The excess cardiovascular risk in patients with SLE has been attributed to corticosteroid usage in the treatment of the condition and as such was given as the explanation of the increased atherosclerosis (Petri M, 1992, 1996). Although, corticosteroid therapy can itself cause hypertension, diabetes and dyslipidaemia, the cumulative steroid dose is also a surrogate marker for disease severity. Studies have also shown that patients with the condition are more hypertensive and have an increased tendency to be smokers (Asanuma Y, 2003). However, a separate study showed that despite a higher incidence of hypertension, diabetes and an earlier menopause, the 10 year Framingham risk score was the same as matched healthy controls (Bruce IN, 2003). This would suggest that the risk factors present in SLE are not adequately explained by the conventional cardiovascular risk assessment model. In fact, SLE itself is a strong independent risk factor for atherosclerosis. Due to the inflammatory nature of SLE it is consistent with the recent paradigm shift towards the concept of atherosclerosis as a disease of vascular inflammation. Vascular inflammation leads to endothelial and vascular damage which can predispose to atherosclerosis (Ross R, 1999).