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Chronic obstructive pulmonary disease (COPD) is predicted to become the sixth leading cause of disability and the third most common cause of death by 2020. Reduced forced expiratory volume in 1 s, a hallmark of COPD, is ranked second to smoking and above blood pressure and cholesterol as a predictor of all-cause and cardiovascular mortality. Even in mild to moderate COPD patients succumb to cardiovascular disease rather than respiratory failure although the causative mechanism is unknown.1
Over the past decade it has become apparent that during an exacerbation of COPD, classically defined by the combination of worsening dyspnoea with increased sputum volume and/or purulence, there is subclinical myocardial damage typified by an increase in troponin level and other biomarkers which predict mortality.2–4 The key question relates to the mechanisms behind this rise, since without an understanding of the mechanisms the ability to identify an appropriate intervention that will improve outcome is hindered.
Søyseth and colleagues5 seek to further the understanding of this relationship. Specifically they addressed the important issue as to whether the raised levels of troponin found at exacerbation are chronically raised or are a phenomenon related to the exacerbation itself, and found that the troponin levels were significantly higher in the exacerbator group compared with stable patients. The study compared those patients admitted to hospital for an exacerbation with those from a pulmonary rehabilitation clinic. It is however questionable whether these groups really represent similar populations in …
Contributors ISS and NCB were responsible for the conception of the manuscript. ISS was responsible for writing and editing of the manuscript while NCB and SEP contributed through the critical appraisal of the manuscript. All authors approved the final draft for publication (NCB is guarantor).
Funding ISS is an employee of Barts Health NHS trust who has received a research grant from GlaxoSmithKline. NCB is directly funded by Barts Health NHS trust. SEP was directly funded by the National Institute for Health Research Cardiovascular Biomedical Research Unit at Barts.
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.
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