Association of deep learning–derived epicardial fat volume with target organ damage in subjects with nonobstructive coronary artery disease

다국어 초록 (Multilingual Abstract)

Background Epicardial fat exerts both protective and deleterious effects on organs through diverse cytokinemediated pathways. This study aimed to investigate computed tomography (CT)-based indexed epicardial fat volume (EFVi) in association with target organ damage parameters.
Methods The prospectively enrolled cohort of 75 patients with nonobstructive coronary artery disease underwent electrocardiogram-gated CT and was evaluated for target organ damage parameters: estimated glomerular filtration rate, proteinuria, echocardiographic septal e′ velocity, E/e′ and tricuspid regurgitation velocity, brachial-ankle pulse wave velocity, and ankle-brachial index. EFVi was measured from semiautomated 3D segmentation of electrocardiogram- gated CT. Partial correlation, multiple linear regression, and receiver operating characteristic (ROC) analyses were conducted.
Results Age and EFVi showed moderate positive linear correlation (r = 0.567, P < 0.001). After adjusting for age, EFVi was significantly correlated with the septal e′ velocity (r = − 0.489, P < 0.001) and E/e′ (r = 0.256, P = 0.034), but not with other target organ damage parameters (P > 0.05). Multiple linear regression analysis showed that the correlations of the EFVi with the septal e′ velocity (β = –0.0003, P = 0.007) and E/e′ (β = 0.0606, P = 0.024) remained significant after adjusting for potential confounders. ROC analysis identified optimal EFVi thresholds: 95.78 cm3/ m2 for reduced septal e’ velocity (area under the ROC curve [AUC], 0.750; sensitivity, 88.2%; specificity, 56.8%) and 91.68 cm3/ m2 for elevated E/e’ (AUC, 0.692; sensitivity, 71.4%; specificity, 64.8%).
Conclusions EFVi was related to left ventricular diastolic function more than other target organ damage parameters, including renal function and arterial stiffness, which suggests that the epicardial fat may have a role in the pathogenesis of left ventricular diastolic dysfunction.