Abstract 12457: Carotid Intima-Media Thickness and Aortic Stiffness are Elevated in Chronic Obstructive Pulmonary Disease (COPD) Subjects Compared to Controls and Not Associated With Systemic Inflammation

Abstract

Introduction: COPD is associated with increased cardiovascular risk, independent of established risk factors. Carotid intima thickness (CIMT) and carotid-femoral aortic pulse wave velocity (aPWV) are surrogate measures of cardiovascular risk and small studies have suggested elevated CIMT and aPWV in COPD are associated with systemic inflammation. We investigated this further as part of the ERICA (Evaluation of Role of Inflammation in Chronic Airways disease) multi-centre UK study: the largest cohort study focussing on cardiovascular manifestations in COPD. Hypothesis: COPD subjects have increased CIMT and aPWV compared to controls and CIMT and aPWV are associated with systemic inflammation in COPD. Methods: Spirometry, cardiovascular history and assessment, CIMT and haemodynamic measures including aPWV were performed in 432 COPD patients recruited from Cambridge and Cardiff study centres only. Age and gender matched healthy controls (n=324) were evaluated for comparison. Possible determinants for CIMT and aPWV in COPD subjects were assessed by linear regression analysis. Results: Mean age of COPD and control subjects was 67 years (SEM±0.41), 61% were male. COPD subjects, when compared to controls had increased CIMT (0.85±0.01mm vs 0.70 ±0.08mm, p=0.0001) and aPWV (10.35±0.12m/s vs 8.22 ±0.1m/s, p=0.0001), which were maintained after adjustment for mean arterial pressure (MAP) and heart rate (HR). COPD subjects also had higher brachial systolic BP (Δ 12±0.2mmHg, p=0.0001), and central systolic BP (Δ 12±0.2mmHg, p=0.0001). COPD was an independent determinant of CIMT and aPWV in pooled analysis of COPD and controls (p=0.0001 respectively). In COPD, age and systolic BP were independently associated with CIMT; and age, MAP and HR were determinants of aPWV. Inflammatory markers (fibrinogen, CRP, WCC), smoking status and pack years smoked were not associated with CIMT or aPWV. Conclusions: These data support the theory of accelerated ageing in COPD subjects compared to matched controls, which may partly explain the excess cardiovascular risk seen. As systemic inflammatory biomarkers did not relate to CIMT or aPWV, consideration of novel therapeutic targets to ameliorate premature arterial stiffening in COPD, merits further investigation.