Impact of Inhaled Treprostinil Sodium on Ventilation Perfusion Matching
Pulmonary Arterial Hypertension
Chronic Obstructive Pulmonary Disease
|Study Design:||Observational Model: Case-Only
Time Perspective: Prospective
|Official Title:||An Open-Label Study to Explore the Impact of Inhaled Treprostinil Sodium on Ventilation Perfusion Matching When Used for Treatment of Group 1 Pulmonary Arterial Hypertension in Patients With Concomitant Chronic Obstructive Pulmonary Disease (COPD)|
- Change in Oxygen saturation in subject initiated on inhaled treprostinil sodium for treatment of PAH who have concomintant COPD. [ Time Frame: Dec 2014 ]
- Change in 6MWT in subject initiated on inhaled treprostinil sodium for treatment of PAH who have concomintant COPD. [ Time Frame: December 2014 ]
- SGRQ questionaires [ Time Frame: December 2014 ]
|Study Start Date:||November 2011|
|Study Completion Date:||December 2014|
|Primary Completion Date:||December 2014 (Final data collection date for primary outcome measure)|
In patients with severe COPD where the FEV1 is 50% or less than predicted, emphysema and obliterating bronchiolitis presenting a "ceiling" to any improvement in function that can be achieved by therapies that dilate the airways or lessen inflammation. Such severe COPD is commonly associated with pulmonary hypertension at rest or during exercise. Although hypoxia has been classically considered to be the major pathogenic mechanism of pulmonary hypertension in COPD and oxygen has been the mainstay of therapy, other mechanisms may play important roles. Indeed, endothelial dysfunction can be observed in patients with mild to moderate COPD who do not have hypoxemia and in smokers with normal lung function. In addition, long-term oxygen therapy does not generally result in resolution of the pulmonary hypertension. A key question that remains is whether the newer therapies for pulmonary arterial hypertension (PAH) could improve pulmonary hypertension and therefore exercise tolerance in COPD.
Unfortunately the use of non-selective pulmonary vasodilator therapy in oral, intravenous or subcutaneous form for PAH patients who have unrelated concomitant COPD, is known to cause worsening gas exchange and intensification of symptoms despite a decrease in pulmonary vascular resistance and arterial pressures.
We hypothesize that an inhaled pulmonary vasodilator may not worsen ventilation-perfusion mismatching by selectively vasodilating well ventilated areas in PAH patients with concomitant COPD and in fact may improve ventilation perfusion matching leading to preservation or improvement of oxygenation.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01494896
|United States, Florida|
|University of Florida, Jacksonville|
|Jacksonville, Florida, United States, 32209|
|Jacksonville, Florida, United States, 32224|
|Cleveland Clinic Florida|
|Weston, Florida, United States, 33331|
|Principal Investigator:||Abubakr A Bajwa, MD, FCCP||University of Florida|