Narrative mini-review discusses mechanisms driving coronary atherosclerosis in patients with systemic lupus erythematosus

This publication is classified as a narrative mini-review focusing on patients with systemic lupus erythematosus. The scope encompasses the comprehensive relationship between systemic lupus erythematosus and coronary atherosclerosis, examining underlying biological processes rather than clinical trial outcomes. The authors do not report a specific sample size or follow-up duration.

Key findings indicate that premature coronary atherosclerosis remains a primary driver of late-stage mortality in systemic lupus erythematosus. Chronic systemic inflammation modifies the lipoprotein profile toward a pro-oxidant state, characterized by dysfunctional HDL and elevated oxidized LDL. Type I interferon-driven cascades, excessive neutrophil extracellular trap release, and biased macrophage polarization toward pro-atherogenic phenotypes are described as central to vascular pathology mechanisms.

The review also further explores roles of pathogenic autoantibodies, genetic susceptibility, and the metabolic impact of specific immunosuppressants. However, the source explicitly notes that it is a mini-review, not a primary trial. Findings are mechanistic insights rather than clinical outcome data. The text describes mechanistic pathways underpinning atherosclerosis but does not report clinical trial data establishing causality.

Integrating these mechanistic insights is essential for refining cardiovascular risk assessment and identifying novel immunomodulatory interventions. Understanding the unique systemic lupus erythematosus–atherosclerosis axis provides a foundation for reducing cardiovascular morbidity and improving long-term outcomes in this vulnerable population.