Rheumatoid arthritis (RA; Table 1) is a chronic systemic autoimmune disorder primarily affecting synovial joints, characterized by persistent inflammation, progressive cartilage and bone destruction, and substantial functional disability if left untreated (Figure 1). Beyond articular manifestations, RA is increasingly recognized as a multisystem disease with wide-ranging comorbidities. Among these, cardiovascular disease (CVD) represents a leading cause of premature morbidity and mortality [1]. Epidemiological studies have consistently shown that patients with RA face a 1.5–2-fold higher risk of myocardial infarction, stroke, and cardiovascular death compared to the general population, a burden that cannot be fully explained by traditional risk factors such as hypertension, diabetes, or smoking [2]. Instead, chronic systemic inflammation, dysregulated immune pathways, and disease-related metabolic alterations appear to accelerate atherogenesis, placing CVD at the forefront of extra-articular RA complications. Within this context, lipoprotein(a) [Lp(a)] has emerged as a potential mediator of excess cardiovascular risk [3,4]. Lp(a) is a genetically determined low-density lipoprotein (LDL)–like particle in which apolipoprotein B-100 (apoB-100) is covalently bound to apolipoprotein(a) [apo(a)]. This unique structure confers pro-atherogenic, pro-thrombotic, and pro-inflammatory properties. Elevated plasma Lp(a) levels have been robustly established as an independent, causal risk factor for CVD in the general population, supported by large epidemiological cohorts and Mendelian randomization studies [5]. However, its role in the specific context of RA remains incompletely understood. Early investigations suggested that Lp(a) may be elevated in RA patients and linked to both inflammation and cardiovascular events, yet methodological inconsistencies and limited sample sizes prevented firm conclusions. More recently, advances in genetic, molecular, and biomarker research have reinvigorated interest in Lp(a), particularly as a mechanistic bridge between autoimmunity, vascular inflammation, and accelerated atherosclerosis [3,6].

The rationale for this review is to synthesize both longstanding discoveries and recent advances regarding Lp(a) in RA. By revisiting the historical evidence and integrating new insights from molecular biology, clinical studies, and emerging therapeutics, we aim to clarify the relevance of Lp(a) to cardiovascular and disease-specific outcomes in RA. The specific objectives of this review are fourfold: (i) to summarize the historical context of Lp(a) research in RA; (ii) to outline current understanding of its biological mechanisms in inflammation and atherogenesis; (iii) to appraise current evidence linking Lp(a) to cardiovascular risk and joint disease activity in RA; and (iv) to highlight emerging therapeutic opportunities and research priorities.