Traditional and autoimmune-related mechanisms of cardiovascular disease in systemic lupus erythematosus and antiphospholipid syndrome. A complex interaction between traditional and disease-specific traits leads to premature atherosclerosis process. Several risk factors (left) have been described since the Framingham heart study, known as classic risk factors, which over time conduce to endothelial dysfunction, subclinical atherosclerosis, and CV event manifest. In the autoimmune setting (right), several novel risk factors contribute to development of premature vascular damage. This damage is represented by impaired endothelial function and early increase of intima-media thickness, which are surrogates of the accelerated atherosclerosis process. These associations are even more pronounced in this case of polyautoimmunity (SLE and APS in the same individual), where risk factors have additive effects and atherosclerosis develops earlier. The cornerstone of management of CV risk includes an aggressive treatment of disease activity, the continuous monitoring and treatment of modifiable CV risk factors, and the use of other medications in order to diminish the CV burden. ACE-I: angiotensin-converting enzyme inhibitors; AMs: antimalarials; APS: antiphospholipid syndrome; AT-II blockers: angiotensin II receptor blockers; Auto-Ab: autoantibodies; AZA: azathioprine; CIC: circulating immune complex; CYC: cyclophosphamide; CVD: cardiovascular disease; HDL: high-density lipoprotein; HRT: hormone replacement therapy; IR: insulin resistance; MetS: metabolic syndrome; MMF: mycophenolate mofetil; oxLDL/β2GPI complex: oxidized low-density lipoprotein/2 glycoprotein I; SLE: systemic lupus erythematosus; T2DM: type 2 diabetes mellitus.
