Pulmonary hypertension in COPD: A review and consideration of the role of arterial vasodilators

Abstract

The possibility that pulmonary hypertension (PH) may develop in patients with chronic obstructive pulmonary disease (COPD) is well established, but prevalence data vary. The current World Health Organization clinical classification includes COPD in diagnostic group III: PH associated with disorders of the respiratory system or hypoxemia. The National Institute of Health defines PH as a mean pulmonary artery pressure of greater than 25 mmHg. Approximately 10 of the patients seen over the last decade in the PH Clinic at Mayo Clinic in Jacksonville, Florida, have PH due to COPD. The pathophysiology is likely complex and involves hypoxic pulmonary vasoconstriction. Ultimately, chronic hypoxia results in vascular remodeling with narrowing of the vascular lumen. The right heart is forced to generate increased driving pressures to overcome the increased vascular resistance. As the disease progresses, cor pulmonale may develop. The mortality in this setting is increased with five-year survival of 20 to 36 and seems to correlate with worsening PH and age. Fortunately, the PH in most cases is mild and occurs primarily in those with severe hypoxemia. Only 1 to 4 of patients have PH seemingly out of proportion to the severity of the COPD. This disproportionate subgroup may represent an important phenotype that requires a different therapeutic approach. Although supplemental oxygen remains the primary treatment for all PH in association with chronic hypoxia, pulmonary arterial vasodilators may have a therapeutic role in this subgroup. Vasodilators may worsen gas exchange, however, and to date, have no proven benefit. Rigorous future study will be required to determine whether there is a role for using pulmonary arterial vasodilators in this setting.