Corresponding Diagnoses Ischaemic heart disease, Pulmonary artery hypertension, Gastroesophageal reflux disease and Osteoporosis Results 1000 CT chest scans were reviewed. Here is analysis from first 227 scans. Common reasons for requesting imaging: lung transplant assessment (29%), excluding bronchiectasis (18%), acute exacerbation of COPD(12%) and LVRS assess- ment. Retrospective analysis of 227 CT Thorax scans showed a total of 450 pulmonary (138) and extra pulmonary (312) findings. (figure 1) Pulmonary findings Bronchiectasis: 40% (90/227), lung nodules: 6% (13/227) of which new cancer diagnoses were 23% (3/13), Consolidation 4% (9/227), Small airway changes 3% (7/227), Interstitial lung changes:6% (14/ 227), Pleural plaques 2% (5/227). Extra pulmonary findings Hiatus hernia: 18.5% (42/227), Vertebral fractures: 17% (39/ 227), Enlarged Pulmonary artery diameter (more than or equal to 29 mm): 38% (87/227), Coronary artery plaques: 55% (124/227). Summary Preliminary analysis indicates a high incidence of potentially treatable extra pulmonary comorbidities. Incidence of co-existing radiological bronchiectasis is 40%. Conclusions To our knowledge this is the first report quantify- ing the added value of non-contrast CT Thorax in the assess- ment of COPD patients. Our recommendation is that a list of imaging diagnoses linked to well recognised COPD comorbid- ities should be part of the standard work up in the assessment of COPD patients undergoing CT Thorax. REFERENCE 1. Martinez CH, Miguel DJ, Mannino DM. Defining COPD-related comorbidities, 2004–2014. J COPD F.2014;1(1):51–63. P94 CARDIORESPIRATORY PHYSIOLOGY IN PATIENTS WITH COPD ACCORDING TO BLOOD EOSINOPHILIA: DATA FROM THE ERICA COHORT 1 L Buss, 1 TM McKeever, 2 D Mohan, 3 K Maki-Petaja, 3 J Forman, 3 CM McEniery, 3 J Cheryian, 4 N Gale, 4 JR Cockcroft, 5 PM Calverley, 6 W MacNee, 2 R Tal-Singer, 7 M Polkey, 3 IB Wilkinson, 1 CE Bolton. 1 University of Nottingham, UK; 2 GSK King of Prussia, US; 3 University of Cambridge, UK; 4 Cardiff University, UK; 5 Liverpool University, UK; 6 Edinburgh University, UK; 7 Royal Brompton Hospital, London, UK 10.1136/thoraxjnl-2017-210983.236 Introduction Blood eosinophils level in Chronic Obstructive Pulmonary Disease (COPD) is a candidate biomarker for Reg- ulatory qualification as a drug development tool identifying individuals who may benefit from targeted therapies. Current evidence focused on association with exacerbations and response to therapy, however the association of eosinophilia with cardiorespiratory physiology has not been determined. Methods The ERICA (Evaluating the Role of Inflammation in Chronic Airway Disease) study is a large multicentre study of patients with COPD. 1 Aortic pulse wave velocity (PWV), caro- tid intimal thickness (CIMT) and spirometry were measured. Health Status (CAT) was recorded. From the full blood count, both absolute and percentage eosinophil counts were consid- ered. We used previously validated cut offs 2 of 0.3 × 10 9 cells/L and 2% to compare aortic PWV, CIMT and spiro- metry variables using a Student’s t-test. A multivariate model was then built to examine the effect after adjusting for con- founding factors. Results 519 subjects were included in this analysis. Of these, 58% were men, mean (SD) age of 66.9 (7.6) years with a median smoking history of 42 pack years. Mean (SD) resting heart rate was 75 (13)bpm, mean arterial pressure 104 (12) mmHg and percentage predicted FEV 1 52.5 (16.1)%. When comparing high and low eosinophil groups at both 0.3 × 10 9 cells/L and 2% cut-offs there was no difference in smok- ing status or pack years, spirometry variables or CAT score. There was no difference in prevalence of ischaemic heart dis- ease, stroke or diabetes. Aortic PWV or CIMT were not differ- ent between groups. Multiple regression confirmed this (Table). Conclusions A phenotype defined by blood eosinophilia does not relate to cardiorespiratory physiological variables in sub- jects with COPD. REFERENCES 1. Mohan D et al. Journal of COPD 2015. 2. Negewo N et al. Respirology 2017. Abstract P94 Table 1 Cardiorespiratory variables * Absolute eosinophil count Percentage eosinophil count Beta co- efficient 95% CI p- value Beta co- efficient 95% CI p- value Aortic PWV (m/s) 0.23 À1.3 to 1.7 0.77 0.090 À0.29 to 0.47 0.64 CIMT (mm) Diameter right Diameter left 0.16 0.17 À0.60 to 0.91 À0.56 to 0.89 0.69 0.65 0.04 0.05 À0.15 to 0.23 À0.13 to 0.23 0.71 0.59 FEV 1 (L) 0.10 À0.11 to 0.51 0.21 0.06 À0.02 to 0.13 0.15 FVC (L) 0.17 À0.29 to 0.64 0.46 0.12 0.01 to 0.23 0.04 * Adjustment for sex, age, MAP, HR, FEV 1 , FVC, smoking pack years, history of diabetes and peripheral vascular disease P95 CHRONIC OBSTRUCTIVE PULMONARY DISEASE IN SYMPTOMATIC AORTIC STENOSIS: A MAIN UNDERLYING DIAGNOSTIC CONFOUNDER AND PROGNOSTIC FACTOR 1 M Rigolli, 2 A Rossi, 3 PL Temporelli, 2 G Benfari, 4 G Cioffi, 5 S Nistri, 6 N Gaibazzi, 7 F Guidetti, 1 M Bafadhel, 7 P Faggiano. 1 University of Oxford, Oxford, UK; 2 University of Verona, Verona, Italy; 3 Fondazione Salvatore Maugeri, Veruno, Italy; 4 Villa Bianca, Trento, Italy; 5 Veneto Medica, Altavilla Vicentina, Italy; 6 University of Parma, Parma, Italy; 7 University of Brescia, Brescia, Italy 10.1136/thoraxjnl-2017-210983.237 Introduction and Objectives COPD is associated with increased prevalence of cardiovascular comorbidities and mortality from cardiac pathologies. In heart valve diseases, the onset of dysp- noea is the main determinant of outcome and treatment. Thus, COPD may represent a confounding factor in patients with severe aortic stenosis (AS) whilst influencing management. Moreover, the correct diagnosis of COPD in symptomatic AS is extremely challenging. We investigate the prevalence of COPD in patients with symptomatic AS and its relation with all-cause mortality. Methods Consecutive patients with symptomatic severe AS referred to a cardiology tertiary centre for their clinical man- agement were recruited. The severity of aortic valve disease, diagnosis of COPD and symptomatic status were recorded. Patients were treated with either surgical or percutaneous Poster sessions A134 Thorax 2017;72(Suppl 3):A1–278