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

BACKGROUND. Psoriasis is a chronic inflammatory skin disease associated with increased obesity, noncalcified coronary artery burden (NCB), and incident myocardial infarction. Here, we sought to assess the relationship among 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 underwent coronary CT angiography to quantify NCB and abdominal CT to calculate VAT at baseline (n = 237), 1 year (n = 176), and 4 years (n = 50). RESULTS. Patients with high levels of high-sensitivity C-reactive protein (hs-CRP) had significantly greater visceral adiposity (17,952.9 849.2 cc3 vs. 13370.7 806.8 cc3, P < 0.001) and noncalcified coronary burden (1.26 0.03 vs. 1.07 +/- 0.02 mm2) than those with low levels of hs-CRP. Those with higher levels of VAT had more systemic inflammation (hs-CRP, median [IQR], 2.5 mg/L [1.0-5.3 mg/L] vs. 1.2 mg/L [0.6-2.9 mg/L]), with approximately 50% higher NCB (1.42 +/- 0.6 mm2 vs. 0.91 +/- 0.2 mm2, P < 0.001). VAT associated with NCB in fully adjusted models (beta = 0.47, P < 0.001). At 1-year follow-up, patients who had worsening hs-CRP had an increase in VAT (14,748.7 +/- 878.1 cc3 to 15,158.7 +/- 881.5 cc3; P = 0.03), whereas those who had improved hs-CRP improved their VAT (16,876.1 +/- 915.2 cc3 to 16310.4 +/- 889.6 cc3; P = 0.04). At 1 year, there was 10.3% reduction in NCB in those who had decreased VAT (beta = 0.26, P < 0.0001), which persisted in a subset of patients at 4 years (beta = 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 effect on early atherogenesis.