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Authors' response
  1. C L Chang1,
  2. R J Hancox1,2
  1. 1Department of Respiratory Medicine, Waikato Hospital, Hamilton, New Zealand
  2. 2Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand
  1. Correspondence to Dr C L Chang, Department of Respiratory Medicine, Waikato Hospital, Level 01 Menzies Building, Waikato Hospital, Hamilton 3204, New Zealand; contact_cat{at}

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We thank Bertoletti and colleagues for raising the important issue of pulmonary embolism (PE) in the exacerbation of chronic obstructive pulmonary disease (COPD).1 Although we did not routinely investigate for PE in our cohort, we excluded any patients with suspected or confirmed PE from the study.2 Unfortunately, it is difficult to detect thromboembolic events in this population and it is possible that we included some patients with subclinical pulmonary emboli. It is also plausible that this contributed to the association between elevated cardiac biomarkers and mortality. However, we think that this is unlikely to be the only mechanism.

Thromboprophylaxis was administered to some patients during their admission depending on their immobility and other risk factors, but this would not have influenced the NT-proBNP or troponin T results obtained on presentation. We did not collect information on pre-existing anticoagulation therapy on admission to the study.

Further research into the mechanism linking elevated cardiac biomarkers and mortality in COPD exacerbation is needed. We agree with Bertoletti and colleagues that investigating the contribution of concurrent PE is important, as this is something that can be treated.


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  • Linked article 200416

  • Competing interests None.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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