Cardiovascular Disease in Latin American Patients with Systemic Lupus Erythematosus: A Cross-Sectional Study and a Systematic Review

Figure 2

Traditional and autoimmune-related mechanisms of cardiovascular disease in systemic lupus erythematosus. A complex interaction between traditional and disease-specific traits leads to premature atherosclerotic 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), a broad spectrum of novel risk factors contribute to development of premature vascular damage. This damage is represented by impaired endothelial function and early increased of Intima-Media Thickness which are surrogates of the accelerated atherosclerosis process, which is perpetuated by a chronic proinflammatory milieu. The cornerstone of management of CV risk include an aggressive treatment of disease activity, the continuous monitoring and treatment of modifiable CV risk factors, as well as the use of other medications in order to diminish de CV burden. CVD: cardiovascular disease, SLE: systemic lupus erythematosus, MetS: metabolic syndrome, T2DM: type 2 diabetes mellitus, IR: insulin resistance, HRT: hormone replacement therapy, CIC: Circulating Immune complex, oxLDL/B2GPI complex: oxidized-low density lipoprotein/β2 glycoprotein I, HDL: high density lipoprotein, Auto-Ab: auto-antibodies, AMs: antimalarials, CYC: cyclophosphamide, AZA: azathioprine, MMF: mycophenolate mofetil, ACE-I: angiotensin-converting enzyme inhibitors, AT-II blockers: angiotensin II receptor blockers.