Abstract P390: Insulin Resistance Determines Severity of Vascular Inflammation by 18-Fluorodeoxy Glucose PET-CT in Psoriasis
Introduction: Psoriasis (PSO), an inflammatory skin disease is associated with increased cardiovascular disease (CVD) risk. We have previously shown the presence of insulin resistance (IR) in psoriasis, however how this relates to subclinical vascular disease is unknown. Here, our aim was to determine whether IR relates to vascular inflammation (VI) measured by 18FDG PET-CT in a well-phenotyped psoriasis cohort (NCT 01778569).
Hypothesis: We assessed the hypothesis that an increase in IR is associated with greater VI.
Methods: We performed 18FDG PET-CT scans on 86 consecutive patients with psoriasis (Siemens Biograph). Target-to-background ratio (TBR) was used as the VI measure. Fasting plasma samples were collected and homeostatic model assessment of IR (HOMA-IR) was used to stratify the study group into normal (n=41) vs high (n=45) HOMA-IR groups using an accepted cut-off value (3.0). Lipid profile and lipoprotein characteristics were also obtained using NMR spectroscopy (Liposcience, USA).
Results: Our study cohort was middle aged with mild to moderate PSO (Table 1). There was increased VI by TBR in this sample (mean 1.8±0.3) as compared to published values for CAD (mean 1.6±0.3). The high HOMA-IR group had greater skin involvement by psoriasis, an increased incidence of CVD risk factors and an atherogenic lipid profile on NMR spectroscopy when compared to the normal HOMA-IR group. There was greater VI in the high HOMA-IR group (Mean±SD: 1.91±0.3 vs 1.69±0.2, p<0.001) which was robust to multivariate adjustment for age, gender, CVD risk factors and BMI (beta 0.38, p <0.01). Finally, on likelihood ratio testing, we observed an incremental effect when HOMA-IR was added to a fully adjusted model with BMI as a covariate (chi2 5.65, p = 0.02).
Conclusion: Psoriasis increases VI by 18FDG PET-CT, which is strongly related to the presence of IR beyond traditional CVD risk factors and BMI. This suggests that inflammatory IR may have direct impact on the development of vascular inflammation.
Author Disclosures: B. Natarajan: None. T. Salahuddin: None. J. Dave: None. M. Playford: None. J. Doveikis: None. P. Herscovitch: None. N. Mehta: None.
- © 2015 by American Heart Association, Inc.