Large increases in mortality related to premature atherosclerosis with coronary artery disease have been reported in patients with systemic lupus erythematosus (SLE). The current pathogenic hypothesis for atherosclerosis involves not only the classic factors identified in the Framingham study, but also includes chronic inflammation, corticosteroid therapy, excess of traditional risk factors, autoantibodies, immune complexes (containing antibodies to phospholipids, to oxidized low-density lipoproteins, and to endothelial cells), and cytokine-producing activated T cells. Early risk factor intervention and effective control of inflammation should be incorporated into the management of SLE to protect against atherosclerosis.