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.

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 used cross-sectional data on 2,660 black and 2,611 Mexican-American adult participants in the National Health and Nutrition Examination Survey (1999–2006) to investigate the association between metropolitan-level racial/ethnic residential segregation and obesity and to determine whether it was mediated by the neighborhood socioeconomic environment. Residential segregation was measured using the black and Hispanic isolation indices. Neighborhood poverty and negative income incongruity were assessed as mediators. Multilevel Poisson regression with robust variance estimates was used to estimate prevalence ratios. There was no relationship between segregation and obesity among men. Among black women, in age-, nativity-, and metropolitan demographic-adjusted models, high segregation was associated with a 1.29 (95% confidence interval (CI): 1.00, 1.65) times higher obesity prevalence than was low segregation; medium segregation was associated with a 1.35 (95% CI: 1.07, 1.70) times higher obesity prevalence. Mexican-American women living in high versus low segregation areas had a significantly lower obesity prevalence (prevalence ratio, 0.54; 95% CI: 0.33, 0.90), but there was no difference between those living in medium versus low segregation areas. These associations were not mediated by neighborhood poverty or negative income incongruity. These findings suggest variability in the interrelationships between residential segregation and obesity for black and Mexican-American women.

Racial residential segregation is the systematic separation of groups into different neighborhoods by race. While largely thought to be caused by structural discrimination (eg, in housing and lending markets), differential residential preferences by race are believed to play a role as well.^1,2 Residential segregation has been identified as a fundamental cause of black-white health disparities because of its effect on access to a wide range of health-promoting resources and opportunities, including quality education, jobs, healthy food options, and social capital.^3-6 Some cross-sectional evidence suggests that the greater the segregation, the higher the hypertension prevalence in black communities.^7-9 To our knowledge, no study has yet investigated the association of changes in exposure to segregation with changes in blood pressure or the association of moving to less segregated neighborhoods with improvements in blood pressure. Longitudinal analyses are required to strengthen these causal inferences and to determine whether policies that reduce segregation have beneficial effects on blood pressure.

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.