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Stress-Associated Neurobiological Pathway Linking Socioeconomic Disparities to Cardiovascular Disease.

ABSTRACT: BACKGROUND:Lower socioeconomic status (SES) associates with a higher risk of major adverse cardiac events (MACE) via mechanisms that are not well understood. OBJECTIVES:Because psychosocial stress is more prevalent among those with low SES, this study tested the hypothesis that stress-associated neurobiological pathways involving up-regulated inflammation in part mediate the link between lower SES and MACE. METHODS:A total of 509 individuals, median age 55 years (interquartile range: 45 to 66 years), underwent clinically indicated whole-body 18F-fluorodeoxyglucose positron emission tomography/computed tomography imaging and met pre-defined inclusion criteria, including absence of known cardiovascular disease or active cancer. Baseline hematopoietic tissue activity, arterial inflammation, and in a subset of 289, resting amygdalar metabolism (a measure of stress-associated neural activity) were quantified using validated 18F-fluorodeoxyglucose positron emission tomography/computed tomography methods. SES was captured by neighborhood SES factors (e.g., median household income and crime). MACE within 5 years of imaging was adjudicated. RESULTS:Over a median 4.0 years, 40 individuals experienced MACE. Baseline income inversely associated with amygdalar activity (standardized ?: -0.157 [95% confidence interval (CI): -0.266 to -0.041]; p = 0.007) and arterial inflammation (?: -0.10 [95% CI: -0.18 to -0.14]; p = 0.022). Further, income associated with subsequent MACE (standardized hazard ratio: 0.67 [95% CI: 0.47 to 0.96]; p = 0.029) after multivariable adjustments. Mediation analysis demonstrated that the path of: ? neighborhood income to ? amygdalar activity to ? bone marrow activity to ? arterial inflammation to ? MACE was significant (?: -0.01 [95% CI: -0.06 to -0.001]; p < 0.05). CONCLUSIONS:Lower SES: 1) associates with higher amygdalar activity; and 2) independently predicts MACE via a serial pathway that includes higher amygdalar activity, bone marrow activity, and arterial inflammation. These findings illuminate a stress-associated neurobiological mechanism by which SES disparities may potentiate adverse health outcomes.

SUBMITTER: Tawakol A

PROVIDER: S-EPMC6767929 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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Stress-Associated Neurobiological Pathway Linking Socioeconomic Disparities to Cardiovascular Disease.

Tawakol Ahmed A Osborne Michael T MT Wang Ying Y Hammed Basma B Tung Brian B Patrich Tomas T Oberfeld Blake B Ishai Amorina A Shin Lisa M LM Nahrendorf Matthias M Warner Erica T ET Wasfy Jason J Fayad Zahi A ZA Koenen Karestan K Ridker Paul M PM Pitman Roger K RK Armstrong Katrina A KA

Journal of the American College of Cardiology 20190701 25

<h4>Background</h4>Lower socioeconomic status (SES) associates with a higher risk of major adverse cardiac events (MACE) via mechanisms that are not well understood.<h4>Objectives</h4>Because psychosocial stress is more prevalent among those with low SES, this study tested the hypothesis that stress-associated neurobiological pathways involving up-regulated inflammation in part mediate the link between lower SES and MACE.<h4>Methods</h4>A total of 509 individuals, median age 55 years (interquart ...[more]

PMID: 31248544

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Project description:BackgroundChronic exposure to socioeconomic or environmental stressors associates with greater stress-related neurobiological activity (ie, higher amygdalar activity [AmygA]) and higher risk of major adverse cardiovascular events (MACE). However, among individuals exposed to such stressors, it is unknown whether neurobiological resilience (NBResilience, defined as lower AmygA despite stress exposure) lowers MACE risk. We tested the hypotheses that NBResilience protects against MACE, and that it does so through decreased bone marrow activity and arterial inflammation.MethodsIndividuals underwent 18F-fluorodeoxyglucose positron emission tomography/computed tomography; AmygA, bone marrow activity, and arterial inflammation were quantified. Chronic socioeconomic and environmental stressors known to associate with AmygA and MACE (ie, transportation noise exposure, neighborhood median household income, and crime rate) were quantified. Heightened stress exposure was defined as exposure to at least one chronic stressor (ie, the highest tertile of noise exposure or crime or lowest tertile of income). MACE within 5 years of imaging was adjudicated. Relationships were evaluated using linear and Cox regression, Kaplan-Meier survival, and mediation analyses.ResultsOf 254 individuals studied (median age [interquartile range]: 57 years [46-67], 36.7% male), 166 were exposed to at least one chronic stressor. Among stress-exposed individuals, 12 experienced MACE over a median follow-up of 3.75 years. Among this group, higher AmygA (ie, lower resilience) associated with higher bone marrow activity (standardized β [95% CI]: 0.192 [0.030-0.353], P=0.020), arterial inflammation (0.203 [0.055-0.351], P=0.007), and MACE risk (standardized hazard ratio [95% CI]: 1.927 [1.370-2.711], P=0.001). The effect of NBResilience on MACE risk was significantly mediated by lower arterial inflammation (P<0.05).ConclusionsAmong individuals who are chronically exposed to socioeconomic or environmental stressors, NBResilience (AmygA <1 SD above the mean) associates with a >50% reduction in MACE risk, potentially via reduced arterial inflammation. These data raise the possibility that enhancing NBResilience may decrease the burden of cardiovascular disease.

Project description:Background Observational studies demonstrate that communities of low socioeconomic status have higher blood pressure and worse cardiovascular outcomes. Yet, whether the clinical outcomes resulting from antihypertensive therapy vary by socioeconomic context in a randomized clinical trial, in which participants are treated under a standard protocol, is unknown. Methods and Results We used data from ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial) to study the effect of socioeconomic context, defined as the county-level median household income, of study sites. We stratified sites into income quintiles and compared characteristics, blood pressure control, and cardiovascular outcomes among ALLHAT participants in the lowest- and highest-income quintiles. Among 27 862 qualifying participants, 2169 (7.8%) received care in the lowest-income sites (quintile 1) and 10 458 (37.6%) received care in the highest-income sites (quintile 5). Participants in quintile 1 were more likely to be women, to be black, to be Hispanic, to have fewer years of education, to live in the South, and to have fewer cardiovascular risk factors. After adjusting for baseline demographic and clinical characteristics, quintile 1 participants were less likely to achieve blood pressure control (<140/90 mm Hg) (odds ratio, 0.48; 95% CI, 0.37-0.63) and had greater all-cause mortality (hazard ratio [HR], 1.25; 95% CI, 1.10-1.41), heart failure hospitalizations/mortality (HR, 1.26; 95% CI, 1.03-1.55), and end-stage renal disease (HR, 1.86; 95% CI, 1.26-2.73), but lower angina hospitalizations (HR, 0.70; 95% CI, 0.59-0.83) and coronary revascularizations (HR, 0.71; 95% CI, 0.57-0.89). Conclusions Despite standardized treatment protocols, ALLHAT participants in the lowest-income sites experienced poorer blood pressure control and worse outcomes for some adverse cardiovascular events, emphasizing the importance of measuring and addressing socioeconomic context. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00000542.

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Stress-Associated Neurobiological Pathway Linking Socioeconomic Disparities to Cardiovascular Disease.

Publications

Stress-Associated Neurobiological Pathway Linking Socioeconomic Disparities to Cardiovascular Disease.

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