View clinical trials related to Pulmonary Arterial Hypertension.
Filter by:To evaluate the effect of inhaled treprostinil compared to placebo on exercise capacity and time to clinical worsening.
It has been hypothesized that one of the benefits of bosentan relates to pulmonary vascular remodeling. The investigators believe that this study will help document the nature of beneficial changes that occur in patients with Pulmonary Arterial Hypertension (PAH) in response to bosentan therapy. In turn, demonstrating that changes in pulmonary vascular structure and function accompany clinical improvement.
A multinational, multicenter, double-blind, randomized, placebo-controlled, Phase III study to assess the efficacy and safety of BPS 314d-MR in subjects with pulmonary arterial hypertension currently receiving treatment with an Endothelin Receptor Antagonist (ERA) and/or a Phosphodiesterase-5 Inhibitor (PDE-5 inhibitor). Approximately 100 centers will be participating in the study. Approximately 630 eligible subjects will be randomized 1:1 into two groups, BPS-314d-MR (active) or placebo study drug.
Treatment of PAH includes exercise limitation, non specific agents (anticoagulants, diuretics and supplemental oxygen), pulmonary specific vasodilators and antiproliferative agents. Recent data obtained by our group, within rat PAH models, showed that the antihyperglycemic drug metformin, used in France since 1959 in diabetic type II patients, significantly acts at the pulmonary arteries level. According to these results, and knowing that metformin is a widely used drug, with a favorable safety profile, the investigators decided to set up a pilot study, in order to evaluate the activity of metformin in PAH treatment. In parallel, the investigators will focus on metformin mechanism of action.
The study is to assess if sitaxsentan and ritonavir will affect the blood levels of each other when coadministered.
This study will assess how rifampin will affect the blood levels of sitaxsentan. Safety of sitaxsentan given alone and with rifampin will also be assessed.
To determine the prevalence of myelofibrosis in patients with primary pulmonary hypertension, and to discover if the fibrosis in these patients is primary (AMM) or secondary.
Pulmonary Arterial Hypertension (PAH) in the setting of Idiopathic Pulmonary Fibrosis(IPF)is a risk factor for morbidity and mortality in the peri-lung transplant(LT) setting. Currently there is no significant data to support the use of pulmonary vasodilators for PAH in the setting of interstitial lung disease such as IPF. The majority of IPF patients have PAH either at rest or during exercise. The study hypothesis is that bosentan may improve morbidity and mortality in the peri-LT setting in both IPF cohorts with either resting or exercise PAH.
Pulmonary Arterial Hypertension (PAH) in the setting of Idiopathic Pulmonary Fibrosis(IPF)is a risk factor for morbidity and mortality in the peri-lung transplant(LT) setting. Currently there is no significant data to support the use of pulmonary vasodilators for PAH in the setting of interstitial lung disease such as IPF. The majority of IPF patients have PAH either at rest or during exercise. The study hypothesis is that sildenafil may improve morbidity and mortality in the peri-LT setting in both IPF cohorts with either resting or exercise PAH.
Our goal is to determine clinically in Pulmonary Arterial Hypertension patients if associations exist between the efficacy and toxicity of sitaxsentan, bosentan, and ambrisentan and several gene polymorphisms in several key disease-specific and therapy specific genes. Also characterized is the relationship between these polymorphisms and the severity of Pulmonary Arterial Hypertension using either baseline hemodynamic or clinical surrogates for disease severity. Hypothesis: Polymorphisms influence the efficacy and toxicity of specific Pulmonary Arterial Hypertension therapy as well as development/severity of PAH via their effect on PA remodeling, drug response, or metabolism. This study requires a one time 8.5 ml blood sample and clinical data to be obtained at initiation of therapy, 4 months after initiation of therapy and 12 months after initiation of therapy.