Abstract P293: Perivascular Adipose Tissue of the Descending Aorta is Associated with SLE and Vascular Calcification

Abstract

Introduction: Women with systemic lupus erythematosus (SLE) have an increased risk of cardiovascular disease (CVD). Traditional CVD and SLE related risk factors have been implicated, but do not fully account for this increased risk. Adipose produces pro-atherogenic components and visceral adipose is most strongly associated with vascular dysfunction and metabolic disorder. The proximity of perivascular adipose tissue (PVAT) to blood vessels may exacerbate vascular dysfunction and progression of CVD. Hypothesis: We hypothesized that SLE participants have increased PVAT surrounding the descending thoracic aorta with increased coronary artery calcification (CAC) and aortic calcification (AC) compared to healthy controls. PVAT is hypothesized to be positively associated with increased CAC and AC. Methods: Women participating in the: “Heart Effects on Atherosclerosis and Risk of Thrombosis in SLE” (HEARTS) study were clinically CVD-free, diagnosed with SLE for 2 years and age and race matched to healthy women, excluding those with diabetes (SLE, n=153; Control, n=158). The EBT scans were performed using an Imatron C-150 scanner. CAC/AC were quantified using Agatston scores and the PVAT was quantified using standard attenuations values for adipose tissue (−190 to −30 HU) on commercially available software. The total PVAT volume (tPVAT) was calculated by summing the areas and multiplying by the length of the participant’s aorta. Results and Conclusions: The SLE group had a greater tPVAT than the control group (p=0.0071) despite no differences in age, BMI, metabolic syndrome (MS), or waist or hip circumference. The SLE group was more likely to be hypertensive (p<0.0001) and had a larger waist to hip ratio (p=0.001 ) reflecting vascular dysfunction and a different adipose distribution. Total PVAT was associated with SLE (OR: 1.02, p=0.020) and the association remained significant after adjusting for CVD risk factors including BMI and MS (OR: 1.03, p=0.028). Based on linear regression analysis, the tPVAT in both SLE and controls was influenced by postmenopausal status, CRP, BMI, and MS, while history of smoking also influenced the control tPVAT. Unadjusted AC was associated with SLE by a factor of 2.3 (p=0.01), while there was no statistical difference between SLE and control for CAC. In logistic regression analysis, tPVAT was associated with AC (1.07,p<0.0001), which remained significant after adjusting for CVD and inflammatory factors including BMI and MS. The CAC (1.05,p<0.0001) association was attenuated with BMI and MS. In conclusion, tPVAT is greater in clinically CVD-free SLE versus control participants and is associated with AC independent of overall adiposity.