Abstract 16281: Non-calcified Coronary Plaque Burden is Related to Epicardial Adipose Tissue and Peri-coronary Adipose Tissue Attenuation in Heart Failure With Preserved Ejection Fraction

Abstract

Introduction: Coronary inflammation may be a factor in developing heart failure with preserved ejection fraction (HFpEF). Epicardial fat volume (EFV) measured using non-contrast computed tomography (CT) and pericoronary adipose tissue (PCAT) attenuation on coronary CT angiography (CCTA) are considered to be inflammatory mediators, which play an important role in the development of coronary plaque. Hypothesis: We hypothesize that there is an interrelationship between these measures in HFpEF and no obstructive coronary artery disease (CAD). Methods: 28 subjects with HFpEF (European Society of Cardiology criteria), with coronary CCTA-documented absence of obstructive CAD. Non-calcified plaque (NCP), low-density non-calcified plaque (LDNCP), PCAT attenuation were quantified using semi-automated software and EFV was quantified using QFAT software. PCAT attenuation in Hounsfield Units (HU) was measured in a standardized 40 mm segment around the proximal right coronary artery. Statistical analysis was performed using Spearman correlation and multivariable regression models adjusted for age, BMI, EFV, and PCAT tested relations to NCP burden. Results: Overall, the mean age of 64.8±12 years, 74% women, BMI 29.3±4, total cholesterol 162±41mg/dl, LDL 85±29 mg/dl, HDL 55±14 mg/dl, systolic BP 132±22mmHg, diastolic BP 77±12mmHg, EFV 139±73 cm 3 and, PCAT attenuation -78±8 HU. Mean total NCP burden 34±13%, total LDNCP burden 3±1.8 %, and coronary calcium score (CCS) 414±920. EFV and PCAT attenuation correlated with the coronary risk markers including CCS and NCP burden variables (Table). In multivariable analysis, age and PCAT (β±SE=0.43±0.2, p=0.04, 0.64±0.3, p=0.03 per 1%-change in NCP burden respectively) were related to NCP burden. Conclusions: EFV and PCAT attenuation are associated with non-calcified plaque burden and may play an important role in the pathophysiological process of HFpEF. Further studies are needed to further understand these findings.