View clinical trials related to Pulmonary Arterial Hypertension.
Filter by:Patients with scleroderma can develop heart failure due to high blood pressure in the lungs (a condition called pulmonary arterial hypertension). It is important to find pulmonary arterial hypertension early, so that it can be treated before heart failure develops. However, the tests that we now use to find the earliest form of this disease in scleroderma patients are not good enough. This study will examine whether tests performed during exercise can improve our ability to find early pulmonary arterial hypertension. The study will also try to identify genes that are responsible for the development of pulmonary arterial hypertension.
The purpose of this study to look at differences in the way the heart functions in people with pulmonary hypertension (PH) who have near normal right ventricle (RV) function and people with pulmonary hypertension who have impaired RV function. The right ventricle is a chamber of the heart that pumps blood into the pulmonary artery (the artery that carried blood from the heart to the lungs). Learning more about how the heart is working in people with pulmonary hypertension may help researchers to understand how to better treat pulmonary hypertension and prevent the disease from getting worse. To do this, we will use two imaging techniques, MRI (Magnetic Resonance Imaging) and PET/CT (Positron Emission Tomography/Computed Tomography). MRI uses a strong magnet and radio waves to take pictures of your heart. A PET/CT scan combines a PET and CT scan into one machine. A CT scan uses x-0rays to take a 3-day picture of the inside of your body, while a PET scan measures small amounts of radiation from a dye called a "tracer" that we inject into your veins. You will be given two tracers as part of the PET/CT scan. A tracer is a special type of dye with a small amount of radioactivity in it. The tracers that are used in this study are called [18F]fluorodeoxyglucose (FDG) and [11C]-acetate. In order to take part in this study, you must also have agreed to take part in a companion study. In the companion study, we are trying to learn whether the drug ranolazine is safe and effective in people with PH.
This clinical trial will study the safety, tolerability, and pharmacodynamics of single doses of MK-8892 in participants with pulmonary arterial hypertension (PAH). The primary objective is to estimate the measured peak effect of the highest acutely tolerated (HAT) single oral dose of MK-8892 on pulmonary vascular resistance (PVR).
A sub-study to the TDE-PH-304 protocol to assess the pharmacokinetics of patients transitioning from a twice daily dosing regimen of oral treprostinil to a three times daily dosing regimen.
This study will evaluate the safety, tolerability, and PK of MK-8892 in participants with pulmonary arterial hypertension. The primary hypothesis is that the geometric mean of MK-8892 area under the concentration time-curve from Hour 0 to 24 hours (AUC0-24hr) in participants with PAH, will be equal to or greater than the efficacious exposure in humans of 0.6 μM•hr.
This is a multicenter, double-blind, randomized, placebo-controlled Phase 3 study, to assess the efficacy and safety of BPS-314d-MR when added-on to inhaled treprostinil (Tyvaso®)in patients with pulmonary arterial hypertension. Patients new to Tyvaso, will enter a run-in period on inhaled treprostinil until 90 days of experience is achieved to ensure drug tolerability before enrolling in the study. Treatment groups consist of one active and one placebo group. Subjects will be randomly allocated in a 1:1 ratio to one of the two treatment groups.
Pulmonary arterial hypertension (PAH), or high blood pressure in the lungs, is a rare condition that can shorten life. Although the cause of this disease is usually unknown, in about 70% of heritable and 15-20% of idiopathic cases there is a change in a gene (a mutation) that controls how blood vessels grow and function. The gene is called bone morphogenetic protein type receptor 2 (BMPR2). Although mutations in BMPR2 are a risk factor for PAH, not everyone with a mutation gets the disease. Additional genetic and environmental factors are likely to contribute. The investigators suspect that mutations in other genes are responsible for some cases of PAH. In this study the investigators aim to recruit all patients with PAH and some of their relatives and follow them up for several years. The investigators hope to discover new mutations for this disease and to determine what factors lead to poor outcome, and to understand what triggers disease in patients with mutations. Who can participate? Adults with PAH, their relatives and controls (one off blood sample)
Pulmonary arterial hypertension is a disease characterised by pathological changes in the pulmonary arteries leading to a progressive increase in pulmonary vascular resistance and pulmonary artery pressure. Right ventricular failure is the main cause of death in patients with pulmonary arterial hypertension, and the ability of the right ventricle to adapt to the progressive increase in pulmonary vascular resistance associated with changes to the pulmonary vasculature in pulmonary arterial hypertension is the main determinant of a patient's functional capacity and survival. Right ventricular dyssynchrony was present in a substantial proportion of patients with pulmonary arterial hypertension and this dyssynchrony adversely affected right ventricular function.
The purpose of this study is to provide Sildenafil therapy for subjects who completed A1481156 study and are judged by the investigator to derive clinical benefit from continued treatment with Sildenafil, prior to reimbursement and availability for subjects in the Russian Federation.
Our hypothesis is that optimal treatment of the dysfunctional metabolic pathways which underlie PAH will improve pulmonary vascular function and consequences of the disease.