Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in patients with rheumatoid arthritis (RA) and psoriatic arthritis (PsA). Both conditions are characterized by systemic inflammation that contributes to an increased risk of CVD, yet the underlying mechanisms and associated risk factors differ. This review investigates the immunological responses, inflammatory pathways, and genetic predispositions that influence the risk of cardiovascular disease (CV) in people with RA and PsA. Endothelial dysfunction and atherosclerosis in RA are primarily caused by pro-inflammatory cytokines, specifically interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α), as well as the existence of autoantibodies such as anti-citrullinated protein antibodies (ACPA). Additionally, RA displays a "lipid paradox," in which a decreased risk of CVD is paradoxically correlated with a higher risk of cholesterol, most likely as a result of ongoing systemic inflammation. Different paths of CV impact are indicated by unique lipid profile changes and less prominent autoantibody participation in PsA, despite the fact that the risk of CVD is also enhanced. Genetic factors like HLA-DRB1 are more prominent in RA, while PsA has a unique association with metabolic syndrome and obesity-related inflammation. Despite the well-established CV risk in both RA and PsA, current risk calculators do not include PsA, and only two models account for RA. This review highlights the need for better risk assessment tools that incorporate disease-specific factors. Recognizing the overlapping and divergent mechanisms in RA and PsA can enhance the development of more targeted strategies for managing CV health and guide personalized treatment approaches.