Abstract 4122389: Accumulation of Epicardial Adipose Tissue as a Marker of Diastolic Dysfunction in Patients With Preserved Left Ventricular Ejection Fraction Undergoing Coronary Computed Tomography Angiograph

Background: Left ventricular diastolic dysfunction (LVDD) plays a major role in the pathophysiology of progression to heart failure with preserved left ventricular (LV) ejection fraction (EF). Although epicardial adipose tissue (EAT) is attracting attention for the underlying pathophysiology, whether increased EAT and coronary plaque burden are associated with LVDD is unclear in patients with chronic coronary artery disease (CAD) and preserved LVEF. Aims: To investigate the association between LVDD and EAT accumulation in chronic CAD patients with preserved LVEF. Methods: We included three hundred fourteen chronic CAD and preserved LVEF patients without history of heart failure (mean age: 66±13 years; 48% female). Thoracic tissue doppler echocardiography (TTDE) analysis included LVDD parameters, including left atrial volume index (LAVI), e’, E/e’ and tricuspid regurgitation (TR) velocity. LVDD was defined according to the American Society of Echocardiography guidelines. Coronary computed tomographic angiography (CCTA) analysis included EAT volume index (EAVi), coronary artery calcium score (CACS), and coronary plaque volume (%PV). Patients were divided into three groups according to EAVi: Group A as normal (<68.1 ml/m 2 , n=127), group B as low (68.1-89.4 ml/m 2 , n=95), and group C as high EATVi (>89.4 ml/m 2 , n=92). Multivariable logistic regression analysis was performed to investigate the association between the clinical parameters, TTDE and CCTA findings, and the presence of LVDD. Results: Compared with Group A, group C was older and more frequently suffered from renal dysfunction. Among the three groups, we observed significant differences in LV mass index, e’, E/e’, and CACS. The EAVi correlated with each LVDD diagnostic component, including e’, E/e’, left atrial volume index (all p<0.05), except for tricuspid regurgitation velocity. A multivariate model showed that age [odds ratio (OR), 1.13; 95% CI, 1.06-1.20; p<0.001] and EAVi (OR, 1.03; 95%CI, 1.01-1.04; p<0.05) were independently associated with LVDD, even after adjusting for LV mass index (OR, 1.1; p < 0.05). There was no independent association of CACS or %PV with LVDD (Table). Conclusion: This study demonstrates that accumulation of EAT and LV mass index but not plaque volume were independent predictors of LVDD in chronic CAD patients with preserved LVEF. Further study is needed to investigate whether EAT predicts the development to heart failure in this population.