Metabolic Syndrome Is Associated with Increased Arterial Stiffness and Biomarkers of Subclinical Atherosclerosis in Patients with Systemic Lupus Erythematosus

Objective. Aortic Pulse wave velocity (PWV) is an independent predictor of risk for atherosclerotic cardiovascular disease. Metabolic syndrome (MetS) is more prevalent in patients with systemic lupus erythematosus (SLE) compared with matched healthy subjects. Aortic PWV is increased in MetS. The purpose of this cross-sectional study wag to determine the association between MetS and aortic PWV and other surrogate biomarkers of subclinical atherosclerosis in SLE. Methods. One hundred twenty-eight patients with SLE were studied. We established the presence of MetS according to the National Cholesterol Education Program Adult Treatment Panel III definition and we measured PWV, glucose, insulin, glycosylated hemoglobin (HbA(1c)), insulin sensitivity (HOMA index), lipid levels, uric acid, homocysteine, fibrinogen, D-dimer, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), interleukin 6 (IL-6) IL-8, IL-10, C3, C4, autoantibodies, SLE Disease Activity Index (SLEDAI), and Systemic Lupus International Collaborating Clinics/ACR Damage Index. Duration of SLE and treatment was also recorded. Multivariate logistic regression analysis was used to identify independent determinants of increased PWV. Results. SLE patients with MetS had higher aortic PWV (9.8 +/- 2.4 vs 8.5 +/- 1.7 m/s: p = 0.002) and increased biomarkers of subclinical atherosclerosis such as CRP, IL-6, C3, uric acid, homocysteine, fibrinogen and D-dimer. compared to those without MetS. HOMA index and insulin and HbA(1c) levels were also higher in this group. No differences were found in variables related to lupus activity (ESR, C4, SLEDAI, IL-8. IL-10, and treatment for SLE). In the multivariate model, increased PWV was associated with age, male sex, MetS, duration of SLE, and CRP. Conclusion. MetS may contribute to the development of accelerated atherosclerosis in SLE. (First Release Sept 1 2009; J Rheumatol 2009,36:2204-11; doi: 10.3899/jrheum.081253)