The latest in systemic lupus erythematosus-accelerated atherosclerosis: related mechanisms inform assessment and therapy

Purpose of Review Accelerated atherosclerosis is a significant comorbidity and the leading cause of death for patients with systemic lupus erythematosus (SLE). It is now apparent that SLE-accelerated atherosclerosis is not driven solely by traditional cardiovascular risk factors, adding complexity to disease characterization and mechanistic understanding. In this review, we will summarize new insights into SLE-accelerated atherosclerosis evaluation, treatment, and mechanism. Recent findings Recent work highlights the need to incorporate inflammatory biomarkers into cardiovascular disease (CVD) risk assessments. This is especially true for SLE patients, in which mechanisms of immune dysfunction likely drive CVD progression. There is new evidence that commonly prescribed SLE therapeutics hinder atherosclerosis development. This effect is achieved both by reducing SLE-associated inflammation and by directly improving measures of atherosclerosis, emphasizing the interconnected mechanisms of the two conditions. SLE-accelerated atherosclerosis is most likely the consequence of chronic autoimmune inflammation. Therefore, diligent management of atherosclerosis requires assessment of SLE disease activity as well as traditional cardiovascular risk factors. This supports why many of the therapeutics classically used to control SLE also modulate atherosclerosis development. Greater understanding of the mechanisms underlying this condition will allow for the development of more targeted therapeutics and improved outcomes for SLE patients.

Automated summary

Accelerated atherosclerosis is a significant comorbidity and leading cause of death in patients with systemic lupus erythematosus (SLE), where traditional cardiovascular risk factors alone do not drive the condition. New insights suggest incorporating inflammatory biomarkers into cardiovascular disease risk assessments, particularly for SLE patients with immune dysfunction likely driving disease progression. Recent evidence shows commonly prescribed SLE therapeutics can hinder atherosclerosis development by reducing inflammation and directly improving measures of atherosclerosis, emphasizing the interconnected mechanisms of the two conditions.