Abstract 14: Cardiac Biomarkers are Associated With Findings on Brain MRI in Older Adults: The Atherosclerosis Risk in Communities (ARIC) Study

Abstract

Background: Cerebrovascular disease is often the consequence of cardiac disease. Our aim was to examine associations of biomarkers of cardiovascular disease, high sensitivity troponin T (hs-cTnT), NT-proBNP, and galectin-3, with cerebrovascular signs: lacunar infarcts, lobar and subcortical microhemorrhages, cortical infarcts, and white matter hyperintensity (WMH) volume. We also examined total cortical and Alzheimer’s Disease (AD) signature region volumes. Methods: We conducted a cross-sectional analysis of 1748 ARIC participants from the 2011-2013 exam who had biomarker measurements, completed a brain MRI, and did not have a clinical history of stroke. We used linear regression to model brain volumes, modeled as Z scores, and logistic regression for all other outcomes; biomarkers were log transformed. We repeated analyses excluding persons with coronary heart disease, atrial fibrillation, and heart failure. Results: The mean age of participants was 76, 62% were female, and 21% were Black. All biomarkers were associated with total cortical volume. Each standard deviation increase in log hs-cTnT was associated with lower total cortical volume (adjusted beta = -0.08, 95% CI: -0.12, -0.05); results for the other biomarkers were similar (Figure). All biomarkers were associated with lobar microhemorrhages. Hs-cTnT and NT-proBNP were associated with WMH volume, but galectin-3 was not. No biomarker was associated with subcortical microhemorrhages or cortical infarcts. Results were similar in persons without coronary heart disease, atrial fibrillation, or heart failure (conditions associated with cerebral thromboembolism). Conclusions: In persons free of clinical cardiovascular disease, biomarkers of cardiac stretch, strain, and fibrosis were associated cerebral small vessel disease and reduced cortical volume, but not in a specific pattern suggestive of AD pathogenesis. This suggests subclinical vascular insults affect brain structure through mixed pathogenic processes.