baseline and 7 weeks. Within and between group differences were analysed using paired and unpaired t-tests respectively. Results Please see table 1. Conclusion SPACE for COPD can improve dyspnoea and endurance capacity over 7 weeks to a similar level to PR, although it remains unclear to its noniferiority to PR. The SPACE for COPD programme does offer a number of health benefits despite it involving limited support and could offer a suitable alternative to patients with COPD who would otherwise not attend conventional rehabilitation. Background There is good evidence that pulmonary rehabilitation (PR) provides benefit for patients with chronic obstructive pulmonary disease (COPD) in terms of quality of life and daily functioning. However it is generally accepted that the benefits diminish over time. REFERENCESMethods We conducted a randomised controlled parallel study of a maintenance programme, following standard PR, consisting of a two hour session of education and strength and endurance training every 3 months versus standard care. Measurements were made, at baseline (prior to a standard PR programme), at randomisation (after successful completion of a PR programme) and after 12 months, of the chronic respiratory questionnaire (CRQ), endurance shuttle walk test (ESWT), EuroQol (EQ5D), hospital anxiety and depression score (HADS) and activity questionnaires. CRQ was also completed every 3 months by post. Results 250 (139 male) patients, mean (SD) age of 69.2 (9.2) years, FEV1 41 (16)% predicted, provided informed consent to participate in the study. The mean (95% CI) improvement in CRQ following the initial PR was 0.76 (0.59, 0.93) units. 148 patients entered the randomised part of the study. There remained a significant improvement in CRQ dyspnoea at 12 months compared to baseline for the group as a whole. However, there was no statistically significant differences detected between the intervention and control groups for the CRQ dyspnoea score, which amounted to 0.19 (-0.26, 0.64) units, or other domains of the CRQ. There was no difference in the ESTW distance between the two groups (109.1 (-100.1 to 318.2) metres) or HADS (-0.2 (-2.41,2) units). There was a higher level of selfreported activity, according to the visual analogue score of 16.2/ 100, in the maintenance group but not the reported metabolic equivalent (MET)-minutes per week. There was no difference in any of the CRQ measures at any of 3 monthly measurements between the intervention and control groups Conclusion A maintenance programme of 3monthly 2 hour sessions does not improve outcomes in patients with COPD after 12 months. We cannot recommend that our maintenance programme is adopted. It is likely that a maintenance programme should commence earlier than 3 months and possibly be more intensive. Introduction In moderate exacerbations of COPD, patients with the eosinophilic phenotype (>2% of the total leukocyte count) have better outcomes with prednisolone. However, it remains unclear whether patients with severe exacerbations displaying the eos...

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IntroductionCOPD is associated with increased cardiovascular events, independent of established risk factors. Arterial stiffness and carotid intima-media thickness (CIMT) are surrogates of cardiovascular risk and we sought to determine their relationship with COPD severity and prognosis in the ERICA (Evaluation of role of inflammation in airways disease) multi-site UK study: the largest cohort study focusing on cardiovascular manifestations in COPD.MethodsSpirometry, haemodynamic measures (aortic pulse wave velocity (aPWV), augmentation index (AIx), peripheral and central blood pressure (BP)) and CIMT (ultrasound measure of carotid artery intima-media layer thickness) were performed in 729 COPD subjects aged ≥40 years. COPD severity was classified by BODE Index [BMI, Obstruction (FEV1), Dyspnoea (mMRC score), Exercise tolerance (6-minute walk distance)], a validated score based on clinical variables and predictor of mortality in COPD.ResultsMean aPWV was 10.3 (SD 2.6) m/s, AIx 27 (10)%, brachial BP 144/82 (18/11) mmHg, central BP 131/82 (18/11) mmHg, CIMT 0.86 (0.4) mm.BODE correlated with aPWV (p < 0.0001) and this was maintained when adjusted for study site, age, supine heart rate (HR) mean arterial pressure (MAP), years smoked and cardiovascular comorbidities (MI, stroke, diabetes, peripheral vascular disease), p < 0.0001. BODE was also associated with AIx when adjusted for site, age, seated HR and MAP, years smoked and cardiovascular comorbidities, p < 0.01. The constituent variables of BODE did not have the same significant association with both aPWV and AIx, Table 1.Abstract S124 Table 1Comparison of linear regression models of BODE constituent variables, cardiovascular comorbidities and established predictors of arterial stiffnessDependent variableaPWV (m/s)Augmentation Index (%)β coefficientp-valueβ coefficientp-valueAge (years)0.4 <0.0001-0.010.7MAP (mmHg)*0.2 <0.00010.26 <0.0001HR (bpm)*0.2 <0.0001-0.49 <0.0001TPYs-0.0010.980.020.63BMI (kg/m2)0.090.01-0.17 <0.0001FEV1 (%)-0.060.090.050.14mMRC (0–4)0.070.090.0030.946MWD (m)-0.030.5-0.010.002MI-0.010.7-0.080.02Stroke-0.010.7-0.020.46Diabetes0.070.03-0.080.02PVD0.10.0040.010.78Study site-0.060.09-0.030.45*Supine for aortic pulse wave velocity (aPWV), seated for Augmentation Index.TPYs: Total pack years smoked, mMRC dyspnoea scale, 6MWD: 6-minute walk distance, MI: Myocardial Infarction, PVD: Peripheral Vascular Disease.Cardiovascular comorbidities: self-reported on questionnaire.An inverse correlation of BODE with central systolic BP (p = 0.003) was observed and this was maintained after adjustment for study site, age and HR p = 0.03. There was no significant relationship between BODE and CIMT.ConclusionsBODE is associated with arterial stiffness in COPD, independent of traditional risk factors. Its negative relationship with systolic pressure suggests increasing arterial stiffness with COPD severity, is independent of blood pressure. The BODE Index composite variables are not on the causal pathway for vascular stiffness, so its positive association likely ...

were no cannabis-only smokers and only 6/62 (9.7%) were never-smokers (tobacco&cannabis).56/62 (90%) abnormal HRCTs were in ex/current tobacco smokers and 27/62 (44%) were in current tobacco&cannabis smokers. There was a higher prevalence of pneumothoraces and bullae with a cannabis and tobacco smoking history than for tobacco alone but this was not statistically significant different (chi-squared STATA) (Table1). Conclusion More than half of tobacco smokers with abnormal HRCTs also had a history of previous and current cannabis smoking. Despite these findings 25% of patients with abnormal HRCTs had no documentation regarding cannabis smoking. This population of ≤50 years olds with abnormal HRCTs did not smoke cannabis without tobacco. While not statistically significant, bullae and pneumothoraces were more frequently observed in patients who smoked tobacco with cannabis compared to tobacco alone. Larger studies are needed to further understand the additive effect of cannabis smoking to tobacco-induced lung damage. These studies will require systematic recording of both tobacco and cannabis smoking histories. Background As cardiovascular disease is a comorbidity and major cause of death in patients with COPD, primary preventative strategies are required. Arterial stiffness, as measured by aortic pulse wave velocity (PWV) is increased in patients with COPD 1 , and is an independent predictor of cardiovascular risk 2 , which is modifiable over the short term. We hypothesised that aortic PWV, would be reduced by six weeks treatment of simvastatin 20mg once daily compared to placebo in selected patients with COPD without concurrent heart disease, diabetes or hypercholesterolemia. Methods Clinically stable patients with confirmed COPD were recruited and randomised to either simvastatin 20mg od (active) or placebo in double blinded fashion. Aortic PWV, blood pressure, spirometry, six minute walking distance, and lipids were measured pre-and post-6 weeks treatment. Primary analysis compared PWV between groups. A predefined subgroup analysis compared those with a baseline PWV≥10m/s. Results The patients were well matched for age, sex, smoking and lung function; active, n = 33 and placebo, n = 37. The recruitment target was met. Compliance was high with the active group achieving significantly lower total cholesterol -between arms mean (95% CI): -1.1 (-1.3, -0.8)mmol/L, p < 0.001. There was no significant change in aortic PWV after treatment in the active compared to placebo group: -0.7 (-1.8, 0.5)m/s, p = 0.24, In the subgroup with aortic PWV≥10m/s, n = 22, aortic PWV improved in the active arm compared to placebo: -2.8 (-5.2, -0.3)m/s, p = 0.03. This latter difference remained statistically significant after adjusting for age and sex. Blood pressure, lung function and six minute walking distance did not change. Conclusions In this pilot study, despite a significant reduction in total cholesterol there was no improvement in aortic PWV in patients with COPD taking simvastatin 20mg compared to placebo over 6 weeks. The p...

Introduction In many chronic diseases vitamin D has been proposed as an adjunctive anti-inflammatory therapy. Vitamin D upregulates MKP1, thereby downregulating p38 phosphorylation and the NFKB inflammatory cascade (Zhang et al, J Immunol. 2012;188(5):2127-35). Steroids exert anti-inflammatory effects via this cascade, and exhibit synergy with vitamin D for some effects (Yu et al, Journal of the National Cancer Institute. 1998;90(2):134-41). Patients with COPD have chronic pulmonary inflammation, with upregulation of NFKB, yet do not exhibit a good response to steroids. Vitamin D therapy has been trialled in COPD patients, albeit with disappointing results (Lehouck et al, Annals of internal medicine. 2012;156(2):105-14). We hypothesised that COPD patients' inflammatory response would differ from health, and that vitamin D would exhibit synergy with steroids in vitro to improve this. Methods PBMCs isolated from 10 COPD patients and 10 healthy control subjects were incubated with LPS, vitamin D, dexamethasone, a p38 MAPK inhibitor or combinations of these agents. Supernatants were harvested for TNF and IL6 measurements (ELISA). Results LPS caused a marked rise in IL6 in both healthy controls (p = 0.044) and COPD patients (p = 0.008). IL6 reduction with vitamin D was only seen in health. IL6 reduction with addition of dexamethasone was not statistically significant (p = 0.636) in COPD. Combinations of agents failed to produce any additional benefit in both health and COPD.The response to vitamin D was heterogeneous; half of healthy subjects showed an anti-inflammatory response but in COPD only 12.5% of patients exhibited this. The difference in response rate was not significant (p = 0.120, Fishers exact test), though this may be due to low power. Similarly reduced response rate to dexamethasone was seen in COPD. Conclusion Vitamin D does not enhance the anti-inflammatory effect of steroids. The anti-inflammatory effects of vitamin D are no different between COPD and health; variability of response may be one reason for lack of effect of vitamin D in clinical trials to date in COPD patients. 2 Several CV risk calculators for the general population exist but it is unclear whether they are applicable for COPD. Hypothesis Standard CV risk calculators do not identify the increased risk in patients with COPD. Methods Subjects with a smoking history >10 pack years, with and without COPD, were assessed at clinical stability, COPD n = 191 and controls n = 106. Post-bronchodilator spirometry and blood pressure were performed, blood taken for lipids and self-reported medical and smoking history recorded. In those without documented established CV disease or diabetes (COPD n = 135 and controls n = 88), 10 year CV risk was calculated using ACC/AHA 3 and NHLBI[4] calculators. Results Both groups were well matched for gender and mean arterial blood pressure (MAP), with the COPD group slightly older, Table 1. Mean CV risk scores were similar between patients with COPD and controls, Table 1, ACC/AHA p = 0.16 and NHLBI p = 0.59. Wh...