The differential increases in blacks as compared to whites may be due to differences in dietary changes in response to developing food insecurity. Previous research has shown racial differences in dietary quality by food insecurity.

Introduction: Racial residential segregation results in increased exposure to adverse neighborhood environments for African Americans; however, the impact of segregation on ideal cardiovascular health (CVH) has not been examined in large, socioeconomically diverse African American samples. Using a novel spatial measure of neighborhood-level racial residential segregation, we examined the association between segregation and ideal CVH in the Jackson Heart Study (JHS). Hypothesis: Racial residential segregation will be associated with worse cardiovascular health among African American adults. Methods: The sample included 4,354 men and women ages 21-93 from the baseline exam of the JHS (2000-2004). Racial residential segregation was assessed at the census-tract level. Data on racial composition (% African American) from the 2000 US Census was used to calculate the local G i * statistic- a spatially-weighted z-score that represents how much a neighborhood’s racial/ethnic composition deviates from the larger metropolitan area. Ideal CVH was assessed using the AHA Life’s Simple Seven (LS7) index which includes 3 behavioral (nutrition, physical activity, and smoking) and 4 biological (systolic BP, glucose, BMI, and cholesterol) metrics of CVH. Multivariable regression models were used to test associations between segregation and the LS7 index continuously (range: 0-14) and categorically (Inadequate: 0-4; Average: 5-9; and Optimal: 10-14). Covariates included age, sex, income, education, and insurance status. Results: The average LS7 summary score was 7.03 (±2.1) and was lowest in the most racially segregated neighborhood environments (High Segregation: 6.88 ±2.1 vs. Low Segregation: 7.55 ±2.1). The prevalence of inadequate CVH was higher in racially segregated neighborhoods (12.3%) compared to neighborhoods that were the least segregated (6.9%). After adjusting for key socio-demographic characteristics, racial residential segregation was inversely associated with ideal CVH (B=-0.041 ±0.02, p=0.0146). Moreover, a 1-SD unit increase in segregation was associated with a 6% increased odds of having inadequate CVH (OR: 1.06, 95% CI: 1.00-1.12, p=0.0461). Conclusion: In conclusion, African Americans in racially segregated neighborhoods are less likely to achieve ideal CVH even after accounting for individual-level factors. Policies aimed at restricting housing segregation/discrimination and/or structural interventions designed to improve neighborhood environments may be viable strategies to improving CVH in this at-risk population.

Background: A combination of social, behavioral, and biological factors are hypothesized to account in large part for racial disparities in obesity, but few studies have shown this empirically. Thus, the goal of this study was to determine the extent to which these factors accounted for racial differences in the development of obesity in men and women over a 30-year period (mean follow-up 21.7 years). Methods: This study includes the 1,617 Black (743 men and 874 women) and 1,950 White (928 men and 1,022 women) CARDIA participants with complete data on all baseline covariates who were not obese at baseline (1985-1986; ages 18-30). A series of gender-stratified Cox proportional hazards models were run adjusting separately for socioeconomic, psychosocial, neighborhood, lifestyle, and physiological factors to determine the extent to which they explained race differences in incident obesity. Results: Among men, 36.9% of Whites and 43.7% of Blacks became obese over follow-up. In women, 33.7% of Whites and 60.3% of Blacks became obese. After adjusting for age and baseline BMI, Black men were 1.39 (95% confidence interval (CI): 1.19, 1.62) times more likely to become obese than White men (Table). Covariate adjustment reduced race differences by 34%; neighborhood factors were the strongest contributors. Black women were 1.63 (95% CI: 1.42, 1.88) times more likely to become obese than White women in the base model. This association was reduced by 57% in fully adjusted models. Lifestyle factors explained the largest proportion of the race difference, followed by individual-level socioeconomic factors and neighborhood conditions. Conclusions: Racial disparities in incident obesity, and the extent to which these disparities were explained by baseline covariates, differ for men and women. Whereas substantial attenuation occurred after adjustment for a wide variety of baseline covariates, race differences in obesity incidence remained significant.

African Americans (AA), both men (M) and women (W), have higher CVD mortality rates than European Americans (E), but AAM have lower prevalence of coronary calcified plaque than WM. AAs also have higher blood pressure (BP) and HDL-C than W; HDL-C is lower in M than W. We tested the hypotheses that AA race is related to higher risk of hypertension (HTN)-related events, and being male is related to higher risk of atherothrombotic (ATH)-related events, placing AAM at particularly high risk for CVD. Methods: We used baseline risk factor data, and adjudicated events through 28 years of follow-up from the CARDIA study which recruited 5,115 participants aged 18-30 years at baseline (1985-6). ATH-related events included acute coronary syndrome with or without MI, coronary revascularization, and CHD and other atherosclerosis death. HTN-related events included heart failure, end-stage renal disease (ESRD), stroke, and death due to cardiomyopathy. CVD events excluded ESRD and included peripheral artery disease procedures. We analyzed time to first event censoring at death without incident CVD and at follow-up end. We built adjusted Cox models with forward selection including race, sex, age, education, and smoking status as forced predictors and selecting among physical activity, anthropometry, glycemia, lipid, and blood pressure risk factors. Results: In unadjusted analyses, risk of HTN-related events was related to race (p Conclusion: Race and sex are differentially associated with early HTN- vs ATH-related events, and AAM were at increased risk for both.

Introduction: There are known racial differences in cardiovascular health behaviors, including smoking, physical activity, and diet quality. A better understanding of factors that explain these differences may suggest novel intervention targets for reducing disparities in cardiovascular disease. Objective: To examine whether socioeconomic, psychosocial and environmental factors mediate racial differences in health behaviors. Methods: We studied 3,028 Black or White CARDIA participants who were enrolled at age 18-30 years in 1985-86 and completed the 30 year follow-up visit in 2015-2016. Health behaviors included smoking (current, former ≤ 12 months, never smoker/quit >12 months), physical activity (inactive, active but not meeting guidelines, meeting guidelines), and a surrogate for healthy eating using fast food and sugar-sweetened beverage consumption (frequency per week ≥ 2, some but < 2, none). Each behavior was assigned a value of 0 for poor, 1 for intermediate or 2 for ideal and summed to calculate an overall health behavior score for each participant (range 0-6). The race difference (β) in health behavior score was estimated using linear regression. Formal mediation analyses computed the proportion of the total effect of race on health behavior score explained by socioeconomic, psychosocial, and environmental factors (see Table footnote). Results: Blacks had a lower health behavior score than Whites in crude analyses (mean difference: -1.04, p Conclusions: Observed racial differences in the health behavior score are predominately mediated by socioeconomic factors, which appear to play a stronger explanatory role than psychosocial and environmental factors.

Background: Cardiovascular health (CVH) is worse among African Americans than whites, yet it is unclear whether differences in health behaviors fully account for these racial disparities. We investigated whether racial differences in CVH factors (blood pressure, glucose, and cholesterol) were explained by body mass index (BMI) and CVH behaviors (smoking and physical activity) in CARDIA. Methods: This cross-sectional analysis included 2,866 African-American and white CARDIA participants from four field centers (Birmingham, AL; Chicago, IL; Minneapolis, MN; and Oakland, CA) who completed the year 30 examination (2015-2016; 71% retention). We created a summary CVH factor score (range 0-6) using poor, intermediate, and ideal levels of blood pressure, glucose, and cholesterol, with higher scores indicative of better CVH. Linear regression was used to evaluate the association of race with the summary score in unadjusted and adjusted models. Results: Mean age (SD) was 55 (3.6) years, 57% were women, and 47% were African-American. The mean CVH factor score (SD) was 4.4 (1.2) for whites and 3.9 (1.3) for African Americans (p Conclusion: The racial disparity in CVH factor score persisted after accounting for BMI and CVH behaviors. Thus, roles of other factors, such as social determinants of health and diet, warrant further investigation.

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.

Background Given increasing rates of heart failure (HF) risk factors (e.g. obesity, diabetes) that disproportionally affect black adults, we sought to describe contemporary trends in HF prevalence and examine differences between blacks and whites. Hypothesis Racial disparities in HF exist and are widening. Methods Non-pregnant adults aged ≥35 years who identified as non-Hispanic black or white from the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2016 were included. Age-adjusted HF prevalence was calculated by two-year cycles and weighted linear regression was used to examine trends over time. Odds ratios (OR) and 95% confidence intervals (CI) of HF in blacks vs. whites were calculated by pooling cycles into six-year periods with adjustment for age, sex, cardiovascular risk factors (CV RF), renal function, and proxies of socioeconomic status (SES: education level and health insurance status). Given a significant interaction between race and age group, analyses were stratified by age groups: 35-64 and 65+ years. Results Of 20,290 participants with mean age 55.3±0.2 years, 52% were women and 12% black. Age-adjusted prevalence of HF per 100,000 increased linearly among blacks from 3921 (2663, 5178) in 1999-2000 to 6568 (4557, 8580) in 2015-2016 (p-trend 0.05). Age and sex-adjusted odds of HF in blacks compared to whites (TABLE) was higher between 2005-10 (period 2) and 2011-16 (period 3). After adjustment for RF and SES, odds of HF remained higher in blacks in periods 2 and 3 by 1.51 (1.11, 2.04) and 1.55 (1.16, 2.06), respectively. This appeared to be primarily driven by differences in HF prevalence between younger blacks and whites (age 35-64 years). Conclusions The prevalence of HF in blacks is increasing and the odds of HF was significantly higher in blacks compared to whites. While the increased odds of HF was attenuated after adjusting for RF and SES, disparities persisted and have widened over time. Research and resources aimed at identifying social determinants of HF, alongside aggressive management of risk factors, are needed to prevent HF and reduce disparities.

Objectives: Little is known about the relationship of acculturation and favorable cardiovascular (CV) health (i.e., low CV risk) in the Hispanic/Latino population. Methods: Age-adjusted prevalences (weighted for sampling probability and non-response) are reported. Logistic regression was used to examine associations of acculturation (measured using nativity and length of residence: 2 ; and no major ECG abnormalities) in 15,047 HCHS/SOL participants (52.4% women) of Central American, South American, Cuban, Dominican, Mexican, Puerto Rican background, and Hispanic/Latino men and women identifying as other or >1 background group. We also tested whether these associations varied by Hispanic/Latino background. Results: Among women, age-adjusted low CV risk prevalence was highest for those living in the US < 10 years (15.4%) and similar for those living in the US ≥ 10 years (9.4%) and born in the US (9.2%). Low CV risk prevalence in was lower in men, but patterns were similar by acculturation ( Conclusions: These findings highlight the role that acculturation plays in shaping cardiovascular health in Hispanics/Latinos.

Introduction: Perceived discrimination is associated with risk factors for type 2 diabetes, including measures of adiposity. However, the relationship between perceived discrimination and incident diabetes is unknown. Objectives: To determine whether perceived discrimination is related to incident diabetes, and whether this association varies by race/ethnicity, age or sex. Methods: Included in this analysis were 5,310 MESA participants aged 45-84 years, without a history of diabetes at baseline. Perceived discrimination was measured using the Lifetime Discrimination scale, which assessed experiences of unfair treatment in 6 life domains (e.g. fired or denied a promotion, unfair treatment by police, not hired for a job, having life made difficult by neighbors). Participants were also asked to attribute their experiences of discrimination to various factors (e.g. race/ethnicity, age, sex, religion). Incident diabetes was identified at four follow-up examinations as fasting glucose ≥126 mg/dL or use of diabetes medications. Multivariable-adjusted Cox proportional hazard regression was used to model lifetime discrimination as a continuous and categorical variable (0, 1, ≥2 domains). Results: A total of 654 incident diabetes cases accrued over a median follow-up of 9.4 years (range 0.9-11.4). Lifetime discrimination reported in ≥ 2 domains (versus none) was associated with a 34% increased risk of incident diabetes, after adjustment for potential confounders or mediators (Table). Similar patterns were observed when we evaluated discrimination attributed to race/ethnicity only, or to a combination of other sources. There were no differences in the strength of association by race/ethnicity, age or sex. Conclusions: Lifetime discrimination was associated with increased risk of incident diabetes, regardless of attribution. These associations were independent of obesity, behavioral and psychosocial factors. Future research is needed to explore the mechanisms of the discrimination-diabetes relationship.

Background— Previous research suggests that neighborhood-level racial/ethnic residential segregation is linked to health, but it has not been studied prospectively in relation to cardiovascular disease (CVD). Methods and Results— Participants were 1595 non-Hispanic black, 2345 non-Hispanic white, and 1289 Hispanic adults from the Multi-Ethnic Study of Atherosclerosis free of CVD at baseline (aged 45–84 years). Own-group racial/ethnic residential segregation was assessed by using the G i * statistic, a measure of how the neighborhood racial/ethnic composition deviates from surrounding counties’ racial/ethnic composition. Multivariable Cox proportional hazards modeling was used to estimate hazard ratios for incident CVD (first definite angina, probable angina followed by revascularization, myocardial infarction, resuscitated cardiac arrest, coronary heart disease death, stroke, or stroke death) over 10.2 median years of follow-up. Among blacks, each standard deviation increase in black segregation was associated with a 12% higher hazard of developing CVD after adjusting for demographics (95% confidence interval, 1.02–1.22). This association persisted after adjustment for neighborhood-level characteristics, individual socioeconomic position, and CVD risk factors (hazard ratio, 1.12; 95% confidence interval, 1.02–1.23). For whites, higher white segregation was associated with lower CVD risk after adjusting for demographics (hazard ratio, 0.88; 95% confidence interval, 0.81–0.96), but not after further adjustment for neighborhood characteristics. Segregation was not associated with CVD risk among Hispanics. Similar results were obtained after adjusting for time-varying segregation and covariates. Conclusions— The association of residential segregation with cardiovascular risk varies according to race/ethnicity. Further work is needed to better characterize the individual- and neighborhood-level pathways linking segregation to CVD risk.

Background Epidemiologic studies have yielded mixed findings on the association of psychosocial stressors with cardiovascular disease ( CVD ) risk. In this study, we examined associations of stressful life events ( SLE ) and social strain with incident coronary heart disease ( CHD ) and stroke (overall, and for hemorrhagic and ischemic strokes) independent of sociodemographic characteristics, and we evaluated whether these relationships were explained by traditional behavioral and biological risk factors. Methods and Results Data from approximately 82 000 Women's Health Initiative Observational Study participants were used for the SLE and social strain analyses, respectively. Participants were followed for events for up to 18.0 years (median, 14.0). Separate Cox proportional hazards models were generated to estimate associations of each stress measure with incident CVD . After adjusting for sociodemographic characteristics and depressive symptoms, higher SLE and social strain were associated with higher incident CHD and stroke (each P trend CHD and 1.14 (1.01, 1.28) for incident stroke among participants reporting high versus low SLE . Findings were similar for social strain. Associations were attenuated with further adjustment for mediating behavioral and biological risk factors. Findings were similar for associations of SLE with ischemic stroke and hemorrhagic stroke, but social strain was only associated with ischemic stroke. Conclusions Higher SLE and social strain were associated with higher incident CVD independent of sociodemographic factors and depressive symptoms, but not behavioral and biological risk factors.

Background: Sleep disturbance is associated with multiple adverse cardiovascular-related health outcomes. Little is known about the relationship between psychological well-being, an independent modifiable risk factor for cardiovascular disease, and sleep disruptions. This study examines cross-sectional and longitudinal associations of optimism with sleep duration and quality. Methods: Data were collected from 3,549 Black and White adults aged 33-45 years who participated in the Coronary Artery Risk Development in Young Adults (CARDIA) study during follow-up years 15 (2000-2001) and 20 (2005-2006). Optimism was assessed in 2000-2001 using the Life-Orientation Test—Revised, with possible scores ranging from 6 (least optimistic) to 30 (most optimistic). Single-item questions on sleep quality and duration in the past month were assessed during 2000-2001 and 2005-2006. Cross-sectional analyses considered optimism and sleep measures at follow-up year 15. Longitudinal analyses considered 5-year incidence of poor sleep quality (fairly/very bad) and duration (short/long sleep) in 2005-2006 by optimism in 2000-2001 (participants with poor sleep quality and duration in 2000-2001 were excluded). Results: Among 3,549 participants (56% female, 46% Black) with complete data on optimism in 2000-2001, 15.9% reported fairly/very bad sleep quality. Sleep duration was distributed as follows: short-sleep (47.9%), sufficient sleep (31.6%), and long-sleep (20.5%). In unadjusted and fully adjusted models, a 1-unit higher optimism score was cross-sectionally associated with 11% lower odds of having fairly/very bad sleep quality and 3-5% lower odds of having short-sleep duration (Table 1). Cross-sectional associations were attenuated after adjustment for depressive symptoms (not shown). Incidence of poor sleep quality in 2005-2006 was 7% lower with each unit higher optimism score, after full adjustment. Conclusion: Optimism is associated with lower incidence of poor self-reported sleep quality over a 5-year period.