Figure 1.

Pro-inflammatory cytokines in SLE like IFN alpha, IL-1, IL-6 and TNF-alpha promotes formation of foam cells, proliferation, platelet adherence, thrombosis and fibrosis. Smoking, hypertension in SLE results in endothelial injury. Impaired glycemic control, DM in SLE can results in endothelial injury and increased lipids. Obesity, sedentary life style in SLE increases LDL and decreases HDL. Pro-atherogenic lipoprotein particles such as LDL infiltrate into the intima of the arterial wall and undergo oxidative modification. Accumulation of these atherogenic particles attracts macrophages that engulf the cholesterol, causing formation of foam cells and subsequent fatty streaks. This process injures the epithelium of the arterial wall, promoting adherence of platelets, release of PDGF, and development of an advanced fibrocalcific lesion. Anti-atherogenic particles such as HDL and apo-A1 promote reverse cholesterol transport and cholesterol efflux from foam cells. They also help to prevent oxidation of LDL and other atherogenic particles. Targets 1 – 8 are proposed to consider for therapeutic interventions to manage cardiovascular disease in SLE.

1 – Drugs used to control inflammation in SLE like hydroxychloroquine, mycophenolate, azathioprine, rapamycin, belimumab, rituximab, cyclophosphamide, steroids, and methotrexate

2 – Anti cytokine therapy like anakinra, anifrolumab

3 – Smoking cessation

4, 5 – Effective treatment of hypertension, diabetes

6 – Diet, and exercise

7 – Statins

8 – Anti platelets and anticoagulants

Abbreviations : Interleukin (IL), Interferon (IFN), TNF – Tumor necrosis factor (TNF), diabetes mellitus (DM), PDGF – Platelet derived growth factor, LDL – low density lipoprotein, HDL – High density lipo protein, ApoA1 – apo lipoprotein A 1, LCAT – Lecithin cholesterol acyl transferase