Cardiovascular (CV) mortality and morbidity are significant challenges in managing patients with systemic lupus erythematosus (SLE). Patients with SLE have a 2-fold higher risk of stroke and a 3-fold higher risk of myocardial infarction than in the general population. Still, the risk is much greater in young women with SLE compared to age-matched women without SLE.1
The higher risk of CV disease in SLE patients is mainly related to accelerated atherosclerosis, leading to sub-clinical disease and clinical manifestations earlier than the general population. A complex interplay between traditional risk factors and SLE-related features is responsible for accelerated atherosclerosis, even though its pathogenesis is not fully understood.2 SLE-related factors contributing to accelerated atherosclerosis include cytokines (e.g., IFN-α, BAFF) and autoantibodies production responsible for endothelial cells dysfunction, hyperactivated T-cells directed against peptides from vascular cells, impairment in lipid profile with increased oxidized LDL and pro-inflammatory (pi)HDL, high dose or high duration of glucocorticoid therapy. Therefore, although there is an increased prevalence of Framingham traditional CV risk factors (e.g. age, hypertension, dyslipidemia, diabetes, current smoking), it is not surprising that they do not fully account for the high CV risk observed in SLE patients.3
New biomarkers have been developed to identify potentially high CV risk SLE patients, including increased circulating leptin, antibodies against apolipoprotein A1, serum cardiac troponin T, and the soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK). In addition, a combination of both traditional (age, diabetes) and SLE-related factors (piHDL, leptin, homocysteine, sTWEAK) has shown better sensitivity (89%) and specificity (79%) than any single biomarker to predict the formation or enlargement of carotid plaques.4 Nevertheless, a biomarker or combination of markers to predict cardiovascular risk accurately in SLE patients is still missing.
Presently, the main objectives to lower the CV risk in SLE should be to monitor and correct traditional CV risk factors while treating the disease to target and maintain remission or low disease activity, prescribing hydroxychloroquine to virtually all patients and minimising corticosteroid use as much as possible.
Yazdany J, et al. Systemic lupus erythematosus; stroke and myocardial infarction risk: a systematic review and meta-analysis. RMD Open 2020;6:e001247.
Skaggs BJ, et al. Accelerated atherosclerosis in patients with SLE--mechanisms and management. Nat Rev Rheumatol 2012 Feb 14;8(4):214–223.
Esdaile JM, et al. Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus. Arthritis Rheum 2001 Oct;44(10):2331–2337.
McMahon M, et al. A panel of biomarkers is associated with increased risk of the presence and progression of atherosclerosis in women with systemic lupus erythematosus. Arthritis Rheumatol 2014 Jan;66(1):130–139.
Describe the morbidity associated with cardiovascular diseases in SLE
Explain the interplay between traditional risk factors and SLE related features responsible for accelerated atherosclerosis
Discuss the most promising biomarkers of CV risk in SLE patients
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