View clinical trials related to Pulmonary Arterial Hypertension.
Filter by:The objective of this project is to determine how pulmonary vascular remodeling in Pulmonary Arterial Hypertension (PAH) at cellular and pathological level is associated with gas exchange physiology changes and hemodynamics (monitored with 129Xe MRI/MRS) and how these signals change with disease progression or treatment.
The purpose of this study is to learn what happens to macitentan and its active metabolite (aprocitentan) in the body of children aged between 1 month and 2 years.
This study will determine the feasibility of a mobile application-based home exercise rehabilitation program for patients with pulmonary hypertension.
The overall objective of this study is to fulfill the Pilot study (miRNA and Myokines Acutely-expressed During Exercise) goal to Investigate the excretion of skeletal muscle-derived miRNA and myokines in patients with pulmonary arterial hypertension during acute exercise that are biologically active and modulate skeletal muscle function during exercise. Pulmonary arterial hypertension (PAH), is characterized by the proliferation of endothelial and smooth muscle cells within the precapillary pulmonary vasculature, if untreated results in increased pulmonary vascular resistance and death. The hallmark perivascular infiltrates in PAH contain inflammatory macrophages and lymphocytes resulting in endothelial dysfunction and involves the dysregulation of distinct inflammatory mechanisms. Idiopathic PAH (iPAH) and scleroderma-associated PAH (SSc-PAH), are related by similar clinical and pathophysiologic features. Patients with PAH experience a central cardiovascular limitation to exercise. Despite effective treatment with pulmonary vasodilators, many resting PAH (rPAH) patients continue to experience exercise intolerance. PAH is increasingly acknowledged as a systemic disease, beyond abnormalities of the pulmonary vasculature. Although other contributions to exercise intolerance in PAH exist, skeletal muscle dysfunction significantly impacts exercise tolerance. The molecular mechanisms behind skeletal muscle dysfunction in PAH remain unclear. Provocative testing with invasive cardiopulmonary exercise testing challenges the cardio-pulmonary-vascular and skeletal muscle systems and elicits a cascade of physiologic events not measurable at rest. Myokines are circulating mediators released from skeletal muscle in an endocrine-like fashion in disease and health influencing many factors but not limited to systemic inflammation, immunity and endothelial function. Myokines have not been well described in PAH. Preliminary data indicate that myokines play important, yet still undescribed, roles in this disease. MicroRNAs (miRNAs) are small non-coding RNA molecules, which negatively regulate gene expression via repressing translation and degrading messenger RNAs through sequence-specific binding. There is a growing literature regarding the biological activity of extracellular miRNAs in PAH and in aerobic exercise. miR-126 has been implicated in skeletal muscle dysfunction in PAH, while miR-133 is skeletal muscle-specific but unlike miR-126 it is not yet implicated in skeletal muscle dysfunction in PAH.
The purpose of the Implantable System for Remodulin (ISR) Post Approval Study (PAS) is to provide evaluation and periodic reporting of the safety and effectiveness of Medtronic market-released ISR, including the catheter and the pump.
Study to evaluate the efficacy, safety, tolerability and pharmacokinetics of JTT-251 administered for 24 weeks in participants with pulmonary arterial hypertension (PAH)
Study of PAH Subjects with LTOT Use that have Demonstrated Improved Exercise Tolerance with the use of Inhaled Nitric Oxide
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 a multicenter, randomized (2:1 oral treprostinil: placebo), double-blind, placebo-controlled study in subjects with Pulmonary Arterial Hypertension (PAH) who are currently receiving background dual therapy (ambrisentan, tadalafil) for at least 30 days at randomization for their PAH. Once randomized, subjects will return for 5 study visits up to Week 28 during the blinded period. After the Week 28 Visit, eligible subjects will transition to the open-label period of the study for up to 20 weeks.
The investigators are doing this research study to find out how blood flow changes in the lungs of people with pulmonary hypertension before and after treatment with ambrisentan (sold under the brand name Letairis). The investigators hope that knowing about these differences will help us to better understand pulmonary hypertension and find new ways to diagnose it earlier.