OBJECTIVE: Morbidity and mortality secondary to premature cardiovascular disease (CVD) in systemic lupus erythematosus (SLE) remain significant issues. The pathogenesis of CVD in SLE patients has not been fully explored. Epicardial adipose tissue (EAT) is believed to contribute to atherosclerosis development, through a paracrine and systemic inflammatory effect. We measured EAT volume in 162 SLE patients and 86 matched controls to assess the association of EAT with markers of atherosclerosis, cardiovascular risk and immunoactivation. METHODS: Clinical and laboratory characteristics collected included anthropomorphic measures, disease activity and damage indices, blood pressure measurement, lipid profile, inflammatory indices, adipokine levels and measures of adiposity. Coronary artery calcium (CAC) and EAT volume were measured using non-contrast cardiac computed tomography. RESULTS: EAT volume was greater in patients with SLE [(mean ± SD) 96.8 ± 45.9 cm(3)] than controls (78.2 ± 40.7 cm(3); P = 0.001). The EAT volume was 31% larger (95% CI, 16.5%-47.4%) in SLE patients than controls (P < 0.001 adjusted for age, sex, and race; after additional adjustment for waist circumference P = 0.007). Within SLE patients, after adjusting for age, race, sex, and waist circumference, EAT volume was associated with cumulative corticosteroid dose (P = 0.007), current corticosteroid use (P < 0.001), HDL cholesterol (P = 0.033), and triglycerides (P = 0.005). EAT was significantly correlated with CAC score (P < 0.001), but the association was attenuated after adjustment for Framingham risk score (P = 0.051). CONCLUSION: The increased EAT volume seen in SLE patients is associated with corticosteroid use. Corticosteroids could have adverse cardiovascular effects in SLE via an increase in EAT volume, a marker of risk in the general population.
OBJECTIVE: Morbidity and mortality secondary to premature cardiovascular disease (CVD) in systemic lupus erythematosus (SLE) remain significant issues. The pathogenesis of CVD in SLEpatients has not been fully explored. Epicardial adipose tissue (EAT) is believed to contribute to atherosclerosis development, through a paracrine and systemic inflammatory effect. We measured EAT volume in 162 SLEpatients and 86 matched controls to assess the association of EAT with markers of atherosclerosis, cardiovascular risk and immunoactivation. METHODS: Clinical and laboratory characteristics collected included anthropomorphic measures, disease activity and damage indices, blood pressure measurement, lipid profile, inflammatory indices, adipokine levels and measures of adiposity. Coronary artery calcium (CAC) and EAT volume were measured using non-contrast cardiac computed tomography. RESULTS: EAT volume was greater in patients with SLE [(mean ± SD) 96.8 ± 45.9 cm(3)] than controls (78.2 ± 40.7 cm(3); P = 0.001). The EAT volume was 31% larger (95% CI, 16.5%-47.4%) in SLEpatients than controls (P < 0.001 adjusted for age, sex, and race; after additional adjustment for waist circumference P = 0.007). Within SLEpatients, after adjusting for age, race, sex, and waist circumference, EAT volume was associated with cumulative corticosteroid dose (P = 0.007), current corticosteroid use (P < 0.001), HDL cholesterol (P = 0.033), and triglycerides (P = 0.005). EAT was significantly correlated with CAC score (P < 0.001), but the association was attenuated after adjustment for Framingham risk score (P = 0.051). CONCLUSION: The increased EAT volume seen in SLEpatients is associated with corticosteroid use. Corticosteroids could have adverse cardiovascular effects in SLE via an increase in EAT volume, a marker of risk in the general population.
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