View clinical trials related to Pulmonary Arterial Hypertension.
Filter by:Background: For patients with out-of-hospital cardiac arrest (OHCA) at the intensive care unit (ICU), oxygen therapy plays an important role in post resuscitation care. During hospitalisation, a lot of these patients occur with pulmonary arterial hypertension (PAH). Currently a wide oxygen target is recommended but no evidence regarding optimal treatment targets to minimise the prevalence of PAH exists. Methods: The RELIEPH trial is a substudy within the BOX (Blood pressure and OXygenation targets in post resuscitation care) trial. It is a single-center, parallel-group randomised controlled clinical trial. 300 patients with OHCA hospitalised at the ICU are allocated to one of the two oxygenation interventions, either a restrictive- (9-10 kPa) or liberal (13-14 kPa) oxygen target both within the recommended range. The primary outcome is the fraction of time with pulmonary hypertension (mPAP >25 mmHg) out of total time with mechanical ventilation. Secondary outcomes are: length of ICU stay among survivors, lactate clearance, right ventricular failure, 30 days mortality and plasma brain natriuretic peptide (BNP) level 48 hours from randomisation. Discussion: This study hypothesises that a liberal target of oxygen reduces the time with PAH during mechanical ventilation compared to a restrictive oxygen target in patients with OHCA at the ICU. When completed, this study hopes to provide new knowledge regarding which oxygen target is beneficial for this group of patients.
The purpose of this study is: - To assess the effect of BIA 5 1058 400 mg on the pharmacokinetics (PK) of sildenafil. - To assess the effect of sildenafil on the PK of BIA 5-1058.
The purpose of this study is: - To investigate CYP2C9 inhibition by BIA 5-1058 through the assessment of its effect on the Pharmacokinetic (PK) of S-warfarin, a substrate of CYP2C9. - To assess the effect of warfarin on the PK of BIA 5-1058.
The overall objective outlined in this study is to determine how pulmonary vascular remodeling in PAH at a cellular and pathological level is associated with changes in gas exchange physiology and hemodynamics (monitored with 129Xe MRI/MRS) and how these signals change with disease progression or treatment.
the purpose of this study is: - To assess the effect of BIA 5 1058 400 mg on the PK of bosentan. - To assess the effect of bosentan on the PK of BIA 5 1058
the purpose of this study is to determine the effect of age on the Pharmacokinetics (PK) profile of BIA 5-1058 at steady state after multiple oral doses
the purpose of this study is: - to determine the rate and routes of excretion of BIA 5-1058 and the mass balance in urine, feces and exhaled air, after a single oral dose of 400 mg 14C labeled BIA 5 1058 containing 3.7 Megabecquerel (MBq) of radiocarbon; - to determine the pharmacokinetics (PK) of total radioactivity (TRA) in plasma and whole blood and to assess the blood-to-plasma ratio; - to determine the PK of BIA 5-1058 and its metabolites in plasma.
The aim of this study is to investigate the effect of food on the pharmacokinetic (PK) profile of BIA 5-1058 after a single dose in healthy subjects.
An Investigator initiated trial (IIT) using a prospective, randomized, double-blind, parallel group, placebo-controlled, clinical study design.
Pulmonary arterial hypertension (PAH) is a progressive disease in which clinically relevant symptoms present a few years after the onset in rise of pulmonary arterial pressure. Increased PA pressure presents an overload on the right ventricle (RV), with RV failure being a common cause of mortality in PAH. Current therapeutic targets help reduce vascular resistance and RV afterload, however, RV dysfunction may continue to progress. Therefore, the reason for RV failure in PAH cannot be contributed to altered vascular hemodynamics alone but may be related to metabolic alterations and failure of adaptive mechanisms in the RV. Providing a better understanding of metabolic remodeling in RV failure may permit the development of RV-targeted pharmacological agents to maintain RV function despite increased pulmonary vascular pressures. This study will evaluate how cardiac metabolism changes in response to pulmonary vasodilator therapy in patients with pulmonary arterial hypertension.