Endothelial Dysfunction in Systemic Lupus Erythematosus: Pathogenesis, Assessment and Therapeutic Opportunities

Systemic Lupus Erythematosus (SLE) is characterised by increased mortality secondary to Cardiovascular Diseases (CVD). Despite being common in SLE, traditional cardiovascular risk factors cannot entirely justify such increase in CVD-associated mortality. The endothelium is a key regulator of the vascular homeostasis; lupus-associated persistent systemic inflammation may impair endothelium functionality, thus initiating a cascade of events that, in concert with traditional CVD-risk factors, leads to atherosclerosis development and progression. Numerous methods have been used for the in vivo assessment of the endothelial function; among all, Flow- Mediated Dilatation (FMD) has been widely validated in clinical trials. Quantification of the endothelial dysfunction by FMD has been confirmed to be an early predictor of CVD in multiple studies involving both non-CVD and CVD-population and it may therefore represent a likewise efficient biomarker of CVD in SLE.

Research and online content related to endothelial function in SLE is reviewed in this article with special attention to the pathophysiology and therapeutic opportunities.

To date, the vast majority of the available data, albeit not all, shows that endotheliumdependent FMD values are lower in SLE patients compared to healthy subjects; further studies, however, will be required in order to confirm the usefulness of the endothelial dysfunction quantification as CVD-predictor in the specific clinical setting of lupus. Notably, FMD variations can also be a sensitive marker for assessing specific therapeutic strategies ability of improving endothelial function in SLE patients.

Endothelial function appears to be affected by SLE potentially contributing to the increased cardiovascular risk observed in SLE patients.