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Laboratory observations regarding interactions of innate immunity and the vascular endothelium have established that inflammation plays a role in all stages of the atherothrombotic process, from early foam cell formation to late plaque rupture.1 Epidemiological evidence supporting the inflammatory hypothesis of atherosclerosis initially derived from studies of those with acute ischaemia2 or from otherwise healthy patient populations3 in which biomarkers of inflammation such as C-reactive protein were observed to predict short- and long-term vascular risk. An equally intriguing set of clinical data linking inflammation to atherosclerosis has come from studies of patients with rheumatoid arthritis, inflammatory bowel disease, and periodontal disorders.4,5 In these studies, patients with systemic chronic inflammatory conditions have consistently been found at elevated vascular risk compared with age-matched controls, even after adjustment for traditional risk factors. Taken together, these laboratory and clinical data have led to a new understanding of atherosclerotic pathophysiology that has implications for both prevention and treatment.In 2006, the paradigm that individuals affected by inflammation have elevated vascular risk was extended by Gelfand and colleagues to include psoriasis, a common prototypical helper T cell type 1 (Th1) inflammatory disorder that leads to scaly erythematous plaques in the skin and in some patients to psoriatic arthritis.6 Using prospective data from the UK General Practice Research Database collected between 1987 and 2002, Gelfand and colleagues initially reported that the incidence of myocardial infarction per 1000 person-years for unaffected controls, those with mild psoriasis, and those with severe psoriasis was 3.58, 4.04, and 5.13, respectively. These investigators also reported that the relative risks of future myocardial infarction associated with psoriasis varied by age and severity, with the greatest risk observed among those with severe disease and young age. Conversely, the lowest risk was observed among those with mild psoriasis … *Corresponding author. Tel: +1 617 732 8790, Fax: +1 617 734 1508, Email: pridker{at}partners.org

Psoriasis, inflammation, and vascular risk: a problem more than skin deep?