Patients with systemic lupus erythematosus (SLE) are prone to premature atherosclerosis and are at risk for the development of cardiovascular disease. Increased arterial stiffness is emerging as a marker of subclinical atherosclerosis. Purpose. To measure proximal aortic stiffness in children and adolescents with SLE. Methods. We studied 16 patients with SLE in activity (mean age years; 16 females), 14 patients with SLE not in activity (mean age years; 4 males, 10 females), and 16 age- and sex-comparable healthy children and adolescents ( years; 4 males, 12 females). Disease activity was determined by the SLE disease activity index (SLEDAI). All subjects underwent echocardiography for assessment of proximal aortic pulse wave velocity (PWV) [Ao distance/Ao wave transit time in the aortic arch]. Venous blood samples were collected for ESR. Results. Patients in activity had significantly higher PWV values than controls ( ), while no significant difference was found between patients not in activity and controls. Conclusions. SLE patients with disease activity demonstrate increased PWV and arterial stiffness of the proximal aorta, while patients without disease activity do not. This suggests that inflammation secondary to SLE activity, and not subclinical atherosclerosis, is the major underlying cause for increased arterial stiffness in this age group. 1. Introduction Patients with systemic lupus erythematosus (SLE) are prone to premature atherosclerosis, and the incidence of atherosclerosis-related myocardial infarction is as much as 50-fold greater in young patients with SLE than in age-matched controls [1]. Potential explanations for accelerated atherosclerosis in SLE include a high prevalence of conventional risk factors [2], long term corticosteroid use [3], the presence of antiphospholipid antibodies [4], and proatherogenic pathophysiologic phenomena inherent to SLE, such as dyslipidemia, immune system activation, endothelial cell apoptosis, oxidative stress [5], and chronic immune complex formation [6], all of which result in a chronic low grade inflammatory state, endothelial dysfunction, and, eventually, atherosclerotic events [5]. SLE patients should therefore be regarded as population at risk for the development of coronary artery disease, similar, for example, to patients with diabetes, in whom prompt identification and stringent treatment of risk factors are recommended [7, 8]. One of the recently accepted ultrasound-derived markers of early, asymptomatic atherosclerosis is increased arterial stiffness, as evidenced by increased pulse wave
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