OBJECTIVE: Women with systemic lupus erythematosus (SLE) have an increased risk of cardiovascular disease (CVD). Traditional CVD and SLE-disease related risk factors do not fully account for this increased risk. Perivascular adipose tissue (PVAT) is a visceral adipose depot in close proximity to blood vessels possibly influencing CVD. We hypothesized that women with SLE have an increased volume of descending thoracic aortic PVAT (aPVAT) associated with increased vascular calcification. METHODS: Using electron beam computed tomography, we quantified the aPVAT in clinically CVD-free SLE women (n = 135) and age-/race-matched healthy controls (HC, n = 152). Coronary artery calcification (CAC) and aortic calcification (AC) were quantified using Agatston scores and the aPVAT was quantified using standard Hounsfield Units (HU) for adipose tissue. RESULTS: Women with SLE had greater median aPVAT (32.2 cm(3) vs HC aPVAT 28.6 cm(3), p = 0.0071) and greater median AC (26.0 vs HC AC 6.0, p = 0.0013) than the healthy control women. Total aPVAT (per 25 cm(3)) remained significantly associated with SLE after adjusting for CVD risk factors (Odds Ratio 1.74 [95% Confidence Interval: 1.04-2.9], p = 0.034), but was attenuated when adjusting for circulating inflammatory markers (p = 0.34). In a logistic regression analysis, SLE aPVAT (per 25 cm(3)) was associated with AC (6.78 [2.0-23], p = 0.0019), which remained significant after adjusting for circulating inflammatory markers (p = 0.0074), and CAC (2.66 [1.4-5.0], p = 0.0028). CONCLUSIONS: Total aPVAT is greater in clinically CVD-free SLE women than in age-/race-matched controls and is associated with calcification in different vascular beds.
OBJECTIVE:Women with systemic lupus erythematosus (SLE) have an increased risk of cardiovascular disease (CVD). Traditional CVD and SLE-disease related risk factors do not fully account for this increased risk. Perivascular adipose tissue (PVAT) is a visceral adipose depot in close proximity to blood vessels possibly influencing CVD. We hypothesized that women with SLE have an increased volume of descending thoracic aortic PVAT (aPVAT) associated with increased vascular calcification. METHODS: Using electron beam computed tomography, we quantified the aPVAT in clinically CVD-free SLEwomen (n = 135) and age-/race-matched healthy controls (HC, n = 152). Coronary artery calcification (CAC) and aortic calcification (AC) were quantified using Agatston scores and the aPVAT was quantified using standard Hounsfield Units (HU) for adipose tissue. RESULTS:Women with SLE had greater median aPVAT (32.2 cm(3) vs HC aPVAT 28.6 cm(3), p = 0.0071) and greater median AC (26.0 vs HC AC 6.0, p = 0.0013) than the healthy control women. Total aPVAT (per 25 cm(3)) remained significantly associated with SLE after adjusting for CVD risk factors (Odds Ratio 1.74 [95% Confidence Interval: 1.04-2.9], p = 0.034), but was attenuated when adjusting for circulating inflammatory markers (p = 0.34). In a logistic regression analysis, SLE aPVAT (per 25 cm(3)) was associated with AC (6.78 [2.0-23], p = 0.0019), which remained significant after adjusting for circulating inflammatory markers (p = 0.0074), and CAC (2.66 [1.4-5.0], p = 0.0028). CONCLUSIONS: Total aPVAT is greater in clinically CVD-free SLEwomen than in age-/race-matched controls and is associated with calcification in different vascular beds.
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