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OCCASIONAL REVIEW |
1 Department of Pathology, University of British Columbia, Vancouver, BC, Canada
2 Department of Medicine, University of British Columbia and Head, Respiratory Division, St Paul’s Hospital, Vancouver, BC, Canada
Correspondence to:
Correspondence to:
Dr J L Wright
Department of Pathology, 2211 Wesbrook Mall, Vancouver, BC, Canada V6T 2B5; jlwright{at}interchange.ubc.ca
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.
Abbreviations: 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
Keywords: chronic obstructive pulmonary disease; pulmonary hypertension; cigarette smoke; vasoactive mediators; emphysema
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