ABSTRACT
Chronic obstructive pulmonary disease (COPD) is defined in terms of airflow obstruction that results from an inflammatory process affecting the airways and lung parenchyma. Despite major abnormalities taking place in bronchial and alveolar structures, changes in pulmonary vessels represent an important component of the disease. Alterations in vessel structure are highly prevalent, and abnormalities in their function impair gas exchange and may result in pulmonary hypertension (PH), an important complication in the natural history of the disease associated with reduced survival and worse clinical course. The prevalence of PH in COPD is not negligible. It can be close to 50% or even greater in patients with advanced disease. In COPD, PH is usually of moderate severity and progresses slowly, without altering right ventricular function in the majority of cases. Nevertheless, a reduced subgroup of patients may present severe PH, which depicts a clinical picture similar to more severe forms of PH and entails high mortality. Studies providing evidence on the important role of the endothelial cell and its derived mediators in the pathogenesis of COPDassociated PH (1) have provided the rationale for the potential use of agents that modulate endothelial function in the treatment of this condition. Although the pathobiology of vascular remodeling in COPD has some similarities with pulmonary arterial hypertension (PAH), studies with drugs used to treat PAH have failed to substantiate any clinical benefit in this clinical setting.
