Literature DB >> 31248544

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

Ahmed Tawakol1, Michael T Osborne2, Ying Wang3, Basma Hammed4, Brian Tung4, Tomas Patrich4, Blake Oberfeld4, Amorina Ishai4, Lisa M Shin5, Matthias Nahrendorf6, Erica T Warner7, Jason Wasfy8, Zahi A Fayad9, Karestan Koenen10, Paul M Ridker11, Roger K Pitman12, Katrina A Armstrong13.   

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 β: -0.157 [95% confidence interval (CI): -0.266 to -0.041]; p = 0.007) and arterial inflammation (β: -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 (β: -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.
Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Entities:  

Keywords:  cardiovascular disease; neurobiology; positron emission tomography; socioeconomic disparities; stress

Mesh:

Substances:

Year:  2019        PMID: 31248544      PMCID: PMC6767929          DOI: 10.1016/j.jacc.2019.04.042

Source DB:  PubMed          Journal:  J Am Coll Cardiol        ISSN: 0735-1097            Impact factor:   24.094


  50 in total

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