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Copyright ©ERS Journals Ltd 2003
Pulmonary hypertension in chronic obstructive pulmonary disease
Dept of Pulmonary Medicine, Institute of Biomedical Research Augusti Pi i Sunyer (IDIBAPS), Hospital Clinic, University of Barcelona, Spain
CORRESPONDENCE: J.A. Barberà, Servei de Pneumologia, Hospital Clínic, Villarroel 170., 08036, Barcelona, Spain. Fax: 34 932275455. E-mail: jbarbera@clinic.ub.es.
Keywords: chronic hypoxaemia, cigarette-smoke effects, endothelium, pulmonary artery, vascular remodelling, vasodilators
Received: December 12, 2002
The authors have been supported, in part, by research grants from Fondo de Investigación Sanitaria (FIS), Sociedad Española de Neumología y Cirugía Torácica (SEPAR), and Societat Catalana de Pneumologia (SOCAP).
Abstract
Pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD). Its presence is associated with shorter survival and worse clinical evolution. In COPD, pulmonary hypertension tends to be of moderate severity and progresses slowly. However, transitory increases of pulmonary artery pressure may occur during exacerbations, exercise and sleep. Right ventricular function is only mildly impaired with preservation of the cardiac output.
Structural and functional changes of pulmonary circulation are apparent at the initial stages of COPD. Recent investigations have shown endothelial dysfunction and changes in the expression of endothelium-derived mediators that regulate vascular tone and cell growth in the pulmonary arteries of patients with mild disease. Some of these changes are also present in smokers with normal lung function. Accordingly, it has been postulated that the initial event in the natural history of pulmonary hypertension in COPD could be the lesion of pulmonary endothelium by cigarette-smoke products.
Long-term oxygen administration is the only treatment that slows down the progression of pulmonary hypertension in chronic obstructive pulmonary disease. Nevertheless, with this treatment pulmonary artery pressure rarely returns to normal values and the structural abnormalities of pulmonary vessels remain unaltered. Vasodilators are not recommended on the basis of their minimal clinical efficacy and because they impair pulmonary gas exchange. Recognition of the role of endothelial dysfunction in the physiopathology of pulmonary hypertension in chronic obstructive pulmonary disease opens new perspectives for the treatment of this complication.
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