Interesting to find an article that apparently belongs to the dermatology field in a cardiology journal. Why read about psoriasis? A disease that, for several years, many colleagues regarded as eminently skin-related and of benign course, especially in its plaque form. As it happens, epidemiological studies^, and an international registry revealed that the risk of cardiovascular (CV) events increased approximately 50% in the group of psoriatic individuals compared to the general population, markedly in younger patients. How to explain this situation? Systemic inflammation seems to be the “missing link” between CV diseases, neoplasms, and chronic systemic inflammatory diseases (e.g., psoriasis or rheumatoid arthritis).

The interest of cardiology in this interdisciplinary theme is not new. In the past two decades, the understanding of atherosclerosis as a systemic vascular inflammatory disease and that sustained systemic inflammatory activity accelerates its physiopathological mechanisms has been consolidated. In 2003, Sattar et al. used rheumatoid arthritis as a physiopathological model to systematize the process of accelerated atherosclerosis. Systemic inflammation would increase the hepatic synthesis of C-reactive protein (CRP), induce lipolysis with the release of free fatty acids, and intensify insulin resistance and oxidation of low-density lipoproteins (LDL), culminating in endothelial dysfunction associated with increased expression of adhesion molecules and accelerating the atherosclerotic disease. In 2011, Boehnck et al. coined the term “psoriatic march” to describe possible mechanisms that could justify the increase in CV events in the physiopathological model of psoriasis. As expected, the foundation and steps of the process are extremely similar to those found in rheumatoid arthritis. The sustained systemic inflammation caused by psoriasis would increase the synthesis of CRP, vascular endothelial growth factor (VEGF), P-selectin, resistin, and leptin. Such proteins would be involved in raising insulin resistance, which ultimately would intensify the endothelial dysfunction and stimulate the expression of adhesion molecules. These steps reveal the importance of the subclinical atherosclerotic phase (endothelial dysfunction, vascular stiffness, and overexpression of vascular adhesion molecules) and biomarkers (CRP, leptin, and resistin) in this physiopathological process. In the article that prompted this short editorial, the authors compared arterial stiffness with pulse wave velocity (PWV), carotid intima-media thickness (IMT), metabolic syndrome data, and CRP levels in a cohort of psoriatic individuals and volunteers. The results reported were statistically significant and corroborated the hypothesis that psoriatic patients with intense disease activity are more prone to have metabolic syndrome, elevated CRP, and signs of subclinical atherosclerosis (increased IMT and arterial stiffness) compared to the control group.

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