Pathophysiologic mechanisms linking atherosclerosis, psoriatic disease and inflammation Atherosclerosis, the underlying process resulting in cardiovascular events, reflects the development of atheromatous plaques in the inner layer of the arteries. It is now widely accepted that atherogenesis is caused by chronic low-grade inflammation that results from an interaction between immune mechanisms and metabolic abnormalities within the vessel wall [Hansson, 2005; Weber and Noels, 2011]. The initial phase involves a qualitative change in the inner lining of the arteries, the endothelial cells. This change includes the expression of adhesion molecules by endothelial cells leading to capture of leukocytes on the surface and their translocation from the blood through the endothelial layer into the intima, the innermost layer of the vessel wall. This process can occur due to irritative stimuli, such as lipid abnormalities or systemic inflammation, as in psoriatic disease [Gonzalez-Juanatey et al. 2007; Tabas et al. 2007]. Several studies have found that the prevalence of endothelial dysfunction, as measured by functional