Introduction

Chronic obstructive pulmonary disease (COPD) is characterised by an irreversible limitation of airflow that is usually progressive.1 A large proportion of patients experience periods with acute exacerbation of COPD symptoms (AECOPD) frequently triggered by airway infections and characterised by local airway and/or systemic inflammation.2 3 COPD is also accompanied by several comorbidities that may represent major health problems for patients. In particular, cardiovascular diseases are common and associated with increased mortality in patients with COPD.4–7 Previous studies have shown that a circulatory marker of myocardial damage, cardiac troponin (cTn), is an independent prognostic marker of mortality in the general population, in patients with stable COPD, and after AECOPD.8–10 The level of cTn has been shown to be inversely related to COPD severity as assessed by spirometry in the stable state.8 10–14 Moreover, the level of cTn has been reported to be higher in patients hospitalised for AECOPD than in patients with COPD in the stable state.15 16 However, prospective studies that examine the trajectory of cTn during the course of COPD are lacking, and whether myocardial damage, as indicated by cTn, progresses during an exacerbated state of COPD has not been determined. Furthermore, the mechanisms that may contribute to elevations in cTn have not been established. We conducted a longitudinal study of cTn in patients with COPD and healthy individuals for 5 years. As our laboratory uses the T-isomere of cTn, we chose T-isomere of cTn as our outcome parameter.

The primary aim of the present study was to test the hypothesis that the cTnT level increases during incident severe AECOPD compared with stable COPD. We also aimed to assess the effect of other hospitalisations on the cTnT level and to elucidate possible mechanism(s) for any increase in cTnT.

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