B-PO04-087 EFFECT OF OBESITY ON LEFT ATRIAL WALL SUBSTRATE IN PATIENTS WITH ATRIAL FIBRILLATION: INSIGHT INTO EPICARDIAL ADIPOSE TISSUE AND FATTY INFILTRATION

Abstract

Obesity and epicardial adipose tissue fat (EAT) contributes to the progression of atrial fibrillation (AF). But, its effect on the left atrial (LA) wall substate is clinically unknown. This study aimed to assess the effect of obesity on the LA substrate. Of 23 AF patients who underwent an initial pulmonary vein isolation (PVI) were enrolled. The 320-row multidetector CT was performed within 2 weeks before PVI. The acquired CT images were transferred to a workstation. EAT was defined as -50 to -200 Hounsfield units (HU). We measured LA EAT volume, EAT thickness adjacent to the LA roof, CT values on the LA roof wall, and LA roof wall thickness using workstation (figure). We compared these parameters between AF patients with and without obesity (≥BMI 25 kg/m2). Both LA EAT volume and EAT thickness were significantly greater in obese group than in non-obese group (LA EAT volume, 50±13 vs. 24±9 ml, P<0.01; EAT thickness, 8.8±2.7 vs. 5.5±1.7 mm, P<0.01). There was a strong positive correlation with LA EAT volume and EAT thickness (r=0.89, P<0.01). The CT value on the LA roof wall was significantly lower in obese group than in non-obese group (21±7 vs. 36±12 HU, P<0.01). The CT value on the LA roof wall correlated negatively with both LA EAT volume (r=-0.80, P<0.01) and EAT thickness (r=-0.72, P<0.01). The LA roof wall thickness did not differ between two groups (2.5±0.5 vs. 2.5±0.3 mm, P=0.88). Our data disclosed different LA wall substrates in obese AF patients. Lower CT values adjacent to thickened EAT may reflect fatty infiltration from EAT, which may explain the pathogenesis of AF in obesity.