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Pulmonary hypertension in chronic obstructive pulmonary disease: current theories of pathogenesis and their implications for treatment
  1. J L Wright1,
  2. R D Levy2,
  3. A Churg1
  1. 1Department of Pathology, University of British Columbia, Vancouver, BC, Canada
  2. 2Department of Medicine, University of British Columbia and Head, Respiratory Division, St Paul’s Hospital, Vancouver, BC, Canada
  1. Correspondence to:
    Dr J L Wright
    Department of Pathology, 2211 Wesbrook Mall, Vancouver, BC, Canada V6T 2B5;


The development of pulmonary hypertension is a poor prognostic sign in patients with chronic obstructive pulmonary disease (COPD), affecting both mortality and quality of life. Although pulmonary hypertension in COPD is traditionally viewed as a result of emphysematous destruction of the vascular bed and/or hypoxia, recent studies indicate that neither of these factors correlates very well with pulmonary artery pressures. New human and animal experimental data are beginning to show that pulmonary hypertension in this setting is probably a result of the direct effect of tobacco smoke on the intrapulmonary vessels with abnormal production of mediators that control vasoconstriction, vasodilatation, and vascular cell proliferation, ultimately leading to aberrant vascular remodelling and aberrant vascular physiology. These changes are in many ways similar to those seen in other forms of pulmonary hypertension and suggest that the treatments used for primary pulmonary hypertension may be beneficial in patients with COPD.

  • eNOS, endothelial nitric oxide synthase
  • ET-1, endothelin-1
  • FEV1, forced expiratory volume in 1 second
  • NO, nitric oxide
  • Pao2, arterial oxygen tension
  • VEGF, vascular endothelial growth factor
  • chronic obstructive pulmonary disease
  • pulmonary hypertension
  • cigarette smoke
  • vasoactive mediators
  • emphysema

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  • This study was supported by grant MOP 62693 from the Canadian Institutes of Health Research. The work is independent of the funders.

  • Competing interests: JLW and AC have received funds from AstraZeneca to examine animal models of emphysema and to test the effectiveness of various compounds under development. RDL has served on advisory boards for Actelion in 2002 ($1000 CAD), 2003 ($2500 CAD) and 2004 ($1200 CAD), has served as a consultant to GlaxoSmithKline ($3375 CAD in 2003) and Northern Therapeutics ($1750 CAD in 2004), and has received fees from Actelion for lecturing at continuing health education activities ($2000 CAD in 2002; $750 CAD in 2003; $1250 in 2004) and $34 000 CAD from Encysive, LP as a research grant for participating in a multicentre clinical trial in 2003–4.