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Psoriasis is a systemic inflammatory disease which contributes to an increased risk for cardiovascular disease, specifically coronary artery disease. Patients with psoriasis tend to have greater total coronary plaque burden and more high risk plaque than healthy controls. This likely contributes to the higher rate of myocardial infarction and 4-5 year reduction in lifespan observed in our psoriasis population. With biologic therapy and improvement in PASI scores, total plaque burden and noncalcified coronary plaque decreases as well. Specifically, ustekinumab decreases intima-media thickness and reduces vascular inflammation. Likewise, TNF-α inhibitors decrease vascular inflammation and reduce cardiovascular events in both sexes, and reduce coronary plaque formation in men with psoriasis. This may be due to elevation in glycoprotein acetylation, which is associated with cardiovascular events and elevated in psoriasis. This elevation has also been shown to decrease with adalimumab usage. Despite all of the knowledge gained on this topic, the incidence of myocardial infarction in psoriasis patients currently remains unchanged when compared to prior years. Consequently, we emphasize the need for further research on the unique pathogenesis of psoriatic coronary plaque formation as well as the effect biologic agents have on this coronary plaque in order to improve the wellbeing of this patient population.

Characterization of Coronary Plaque in Psoriasis and the Impact of Current Therapies