P7.14 SERUM INFLAMMATORY MARKERS ARE POOR PREDICTORS OF VASCULAR INFLAMMATION AND VASCULAR INFLAMMATION DOES NOT DETERMINE AORTIC STIFFNESS IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

Abstract

Background: COPD is independently associated with increased cardiovascular events. Arterial stiffening and systemic inflammation are postulated aetiological factors. We hypothesised that vascular inflammation links systemic inflammation with vascular stiffening and sought to test this in a cohort of COPD subjects undergoing baseline FDG PET/CT either as part of the EVOLVE observational study or EVOLUTION trial (NCT 01541852). Methods: 85 COPD subjects underwent assessments including spirometry, arterial stiffness (aortic pulse wave velocity (aPWV)), inflammatory biomarkers (fibrinogen and hsCRP) and FDG PET/CT imaging (lungs, aorta and carotids) to evaluate inflammation and aortic calcification. Results: 66% of the cohort were male, median age was 68 (IQR 63–73) years, 87% were ex-smokers. Mean aPWV was 9.9 (SEM 0.2) m/s, aortic calcification volume 7156 (1461) mm3, hsCRP 5.2 (0.8) mg/dl, fibrinogen 3.4 (0.08) g/l. Log hsCRP correlated only with carotid FDG uptake (R=0.23, p=0.04) and log fibrinogen did not correlate with FDG uptake in any vascular region. Systemic inflammatory markers were positively associated with aortic inflammation but only weakly. The estimated change in FDG uptake was 0.2 (95% CI 0.11–0.29) and 0.07 (0.06–0.08), for each log unit change in fibrinogen and hsCRP respectively. Aortic inflammation was not a significant determinant of aPWV, but aortic calcification was, adjusted for age, supine HR, MAP and years smoked (p=0.02, β=0.26). Conclusion: HsCRP and fibrinogen are weak predictors of vascular inflammation and therefore likely unsuitable stratification biomarkers of vascular inflammation in COPD. Calcification rather than inflammation appears to be the dominant pathophysiological mechanism underlying arterial stiffness in COPD.