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Socioeconomic Disparities, Amygdalar Activity, and MACE
Study Questions:
What is the mechanism by which lower socioeconomic status (SES) mediates a higher risk of major adverse cardiac events (MACE)?
Methods:
The investigators tested the hypothesis that stress-associated neurobiological pathways involving up-regulated inflammation in part mediate the link between lower SES and MACE. A total of 509 individuals, median age 55 years (interquartile range, 45-66 years), underwent clinically indicated whole-body 18F-fluorodeoxyglucose positron emission tomography/computed tomography imaging and met predefined inclusion criteria, including absence of known cardiovascular disease (CVD) 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. To assess associations with MACE, Cox proportional hazards models were used to derive hazard ratios (HRs) and 95% confidence intervals (CIs).
Results:
Over a median 4.0 years, 40 individuals experienced MACE. Baseline income inversely associated with amygdalar activity (standardized β: -0.157 [95% 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 HR, 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:
The authors concluded that lower SES independently predicts MACE via a serial pathway that includes higher amygdalar activity, bone marrow activity, and arterial inflammation.
Perspective:
This study reports that lower SES is associated with heightened amygdalar activity, arterial inflammation, and risk of subsequent MACE. Furthermore, this analysis supports the hypothesis that lower SES links to MACE through a serial multitissue pathway involving the amygdala, hematopoietic tissues, and arterial inflammation. Overall, the study provides supportive evidence for the existence of a neuroimmune pathway linking lower SES to CVD in adult humans. Additional research is indicated to assess novel interventions that may prevent future heart attacks and strokes and reduce SES-driven health disparities.
Clinical Topics: Cardiovascular Care Team, Diabetes and Cardiometabolic Disease, Noninvasive Imaging, Prevention, Vascular Medicine, Computed Tomography, Nuclear Imaging
Keywords: Amygdala, Arteritis, Bone Marrow, Crime, Fluorodeoxyglucose F18, Inflammation, Metabolic Syndrome, Myocardial Infarction, Neoplasms, Neurobiology, Positron-Emission Tomography, Primary Prevention, Social Class, Stroke, Tomography, X-Ray Computed
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