Cardiovascular diseases (CVD) represent a major cause of morbidity and mortality in people with rheumatoid arthritis (RA) and psoriatic arthritis (PsA), both of which are characterized by systemic inflammation that increases the risk of CVD. Although these two conditions share this common inflammatory component, the specific pathways and associated factors that elevate cardiovascular risk differ. This article delves into the immune system’s response, inflammatory processes, and genetic factors that contribute to cardiovascular complications in RA and PsA. In RA, endothelial dysfunction and the development of atherosclerosis are primarily driven by inflammatory cytokines, particularly interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), along with the presence of certain autoantibodies, such as anti-citrullinated protein antibodies (ACPA). An interesting feature of RA is the “lipid paradox,” where the presence of elevated cholesterol levels paradoxically correlates with a lower incidence of cardiovascular events, possibly due to ongoing inflammation. PsA, while also increasing cardiovascular risk, shows a different mechanism, with variations in the lipid profiles and reduced autoantibody involvement. In this case, factors such as metabolic syndrome and obesity-related inflammation play a more substantial role. Genetic factors, particularly the HLA-DRB1 gene, are strongly associated with RA, while PsA has more significant associations with obesity-driven inflammation. Although the cardiovascular risk in RA and PsA is well-documented, existing risk calculators fail to include PsA and only a limited number of models factor in RA. This review emphasizes the importance of developing more disease-specific tools for cardiovascular risk assessment. By understanding the overlapping and distinct pathways between RA and PsA, clinicians can work toward more individualized and effective strategies for cardiovascular care.
