Abstract and Introduction
Purpose of review: With improved management of the classical disease manifestations of systemic lupus erythematosus (SLE), cardiovascular disease (CVD) has emerged as one of the most important causes of morbidity and mortality. This review in particular focuses on progress over the past year in clinical and basic aspects of SLE-driven accelerated atherosclerosis.
Recent findings: Both subclinical CVD and CV events continue to be recognized at increased frequency in previously unstudied lupus cohorts and populations. Novel associations have been identified between lupus CVD and cognitive impairment, depression, and low-income status. In terms of pathogenesis, there is an ever-increasing focus on the innate immune system and, in particular, type I interferons (IFNs). Recent studies have drawn connections in both human and murine models between neutrophils, plasmacytoid dendritic cells, type I IFNs, and endothelial dysfunction. Whether treatments such as mycophenolate mofetil or statins have a role in prevention of lupus CVD is an area of intensive study.
Summary: CVD is a major complication of lupus and is now a leading cause of death among people living with this disease. As such, additional studies are needed in order to identify the most effective preventive strategies and most predictive vascular risk biomarkers. Type I IFNs may play a critical role in lupus CVD pathogenesis, and it is recommended that vascular outcomes be included in ongoing trials testing the efficacy of anti-IFN biologics.
The prevalence of premature cardiovascular disease (CVD), especially in young women with systemic lupus erythematosus (SLE), is striking, and may be as high as 50-fold depending on the study and outcome measure.[1,2] A significant percentage of patients with SLE have evidence of subclinical vascular disease, such as increased carotid intima-media thickness (CIMT)[1,3,4] and myocardial perfusion abnormalities, findings that are not explained by traditional risk factors.[4,6] Although all-cause mortality in SLE has improved significantly with improved monitoring and immunosuppressive treatments, CVD remains a leading cause of death. The interplay between SLE and CVD is a rapidly expanding area of study and has recently been comprehensively reviewed.[8,9] Here, we will focus on those areas that have seen substantial progress over the past year, primarily focusing on the clinical and basic science of CVD attributable to accelerated atherosclerosis.
Curr Opin Rheumatol. 2013;25(5):597-605. © 2013 Lippincott Williams & Wilkins