Cardiovascular Disease in Systemic Lupus Erythematosus: An Update

Yudong Liu; Mariana J. Kaplan

Disclosures

Curr Opin Rheumatol. 2018;30(5):441-448. 

In This Article

Epidemiology of Vascular Disease in Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is associated with a significant risk of cardiovascular disease (CVD).[1,2] A recent study suggests that patients with SLE have two-fold higher number of atherosclerotic plaques in the carotid and femoral arteries, comparable with what has been reported in rheumatoid arthritis and diabetes mellitus, two other conditions associated to enhanced CV risk.[3] Another recent prospective study reported that during a 5-year follow-up period, 32% of SLE patients developed evidence of carotid atherosclerosis compared with 4% of healthy controls.[4] In addition, individuals with SLE have a two-fold increased rate of ischemic stroke or myocardial infarction (MI) compared with the general population.[1,5] In some patients with lupus, MI may develop even before the diagnosis of SLE or shortly thereafter, suggesting a potential link between autoimmune inflammation and atherosclerosis.[6] SLE patients with lupus nephritis display significantly increased risk of MI and CVD mortality than SLE patients without lupus nephritis.[7] Furthermore, lupus nephritis is associated with twice as often evidence of carotid atherosclerotic plaques when compared with age-matched nonnephritis SLE patients [even those with positivity for antiphospholipid (aPL) antibodies] and population controls.[8] The prevalence of CV events in SLE also shows racial and ethnic variations. Specifically, the risk of MI was recently reported to be lower among Hispanics and Asians compared with Whites, whereas the risk of stroke was elevated among blacks and Hispanics compared with Whites.[9]

Traditional Framingham risk factors do not fully explain the increased CVD risk in SLE.[10] A recent study compared the Framingham score with the recently described SLE-specific CVD risk equation (SLE score) and identified that a large proportion of SLE patients could be reclassified as high CVD risk using a formula that incorporates SLE disease-related parameters.[11] The authors found that the sex preference in SLE and low BMI in women may lead the traditional Framingham score to underestimate the CV risk in female SLE patients. In contrast, the SLE score may capture those patients as having high risk for CVD.[11]

Genetic variants can play important roles in both SLE and CVD. A recent study indicates that an interleukin 19 (IL19) risk allele, rs17581834(T) is associated with stroke/MI in SLE by affecting protein binding. SLE patients with that risk allele had increased levels of plasma-IL10 and aPL antibodies.[12] In addition, an SRP54 Antisense RNA 1-AS1 risk allele, rs799454(G) was associated with stroke/transient ischemic attack in SLE.[12] Another recent study shows that apolipoprotein L1 risk variants associate with atherosclerotic disease in African-American SLE patients.[13]

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