Abstract
Psoriasis is a chronic immune-mediated skin disease that is increasingly understood as a systemic inflammatory condition with implications that extend far beyond the skin. Among its most serious associations is an elevated risk of cardiovascular disease, which has emerged as a leading cause of morbidity and mortality in affected patients. The persistent immune activation characteristic of psoriasis, driven by cytokines such as tumor necrosis factor α (TNFα), interleukin (IL)-17, and IL-23, contributes to endothelial dysfunction, oxidative stress, and atherogenesis. This shared pathophysiology helps explain the increased prevalence of coronary artery calcification, impaired microvascular function, and early-onset myocardial infarction observed in this population. Traditional risk assessment tools often fail to capture the actual cardiovascular burden in patients with moderate to severe disease. Evidence suggests that biologic therapies targeting key inflammatory pathways not only improve dermatologic outcomes but may also mitigate vascular risk, offering systemic benefits that extend beyond skin clearance. Recognizing psoriasis as a multisystem disorder reinforces the need for a more integrated approach to risk assessment and long-term management.