Systemic Lupus Erythematosus (SLE) is a chronic inflammatory disease of unknown cause which can affect any organs, characterized by a wide range of auto-antibodies. Studies of several large cohorts of SLE patients have reported an increased prevalence of symptomatic of sub-clinical coronary artery disease (CAD). It is currently believed that accelerated atherosclerosis in SLE results from a combination of numerous risk factors. In addition to a high prevalence of traditional risk factors, inflammatory processes in SLE are considered to be important in atherogenesis. Chronic activation or damage to the endothelium in SLE may trigger the inflammatory cascade and thereby promoting atherogenesis. Several forms of endothelial insult are being recognized in SLE, including hypercholesterolaemia, hyperhomocysteinaemia, mechanical stress from hypertension, increased oxidative stress and immunological injury as a result of immune complex deposition. Furthermore, autoantibodies directed against oxidised lipoproteins, along with chronic secretion of proinflammatory cytokines and suppression of fibrinolytic pathways may also contribute to atherosclerosis. SLE patients may also be more susceptible to the deleterious effects of the CAD risk factors due to pre-existing inflammation-induced vascular injury. This review updates the modifiable risk factors in SLE. The main focus is on the potential utility of these risk factors. The putative mechanisms of accentuated risk as a result of underlying inflammation, and evidence for association with premature atherosclerosis are discussed. Strategies which may be useful in preventing the development of progression of atheroma in this population include close monitoring and aggressive treatment of the traditional risk factors as in patients with high risk of CAD. The role of antioxidant and immunomodulators are also explored.