Acute exacerbations of chronic obstructive pulmonary disease (COPD) punctuate important disease progression [1]. In-hospital mortality rates for acute exacerbations of COPD vary between 2.5% to 24.5% [2–4]. An integrated clinical score, CURB-65, has been proposed to predict in-hospital and 30-day mortality in acute exacerbations of COPD [5, 6]. According to death-certificate data the most common proximate cause of death in COPD is cardiac disease [7]. An association between elevated cardiac high-sensitivity troponin (hs-cTn) at admission and mortality has been reported in acute exacerbations of COPD [8, 9]. Copeptin has also been associated with poor clinical outcomes and mortality of acute exacerbations of COPD [10], as well as pneumonia [11] and myocardial infarction [12]. Recently, the combination of elevated copeptin and hs-cTn at admission for acute chest pain has been shown to have better discriminative value for acute myocardial injury [13] than troponin alone, as well as strong prognostic value for major cardiac adverse events [14]. We hypothesised that myocardial injury may be an important cause of death in patients admitted with an acute exacerbations of COPD. Accordingly, we investigated whether circulating markers of myocardial injury at the time of presentation to the emergency department (ED) with acute exacerbations of COPD added prognostic value to the CURB-65 score. Initial results were derived in a discovery cohort of 356 consecutive adult patients with acute exacerbations of COPD who presented to the EDs at the Christchurch Heart Institute (New Zealand, n=160), Lariboisière Hospital in Paris (France, n=112), Monastir University Hospital (Tunisia, n=55) and Sivas University Hospital (Turkey, n=29). Median (interquartile range) age was 72 (63–79) years and 57% were male. A prior history of COPD was present in 85%, heart failure in 20% and hypertension in 41% of subjects. At admission, the median systolic blood pressure was 140 (123–160) mmHg, median heart rate was 98 (86–112) min –1 and median respiratory rate was 26 (22–32) min –1. The median length of hospital stay was 4 (1–8) days. 44 patients (12.4%) were admitted to an intensive care unit. 27 patients (7.6%) died during the 30-day follow-up period. An independent validation cohort comprised consecutive patients with acute exacerbations of COPD prospectively enrolled at the Basel University Hospital (Switzerland, n=135). The validation cohort had similar characteristics to the derivation cohort and 30-day mortality was 7.8%. This study was performed in accordance with the declaration of Helsinki. All patients provided written informed consent. CURB-65 was calculated by using information collected upon admission to the ED [5]. The CURB-65 score was indicative of low risk (0–1) in 51% of the derivation cohort, intermediate risk (2) in 32% and high risk (⩾3) of 30-day mortality in the remaining 17%. The primary end-point was 30-day all-cause mortality. Follow-up by phone interview for events to 30 days was completed. Receiver operating characteristic (ROC) curve analysis yielded an area under the curve (AUC) of 0.67 (95% CI 0.57–0.76) for the prediction of 30-day mortality by using the CURB-65 score. Blood samples were collected within 4 h of admission into tubes containing ethylenediaminetetra-acetic acid (EDTA) with immediate separation of plasma, which was stored at −80°C prior to assay. We measured five biomarkers that reflect different pathophysiological pathways: inflammation and/or infection by C-reactive protein (CRP, Abbott laboratories, Abbott Park, IL, USA) and procalcitonin (PCT, Thermo-Fisher B.R.A.H.M.S. AG, Hennigsdorf, Germany); myocardial damage by high-sensitivity cardiac @ERSpublications Acute exacerbated COPD patients with elevated markers of myocardial injury are at high risk of early mortality