Cardiovascular Disease in Systemic Lupus Erythematosus: An Update

Yudong Liu; Mariana J. Kaplan


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

In This Article



A number of studies have indicated that statins may promote autoimmune responses.[69,70] In a recent population-based cohort study assessing the association between statin use and the risk of developing SLE, the authors failed to identify any association between current statin use with the risk of developing SLE among patients 40 years and older.[71] Instead, they observed a decreased SLE risk among current statin users who continued their therapy for more than 1 year.[71] Studies on whether statins can prevent CVD in SLE have given inconsistent results. Atorvastatin improved endothelial cell-dependent vasodilation in a short-term (8-week) trial,[72] but failed to exert vasculoprotective effects in a longer (2-year) trial.[73] A recent study indicated that statin therapy might reduce the risk of mortality and CVD in SLE patients with hyperlipidemia.[74] Short-term atorvastatin therapy improved arterial stiffness in middle-aged SLE patients with abnormal PWV. Although these studies suggest that statin may benefit a subset of SLE patients, larger well-controlled, long-term trials are needed to conclude whether current statin regimens are sufficient in decreasing CV risk and what the guidelines for statin use should be in SLE.

Anti-IFN Therapies and Janus Kinase Inhibitors

Targeting the IFN pathway has emerged as a promising therapeutic strategy in SLE.[75,76] Given these promising results and the putative role of IFN in atherogenesis, it will be important to determine whether disrupting this pathway can yield a beneficial therapeutic response in premature atherosclerosis in SLE. A recent study reported that interfering with downstream signaling of this pathway by utilizing the Janus kinase (JAK) inhibitor tofacitinib ameliorates murine lupus and its associated vascular dysfunction.[77] The role of JAK inhibitors and antitype I IFN therapies in vascular prevention in SLE remains to be determined.


Antimalarials may have cardioprotective effects.[78,79] In a recent study, Fasano et al.[80] reported that long-term hydroxychloroquine (HCQ) use in conjunction with low-dose aspirin may provide added efficacy in primary CVD prevention in SLE. However, another recent database prospective cohort study failed to demonstrate the protective effect of long-term HCQ in reducing vascular events in SLE.[81] Ruiz-Arruza et al.[82] recently showed that, those SLE patients that received glucocorticoids later during the course of the disease and at lower doses while receiving more HCQ, displayed significantly decreased incidence of glucocorticoid-related CVD but similar SLE-related damage compared with SLE patients received glucocorticoids earlier and at higher doses. Additional studies are therefore needed to further define the role of antimalarials in CV prevention and the best strategies for treatment (single use versus combination therapy).