Oral Sildenafil for Exercise Capacity, Dyspnea and Cardiopulmonary Function in COPD
Status:
Not yet recruiting
Trial end date:
2025-06-01
Target enrollment:
Participant gender:
Summary
Chronic obstructive pulmonary disease (COPD) is a condition characterized by airway
obstruction. Patients with COPD experience significant shortness of breath on exertion. The
mechanisms responsible for shortness of breath on exertion are well understood in moderate
and severe COPD, but, are poorly understood in mild COPD where symptoms appear
disproportionate to the degree of airway obstruction.
Mild COPD patients show an exaggerated breathing response to exercise, determined by the
breathing response to carbon dioxide production (V̇E/V̇CO2). Recent work suggests that the
increased V̇E/V̇CO2 during exercise in mild COPD is secondary to increased deadspace (i.e.
lung regions with ventilation but no perfusion) and/or ventilation/perfusion (V̇A/Q)
inequality (poor matching of ventilation to perfusion). Researchers have proposed that the
increased deadspace or V̇A/Q inequality is secondary to pulmonary vascular dysfunction and
hypoperfusion of the pulmonary capillaries.
Recently, we have shown that inhaled nitric oxide, a potent dilator of pulmonary vasculature,
reduces shortness of breath and V̇E/V̇CO2, and improves exercise capacity in mild COPD. This
preliminary finding suggests that pulmonary vascular dysfunction is an important contributor
to exercise intolerance in mild COPD. Here, we aim to test whether sildenafil, an oral
pulmonary vasodilator, can improve exercise tolerance and shortness of breath in mild COPD.