Systemic Lupus Erythematosus and Cardiovascular Disease

Abstract

Systemic lupus erythematosus (SLE) is a condition in which autoimmune inflammation affects nearly every organ in the human body; it is characterized by a relapsing-remitting pattern. Systemic inflammation and tissue damage can arise from autoantibodies, the creation of immune complexes, and the deposition of autoantibodies, all defined as autoimmune diseases. Women of reproductive age are at a high risk of developing lupus, a chronic systemic condition. Among women between the ages of 15 and 44 years, the female-to-male ratio for the occurrence of lupus is as high as 13:1, while it is only 2:1 in children and in the elderly. In addition to accelerated atherosclerosis, SLE is associated with an increased risk of cardiovascular (CV) events such as coronary artery disease (CAD), peripheral artery disease (PAD), and cerebrovascular accident (CVA). Several SLE-specific processes, including impaired immunological regulation, impaired endothelial cell (EC) function, impaired vascular repair, hyperleptinemia, and traditional risk factors, contribute to early atherosclerosis in the disease. CAD can occur at any stage of the disease's progression, with younger individuals being much more at risk than their age-matched counterparts. This review article aims to provide a unique insight into the relationship between SLE and cardiovascular disease (CVD) by discussing the pathophysiological role of CVD in SLE, outlining screening criteria, and highlighting the treatment options for CVD in connection with SLE.

Keywords: atherosclerotic cardiovascular disease; autoimmune heart disease; cardiovascular disease; cvd & sle; glucocorticoid-induced cardiomyopathy; pathogenesis of systemic lupus erythematosus; peripheral arterial diseases; systemic lupus erythematosus disease; systemic lupus erythromatosus; women and heart disease.

Figure 1. Summary of endothelial damage in SLE leading to CVD

SLE: systemic lupus erythematosus; CVD: cardiovascular disease; TNF-α: tumor necrosis factor-alpha; VCAM: vascular cell adhesion molecule; ICAM: intercellular adhesion molecule; IL-1: interleukin-1; VEGF: vascular endothelial growth factor; eNOS: endothelial nitric oxide synthase; LDGs: low-density granulocytes; NETs: neutrophil extracellular traps; Treg: regulatory T cells; Th-17: T helper 17 cells; CD4+: cluster of differentiation 4+; CCR5+: cysteine-cysteine chemokine receptor 5+; iNKT: invariant natural killer T; aPL: antiphospholipid antibodies; anti-HDL: anti-high-density lipoprotein antibodies; Apo-A1: apolipoprotein A-I; PON1: paraoxonase 1; TLR: toll-like receptors; anti-PCIgM: IgM antibodies against phosphorylcholine; MDA: malondialdehyde; anti-oxLDL: anti-oxidized LDL; Apo-B100: apolipoprotein B-100