Abstract 14876: Characterizing Regional and Global Effects of Epicardial Adipose Tissue on Left Atrial Function

Abstract

Background: Obesity is associated with left atrial (LA) dysfunction. Excess epicardial adipose tissue (EAT) deposition is one potential mechanism for this dysfunction. However, it is unknown if the effects of EAT on LA function are mediated via adjacency to LA tissue or rather, represent effects of generalized cardiometabolic dysfunction, also common in obesity. We hypothesized EAT located around the LA would be associated with LA function compared to EAT located distally on the left ventricle (LV). Methods: ardiac MRI was performed in 54 middle-aged obese adults (n = 80, age 40-55 yrs) enriched for increased heart failure risk (N-terminal pro-B-type natriuretic peptide >40 pg/mL or high-sensitivity cardiac troponin T >0.6 pg/mL; visceral fat >2kg). EAT was quantified by tracing the area of LV EAT depots on short axis and LA EAT depots on long axis. LA strain was assessed by MRI feature tracking as reservoir strain during LV systole, conduit strain during early LV diastole, and contractile strain during late LV diastole. Linear regression was performed between EAT area and LA strain components. LA function was quantified by LA reservoir, conduit, and contractile strain. Results: LV EAT amount was 12 times higher than LA EAT (66.7 vs 5.3 cm 2 ). LA EAT was associated with decreased LA conduit strain (r = 0.37, 95% CI = 0.12 to 0.58, p = 0.006) and a trend towards lower reservoir strain (r = -0.26, 95% CI = -0.49 to 0.01, p = 0.058). There was no association with contractile strain. There were no relationships between LV EAT and LA function. Conclusion: Increased LA EAT was associated with worse LA strain. In contrast, LV EAT had no demonstrable effect on LA strain. Our results suggest LA EAT may have direct mechanical or paracrine effects on atrial tissue function and may be a therapeutic target for improving LA function in obese patients.