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Chronic obstructive pulmonary disease: a modifiable risk factor for cardiovascular disease?
  1. Ian S Stone1,2,
  2. Neil C Barnes2,
  3. Steffen E Petersen1
  1. 1Centre for Advanced Cardiovascular Imaging, William Harvey Research Institute, Barts and the London NIHR Biomedical Research Unit, The London Chest Hospital, London, UK
  2. 2Department of Respiratory Medicine, The London Chest Hospital, London, UK
  1. Correspondence to Dr Steffen E Petersen, Centre for Advanced Cardiovascular Imaging, William Harvey Research Institute, Barts and the London National Institute of Health Research Biomedical Research Unit, The London Chest Hospital, Bonner Road, London E2 9JX, UK; s.e.petersen{at}qmul.ac.uk

Abstract

Significant cardiac morbidity and mortality exists in patients with COPD. Shared risk factors include age, smoking history and exposure to air pollution and passive smoke. Although the inappropriate under-prescribing of β-blockers contributes, it is now appreciated that the observed cardiac risk is not only due to smoking and conventional cardiovascular risk factors, but also other independent factors. A number of hypotheses exist for the increased cardiovascular morbidity and mortality seen in COPD including inflammation, pulmonary hypertension, lung hyperinflation and shared genetics models. Mounting evidence from large randomised controlled trials suggests that COPD treatment may be cardio-protective. We review the current evidence supporting the aforementioned hypotheses and how their modulation may prevent cardiovascular morbidity and mortality in COPD. The persisting underdiagnosis of COPD may have significant consequences. Further mechanistic studies identifying the onset and impact of individual interventions will develop our understanding of this emerging and highly relevant clinical field.

  • Imaging and diagnostics
  • MRI
  • lung
  • chronic lung disease
  • myocardial disease
  • cardiomyopathy apical
  • cardiomyopathy hypertrophic
  • myocardial fibrosis
  • ventricular hypertrophy

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Footnotes

  • Funding ISS is an employee of Barts and the London NHS trust who has received a research grant from GlaxoSmithKline. NCB is directly funded by Barts and the London NHS trust. SEP was directly funded by the Barts and The London National Institute for Health Research Cardiovascular Biomedical Research Unit.

  • Competing interests None.

  • Provenance and peer review Commissioned; externally peer reviewed.

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