Active clinical trials for "Pulmonary Arterial Hypertension"

The purpose of this study is to compare the bioavailability of a single 1mg dose of treprostinil diethanolamine sustained release (SR) tablets manufactured by two independent facilities.

Administration of iloprost aerosol comparing two nebulizers: FOX and I-Neb

This protocol describes an open-label phase 2 clinical trial of fluoxetine in PAH looking at change in pulmonary vascular resistance (PVR) as the primary endpoint. In this open-label clinical trial, 18 patients with pulmonary arterial hypertension will be given fluoxetine for 24 weeks. A Right Heart Catheterization will be performed at baseline and 24 weeks. Change in PVR will be the primary endpoint; other hemodynamic endpoints, quality of life, QIDS-SR depression scale, functional class and six-minute walk distance will also be evaluated. Primary Hypothesis: Fluoxetine treatment for 24 weeks will lead to significantly lower pulmonary vascular resistance in 18 patients with PAH in patients treated in an open-label clinical trial.

Multicenter, double-blind, randomized, placebo-controlled, cross-over study to demonstrate that a single infusion of tezosentan has minimal effect on blood pressure in patients with pulmonary arterial hypertension, treated with endothelin receptor antagonists, phosphodiesterase-5 inhibitors or a combination of both.

This is a multi-center, open-label study of sitaxsentan sodium 100 mg taken orally once daily by subjects with PAH until sitaxsentan, in a particular country or region, is commercially available for the treatment of PAH or the study is closed.

This study is designed to describe pulmonary arterial hypertension (PAH) participants in terms of their clinical characteristics, therapies used, disease progression, and outcomes (example, death, hospitalization, risk category for predicted mortality risk, and patient-reported outcomes [PROs]) in real-world clinical practice. This study will collect high-quality real-world data that may be used as a stand-alone dataset or in combination with other studies to address relevant research questions (example, serve as an external control dataset to another study) to support development and access to PAH therapies, as well as to contribute to the knowledge base of PAH through publications.

This is a multicenter, single-arm trial to evaluate the safety of the transition from Selexipag to Remodulin® then Oral Treprostinil in Symptomatic Subjects with Pulmonary Arterial Hypertension (PAH). The study will include about 30 subjects at approximately 10 clinical trial centers. The treatment phase of the study will last approximately 16 weeks.

This is an open-label, multicenter, parallel, randomized (1:1 Slow Dose Titration Group; Rapid Dose Titration Group), two-group study to evaluate the safety, tolerability, pharmacokinetics and efficacy of slow and rapid dose titration regimens of subcutaneous Remodulin infusion in subjects with pulmonary arterial hypertension (PAH). The study will include about 50 subjects at up to 10 clinical trial centers in China. The treatment phase of the study will last approximately 16 weeks. Subjects who complete all required assessments will also be eligible to enter a long-term open-label, extension study (CVT-CV-004).

Pulmonary arterial hypertension (PAH) is a disorder of elevated pulmonary vascular resistance characterized by progressive remodeling and obliteration of vessels of the distal pulmonary circulation. Outcomes in PAH could be improved with earlier diagnosis, and with the early deployment of therapies before irreversible changes have occurred. This study tests the sensitivity of positron emission tomography (PET)-CT scanning with [89Zr]-bevacizumab, a radioisotope-conjugated anti-VEGF antibody for detecting pulmonary vascular remodeling in PAH disease. This test could enable non-invasive diagnosis early in the course of the disease, and potentially improve outcomes in PAH,

Pulmonary arterial hypertension (PAH) is a serious and eventually fatal disease damaging the lungs and the heart. It results from narrowing and eventual blockage of small blood vessels in the lung, due to abnormal proliferation of cells in the blood vessel (arterial). Patients with PAH suffer from fatigue, shortness of breath, low oxygen levels, blood clots and heart failure. No therapies reverse the disease process in the lung arteries, however there are three approved drugs that can temporarily dilate the vessels and improve symptoms. However, all three drugs have significant side effects and toxicities, they do not work effectively in many patients, survival remains on average only 2 to 3 years once symptoms begin, and none of these drugs prevent the underlying disease process in the small arteries of the lung. PAH is known to develop in patients with a pre-existing class of bone marrow diseases called myeloproliferative disorders (MPDs). We and others have recently shown that patients with PAH have bone marrow changes similar to those seen in patients with MPDs, even without other signs and symptoms of those bone marrow diseases such as anemia or high platelet and white blood cell counts. Compared to healthy volunteers, patients with PAH have a higher frequency of immature stem and progenitor cells able to produce blood cells and vascular wall cells in their bone marrow. They also have higher circulating numbers of these cells in the blood, and increased localization of these cells in the lung blood vessels. When immature bone marrow cells from PAH patients and normal volunteers were infused into mice, the mice receiving PAH marrow cells developed similar lung and heart problems to PAH patients, suggesting that the bone marrow problem is a primary cause of the lung problems, and that the increased numbers of immature bone marrow cells in the bone marrow and blood of PAH patients causes the lung blood vessel disease. The drug hydroxyurea is used to inhibit the abnormally high level of bone marrow cell proliferation in patients with MPDs. It has been shown to reduce the numbers of circulating immature bone marrow cells in patients with MPDs. Hydroxyurea has been available for almost fifty years, and has been used to treat patients with MPDs, sickle cell anemia, and congenital heart disease for very prolonged periods of time, up to twenty or more years in individual patients. It has an excellent long-term safety profile and few side effects and is generally well tolerated. It does not appear to result in an increased rate of leukemia even with many years of treatment. In the current protocol, we hypothesize that treating patients with PAH with hydroxyurea will decrease the level of circulating immature bone marrow cells and interrupt the abnormal narrowing and occlusion of lung arteries. We will treat patients with moderately severe primary (no known underlying cause) PAH with 6 months of hydroxyurea, carefully monitoring side effects and adjusting dosage as necessary, and measure the effect on circulating immature cells, lung blood vessel pressures, other blood markers of active PAH, and exercise tolerance.