Background: Psychosocial stress and depression correlate with cardiovascular (CV) events; however, association of objective physiologic measures of these psychological stressors with the development of CV disease is unclear. Thus, we examined the relationship between resting-state stress perception center activation, as measured by amygdala FDG uptake, and vascular inflammation (VI) by 18-FDG PET/CT in a resource-limited community-based (CB) cohort.Hypothesis: We hypothesized that amygdala activity by FDG uptake would directly associate with VI by 18-FDG PET/CT in a resource-limited CB cohort.Methods: Patients from the Washington, D.C. Cardiovascular Health and Needs Assessment, an assessment in predominantly African-American churches in resource-limited D.C. areas, underwent detailed phenotyping with cardiometabolic markers and whole-body 18-FDG PET/CT to measure VI and stress perception center activity (amygdala activity).Results: The cohort (N=31) was consecutively recruited, African American, middle-aged, and predominantly female (Table 1). These patients were obese, pre-hypertensive, and had abnormal lipid levels. In univariable analyses, VI significantly associated with sex, hypertension treatment, and CV disease risk by Framingham risk score (FRS) (p<0.05 for all). VI also associated with amygdala activity (β=0.40, p=0.03). The relationship between amygdala activity and VI remained robust with adjustment for FRS, body mass index, and hypertension treatment (β=0.37, p=0.03).Conclusion: Metabolic activity of neuronal tissues involved in stress perception significantly associated with VI, a subclinical marker of developing atherosclerosis, in a resource-limited CB cohort. Future studies should evaluate mechanistic relationships between amygdala activity, subclinical atherosclerosis, and subsequent atherogenesis in at-risk, community-based populations. Larger studies are warranted to confirm these findings.