Premature atherosclerosis (ATS) in SLE patients is an important clinical problem. It is explained not only by excess of traditional risk factors, but also by specific factors linked to disease activity and therapy. Such specific factors include the following: antioxLDL and anti CRP antibodies, immune complexes, mannose-binding lectin, disturbances of metabolism of annexin A5, antiphospholipid syndrome, immunologically determined dyslipidemia, influence of medication. As a conclusion,atherosclerosis in SLE patients results from an interplay between traditional and nontraditional risk factors. Therapeutic influences suggest antiatherogenic effects for hydroxychloroquine and immunosuppressants and a doubtful proatherogenic influence of cortisone.