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Acute exacerbation of COPD is associated with fourfold elevation of cardiac troponin T
  1. Vidar Søyseth1,
  2. Rahul Bhatnagar1,
  3. Nils Henrik Holmedahl2,
  4. Anke Neukamm1,
  5. Arne Didrik Høiseth1,
  6. Tor-Arne Hagve1,
  7. Gunnar Einvik1,
  8. Torbjørn Omland1
  1. 1Department of Medicine, Akershus University Hospital, University of Oslo, Lørenskog, Norway and Faculty of Medicine, University of Oslo, Campus Akershus University Hospital, Lørenskog
  2. 2Glittreklinikken, Hakadal, Norway
  1. Correspondence to Dr Vidar Søyseth, Department of Medicine, Akershus University Hospital, University of Oslo, Sykehusvn 25, Lørenskog 1478, Norway; vidar.soyseth{at}


Objective To investigate if acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is associated with myocardial injury, expressed as elevated high sensitive cardiac troponin T (hs-cTnT), and to identify determinants of hs-cTnT in chronic obstructive pulmonary disease (COPD) patients.

Design In a cross-sectional study, hs-cTnT in patients hospitalised for AECOPD was compared with hs-cTnT in COPD patients in their stable state.

Setting The study was conducted at a teaching and a pulmonary rehabilitation clinic.

Participants Consecutive admissions to participating units for the years 2010–2011 meeting objective, standardised criteria for AECOPD and stable COPD.

Main outcomes Ratio of hs-cTnT in hospitalised AECOPD patients compared with stable COPD patients. Change in the ratio of hs-cTnT per unit increase of relevant covariables.

Results The geometric mean of hs-cTnT in the index group was 25.8 ng/l (95% CI 21.1 to 31.7) compared with 4.55 ng/l (95% CI 3.72 to 5.67) in the reference group. After inclusion of relevant covariables, multiple linear regression analyses showed that the ratio between hs-cTnT in AECOPD patients and the references was 4.26 (95% CI 3.02 to 6.00) and that hs-cTnT increased 1.41-fold (95% CI 1.20 to 1.68), for each quartile increase in leucocyte count in stable COPD but not in AECOPD. Higher hs-cTnT levels were also associated with the presence of pathological q-waves (p=0.012) and electrocardiographic left ventricular hypertrophy (p=0.039), long-term oxygen treatment (p=0.002) and decreasing forced expiratory volume in 1 s (p=0.014). A significant univariable association between cTnT and arterial hypoxaemia was also found but this association was attenuated almost to a zero effect after inclusion of relevant covariates.

Conclusions AECOPD is associated with higher hs-cTnT as compared with stable COPD. In stable COPD, hs-cTnT appears to be positively associated with indices of COPD severity, whereas we were unable to identify significant determinants of hs-cTnT in AECOPD.

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