Chronic inflammation in psoriasis promotes visceral adiposity associated with noncalcified coronary burden over time.

BACKGROUND Psoriasis is a chronic inflammatory skin disease with increased obesity, non-calcified coronary artery burden (NCB), and incident myocardial infarction. We sought to assess the relationship between inflammation, visceral adipose tissue (VAT), and NCB. Furthermore, we evaluated whether improvement in VAT would be associated with reduction in NCB over time in psoriasis. METHODS Consecutive psoriasis patients (PSO) underwent coronary computed-tomography angiography to quantify NCB and abdominal computed tomography to calculate VAT, at baseline (n=237), one year (n=176), and four-years (n=50). RESULTS Patients with high hs-CRP had significantly greater visceral adiposity (17952.9±849.2 vs 13370.7±806.8 cc3, p<0.001) and non-calcified coronary burden (1.26±0.03 vs 1.07±0.02 mm2) than those with low hs-CRP. Those with higher VAT had more systemic inflammation [hs-CRP: 2.5 (1.0-5.3) vs 1.2 (0.6-2.9) mg/L] with ~50% higher NCB (1.42±0.6 vs 0.91±0.2 mm2 , p<0.001). VAT associated with NCB in fully adjusted models (β=0.47, p<0.001). At one-year follow up, patients who had worsening hs-CRP had an increase in VAT (14748.7±878.1 to 15158.7±881.5 cc3; p=0.03), whereas those who improved hs-CRP improved their VAT (16876.1±915.2 to 16310.4±889.6 cc3; p=0.04). At one-year, in those who decreased VAT, there was 10.3% reduction in NCB (β=0.26, p<0.0001), which persisted in a subset at four-years (β=0.39, p=0.003). CONCLUSIONS Inflammation drives development of VAT, increased cardiometabolic risk, and NCB in psoriasis. Reduction of inflammation associated with reduction in VAT, and associated with longitudinal improvement in NCB. These findings demonstrate the important role of inflammation in the development of VAT in humans and its impact on early atherogenesis.