Coronary artery disease and neurocognitive performance among older adults in Uganda

Abstract Background Coronary artery disease (CAD) has been linked with poorer cognitive function, potentially through shared risk factors and vascular pathways linking atherosclerotic disease to cerebral vascular injury. However, the association between CAD and neurocognitive performance remains poorly characterized in African populations. Methods We analyzed data from the Uganda Aging and Dementia Cohort Study among participants with coronary computed tomography imaging and neurocognitive testing data. The primary exposure was imaging-defined CAD, and cognitive performance was evaluated at the global-composite, domain-composite, and individual-test levels. Multivariable linear regression models adjusted for age, sex, and HIV status. HIV-stratified models adjusted for age and sex, and CAD-by-HIV interaction terms assessed effect modification. We examined predicted 10-year atherosclerotic cardiovascular disease (ASCVD) risk > 5% as an alternative cardiovascular-risk exposure. Higher b coefficients indicated poorer performance. Benjamini-Hochberg false-discovery-rate (FDR) correction was applied within outcome tiers. Results Among 512 participants, mean age was 57.9 years (SD, 6.3), 252 (49.2%) were female, 238 (46.5%) were people with HIV (PWH), 42 (8.2%) had CAD, and 203 (39.6%) had ASCVD risk > 5%. CAD was not associated with global cognition (b = 0.093 SD units; 95% CI, − 0.122 to 0.308; P = 0.397). At individual-test level, CAD was associated with poorer performance on Color Trails 2 (a measure of executive function) (b = 0.502; 95% CI, 0.184 to 0.821; P = 0.002; q = 0.026) and nominally associated with poorer performance on Digits Forward (a measure of attention and immediate verbal span) (b = 0.386; 95% CI, 0.028 to 0.744; P = 0.035; q = 0.210). In HIV-stratified analyses, CAD was nominally associated with poorer Digits Forward performance among PWOH (b = 0.552; P = 0.006; q = 0.070) and poorer Color Trails 2 performance among PWH (b = 0.646; P = 0.010; q = 0.121), but neither survived FDR correction and interaction tests did not support effect modification. ASCVD risk > 5% was nominally associated with poorer learning-and-memory domain performance (b = 0.188; 95% CI, 0.026 to 0.350; P = 0.023; q = 0.116) and poorer WHO/UCLA AVLT total recall (b = 0.231; 95% CI, 0.048 to 0.414; P = 0.014; q = 0.162); neither survived FDR correction. Conclusion CAD was not associated with global or domain-level neurocognitive performance. Its association with poorer Color Trails 2 performance may suggest selective vulnerability in executive control, but requires confirmation in larger longitudinal studies.