Objective To understand whether directly-measured psoriasis severity is associated with vascular inflammation assessed by 18F-fluorodeoxyglucose positron emission tomography computed tomography (FDG PET/CT). Approach In depth cardiovascular and metabolic phenotyping was performed in adult psoriasis patients (n=60) and controls (n=20). Psoriasis severity was measured using psoriasis area severity index (PASI). Vascular inflammation was measured using average aortic target-to-background ratio using FDG PET/CT. Results Both the psoriasis patients (28 men, 32 women, mean age 47 years) and controls (13 men, 7 women, mean age 41 years) were young with low cardiovascular risk. PASI scores (Median 5.4; IQR 2.8-8.3) were consistent with mild to moderate skin disease severity. Increasing PASI score was associated with an increase in aortic TBR (β=0.41, p=0.001), an association that changed little after adjustment for age, sex and Framingham risk score. We observed evidence of increased neutrophil frequency (mean psoriasis: 3.7±1.2; vs 2.9±1.2; p=0.02) and activation by lower neutrophil surface CD16 and CD62L in blood. Serum levels of S100A8/A9 (745.1±53.3 vs 195.4±157.8 ng/mL; p<0.01) and neutrophil elastase-1 (43.0±2.4 vs 30.8±6.7 ng/mL; p<0.001) were elevated in psoriasis. Finally, S100A8/A9 protein related to both psoriasis skin disease severity (β=0.53; p=0.02) and vascular inflammation (β=0.48; p=0.02). Conclusions Psoriasis severity is associated with vascular inflammation beyond cardiovascular risk factors. Psoriasis increased neutrophil activation and neutrophil markers, and S100A8/A9 related to both skin disease severity and vascular inflammation.

Background Psoriasis, a chronic inflammatory disease associated with an accelerated risk of MI, provides an ideal human model to study inflammatory atherogenesis in vivo. We hypothesized that the increased cardiovascular risk observed in psoriasis would be partially attributable to an elevated subclinical coronary artery disease (CAD) burden composed of non-calcified plaques with high-risk features. However, inadequate efforts have been made to directly measure CAD in this vulnerable population. As such, we sought to compare total (TB) and non-calcified (NCB) coronary plaque burden, and high-risk plaque (HRP) prevalence, between psoriasis patients (n=105), hyperlipidemic patients eligible for statin therapy under NCEP-ATP III guidelines (n=100) who were ~10 years older, and non-psoriasis healthy volunteers (HV) (n=25). Methods Patients underwent coronary computed-tomography angiography (CCTA) for TB and NCB quantification, and HRP identification, defined as low-attenuation (<30 HU), positive remodeling (>1.10), and spotty calcification. A consecutive sample of the first 50 psoriasis patients were scanned again at 1 year following therapy. Results Despite being younger and at lower traditional risk than hyperlipidemic patients, psoriasis patients had increased NCB (mean±S.D.:1.18±0.33 vs 1.11±0.32, p=0.02), and similar HRP prevalence (p=0.58). Furthermore, compared to HV, psoriasis patients had increased TB (1.22±0.31 vs 1.04±0.22, p=0.001), NCB (1.18±0.33 vs 1.03±0.21, p=0.004), and HRP prevalence beyond traditional risk (OR=6.0, 95% CI: 1.1–31.7; p=0.03). Finally, amongst psoriasis patients followed for 1-year, improvement in psoriasis severity associated with improvement in TB (β=0.45, 0.23–0.67; p<0.001) and NCB (β=0.53, 0.32–0.74; p<0.001) beyond traditional risk factors. Conclusions Psoriasis patients had greater NCB and increased HRP prevalence than HV. Additionally, psoriasis patients had elevated NCB and equivalent HRP prevalence as older, hyperlipidemic patients. Finally, modulation of target organ inflammation (eg. skin) associated with an improvement in NCB at 1 year, suggesting that control of remote sites of inflammation may translate into reduced CAD risk.