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High-sensitivity cardiac troponin in patients with stable chronic obstructive pulmonary disease: looking beyond the lungs
  1. Anke Neukamm,
  2. Arne Didrik Høiseth,
  3. Vidar Søyseth,
  4. Torbjørn Omland
  1. Division of Medicine, Akershus University Hospital, and Institute of Clinical Medicine, University of Oslo, Lørenskog, Norway
  1. Correspondence to Professor Torbjørn Omland, Division of Medicine, Akershus University Hospital, and Institute of Clinical Medicine, University of Oslo, Lørenskog 1478, Norway

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The Authors' reply We thank doctors A Mirrakhimov and E Mirrakhimov for their interest in our work1 concerning cardiac troponins in chronic obstructive pulmonary disease (COPD).2 Cardiac troponins have previously been shown to be strongly associated with the risk of cardiovascular death in the general population and mortality after COPD exacerbations.3

Cardiac troponins are known to be highly specific, yet the potential release mechanisms are still under debate. In addition to myocyte necrosis, apoptosis, transport across a compromised cell membrane and the formation of cytoplasmic membranous blebs during ischaemia have been proposed as possible mechanisms for troponin release. Increased myocardial strain has also been increasingly recognised as a possible cause of chronic, low-grade troponin elevation. This draws the attention to possible relations between structural changes in pulmonary tissue and vasculature and right ventricular strain and remodelling as potential additional explanatory mechanisms for troponin elevation within this particular patient group.4

Doctors Mirrakhimov and Mirrakhimov also address the issue of COPD as a risk factor for diabetes mellitus and renal disease. We share their enthusiasm concerning these recent discoveries. Our study was, however, not primarily designed to investigate this association. The prevalence of diabetes was low (3%), and most of our COPD patients had normal serum creatinine concentrations. In our moderately sized sample, the prevalence of diabetes and renal failure among COPD patients and controls was not significantly different, and no association between diabetes or kidney function and troponin elevation was observed.

We agree that it is of great importance to further investigate potential pathways through which COPD might increase the risk of cardiovascular disease, including diabetes and renal dysfunction, and to relate these pathways to emerging phenotypes of COPD.5 We strongly believe that such studies will be required to better understand, diagnose, treat and prevent the progression and complications of COPD.


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  • Contributors All authors contributed to the manuscript.

  • Competing interests None.

  • Ethics approval Ethics Committee.

  • Provenance and peer review Commissioned; internally peer reviewed.

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