Endothelial Dysfunction in Systemic Lupus Erythematosus

Background: Systemic lupus erythematosus (SLE) patients have a significantly increased risk of coronary heart disease (CHD) that is not fully explained by classic risk factors. Endothelial dysfunction is an early stage in the process of atherogenesis. Our aim was to determine whether endothelial dysfunction occurs in SLE and whether it is associated with the occurrence of classic Framingham risk factors. Methods and Results: We studied 54 women with SLE (1997 revised criteria) and 27 healthy women. Demographic and risk factor data were collected (cholesterol, triglycerides, smoking, diabetes mellitus, systolic and diastolic blood pressure). Endothelial function was assessed by flow-mediated dilation (FMD) in the brachial artery in response to reactive hyperemia. SLE activity was assessed using SLE Disease Activity Index (SLEDAI). Endothelial function was assessed by means of flow mediated dilation (FMD) on brachial artery, using B-mode ultrasonography. The statistical analysis was done using version 17.0 of the SPSS statistical packaget. The group of SLE patients was formed of 54 females, with the mean age of 45,66 ± 8,72 years. The values of FMD were 7,12 ± 4,7 % (SLE group) and 21,32 ± 3,12 % (group control), p < 0.0001. The statistical analysis showed a strong inverse correlation between FMD and SLEDAI, a moderate inverse correlation between FMD and total cholesterol, systolic and diastolic blood pressure. After adjustment for other factors, SLE activity was associated with 1,27% lower FMD compared with control subjects. Conclusions: Endothelial dysfunction is present in SLE patients even in the absence of traditional cardiovascular risk factors, due to disease activity. Patients with SLE have endothelial dysfunction that remained significant even after adjustment for other classic CHD risk factors. Understanding the mechanism(s) of endothelial dysfunction in SLE may suggest novel strategies for CHD prevention in this context.