View clinical trials related to Pulmonary Hypertension.
Filter by:The purpose of this study is to examine if the ingestion of a standard dose of sildenafil enhances the athletic performance of competitive athletes when exercising in a high pollutant environment verses a low air pollutant environment.
The primary objective of this study is to monitor the long-term safety of ambrisentan in adult participants with pulmonary hypertension. The available ambrisentan doses for this study are 2.5, 5, or 10 mg administered orally once daily. Investigators will be able to adjust ambrisentan dose as clinically indicated. A minimum of 4 weeks between dose adjustments is required. Participants receiving other therapies for pulmonary hypertension that are not contraindicated for concomitant use with ambrisentan are permitted to enroll in this study and continue to receive such therapies. Participants enrolled in this study will receive treatment with ambrisentan until such time as the investigator or participant chooses to stop ambrisentan treatment, ambrisentan becomes commercially available, or the sponsor stops the study.
The purpose of the study is is to determine the effect, on the lung circulation, of BQ-123, an investigational compound which is not approved by the FDA.
Pulmonary hypertension (PHT) is an elevation of pulmonary arterial pressure (PAP) that can be the result of heart, lung or systemic disease. PHT also complicates chronic hemodialysis (HD) therapy immediately after the creation of an arteriovenous (AV) access, even before starting HD therapy. It tends to regress after temporary AV access closure and after successful kidney transplantation. Affected patients have significantly higher cardiac output. This syndrome is associated with a statistically significant survival disadvantage. The laboratory hallmark of this syndrome is reduced basal and stimulatory nitric oxide (NO) levels. It appears that patients with end-stage renal disease (ESRD) acquire endothelial dysfunction that reduces the ability of their pulmonary vessels to accommodate the AV access-mediated elevated cardiac output, exacerbating the PHT. Doppler echocardiographic screening of ESRD patients scheduled for HD therapy for the occurrence of PH is indicated. Early diagnosis enables timely intervention, currently limited to changing dialysis modality such as peritoneal dialysis or referring for kidney transplantation.An echocardiographic diagnosis of pulmonary hypertension (PHT) is made when the systolic pulmonary arterial pressure (PAP) exceeds normal values (30 mmHg). In mild PHT, PAP values range up to 45 mmHg, in moderate PHT, PAP is between 45 and 65 mmHg, and in severe PHT, PAP values are greater than 65 mmHg. Systolic PAP equals cardiac output times pulmonary vascular resistance (PVR), (i.e., PAP = cardiac output × PVR). Increased cardiac output by itself does not cause PH because of the enormous capacity of the pulmonary circulation to accommodate the increase in blood flow. Therefore development of PHT requires pathologic, marked elevation of pulmonary vascular resistance. The presence of PH may reflect serious pulmonary vascular disease, which can be progressive and fatal. Consequently, an accurate diagnosis of the cause of PHT is essential in order to establish an effective treatment program. Pulmonary hypertension can occur from diverse etiologies. In 1996 we first noted unexplained PH in some long-term hemodialysis (HD) patients during an epidemiologic study of this disorder (Nakhoul F and Yigla M Rambam Medical Cemter-Haifa). It was assumed that their PHT was related to end-stage renal disease (ESRD) or to long-term HD therapy via an arteriovenous (AV) access. There are several potential explanations for the development of PHT in patients with ESRD. Hormonal and metabolic derangement associated with ESRD might lead to vasoconstriction of pulmonary vessels and increased pulmonary vascular resistance. Values of PAP may be further increased by high cardiac output resulting from the AV access itself, worsened by commonly occurring anemia and fluid overload. Despite almost five decades of HD therapy via a surgically created, often large, hemodynamically significant AV access the long-term impact of this intervention on the pulmonary circulation has received little attention. RD versus AV HD via AV access Proposed Mechanisms: 1. Elevated Parathyroid hormone 2. Metastatic Calcification due to the increase of the calcium-phosphor multiple 3. High cardiac output 4. Nitric oxide-endothelin metabolism 5. A-v Access flow These observations indicate a role for AV access-mediated elevations in cardiac output in the pathogenesis of PH. The correlation between access flow and PAP values has not yet been studied. Since patients undergoing HD therapy via AV access had PH that reversed after successful kidney transplantation and after short AV access compression, we concluded that both ESRD and AV access-mediated elevated cardiac output are required for the development PH. From a physiologic point of view, due to the enormous capacity of the pulmonary microcirculation, increased cardiac output by itself cannot cause PH. It is the inability of the pulmonary circulation of some ESRD patients to accommodate the AV access-mediated elevated cardiac output that leads to the development of PH.
The purpose of this study is to evaluate the efficacy and safety of vardenafil in the treatment of pulmonary arterial hypertension.
This study will determine if a rehabilitation exercise program can help people with pulmonary hypertension (PH) increase their physical activity. Patients with PH have an increase in blood pressure in the pulmonary blood vessels (artery, vein or capillaries) that leads to shortness of breath, dizziness, fainting and other symptoms. Healthy volunteers and people with pulmonary hypertension between 21 and 75 years of age may be eligible for this study. All participants undergo the following tests and procedures: - Medical history and physical examination - 6-minute walk test: Subjects walk as fast as they can for 6 minutes on a walking track to determine their ability to participate in physical activity. - Questionnaires: Subjects complete nine questionnaires related to their fatigue, daily physical activity, mood, and so forth. - Maximum treadmill test: The exercise begins at an easy level and gradually increases until the subject says he or she can no longer continue or the investigator decides it is not safe to continue. Subjects are fitted with a mask, electrodes and light sensors to measure how well the heart is working and how well the muscles use oxygen. Patients with pulmonary hypertension undergo the following additional procedures: - Activity monitoring: Patients wear a monitor for 3 days that measures movement and heart rate. - Group assignment: Patients are randomly assigned to Group 1 (education plus aerobic exercise) or Group 2 (education followed by exercise). - Group 1 patients will attend classes three days a week at either Inova Fairfax Hospital Pulmonary Rehabilitation Center or The National Institutes of Health for 10 weeks. Two sessions a week will include a 1 hour education session as well as a 30-45 minute track or treadmill exercise session. The third session will only include exercise. During the education patients will learn about a healthy lifestyle with pulmonary hypertension. After the 10 weeks of education and exercise, subjects repeat the 6-minute walk test, maximum treadmill test and questionnaires. - Group 2 patients participate in 2; 1-hour educational session at either the Inova Pulmonary Rehabilitation Center or The National Institutes of Health for 10 weeks. After the classes, they repeat the 6-minute walk test, maximum treadmill test and questionnaires. The following 10 weeks will consist of 3 days a week of 30-45 minute track or treadmill walking at either Inova or NIH, after which they again repeat the questionnaires, treadmill and walk tests.
Pulmonary hypertension is a progressive and life threatening condition. It is characterized by severe remodeling of the pulmonary vessel wall, obstructive plexiform lesions, multi-focal thrombosis, and enhanced vasoconstriction. All of these characteristics contribute to increased pulmonary vascular resistance. Circulating endothelial microparticles (EMPs) play an integral role in the pathogenesis and perpetuation of pulmonary hypertension. Levels of EMPs are considered a reliable biological parameter of endothelial injury. We propose to assess the evolution of both circulating and pulmonary venous EMPs in patients with PH. Assessments will be made before and after initiation of Endothelin-1 (ET-1) Receptor blocker therapy, and correlated to their patterns with the changes in mean PAP, the 6 Minutes Walking Distance test, and circulating Endothelin-1 values. Measurements of the endothelial microparticle circulating levels (assessed by flow cytometry methods) will be made before, 1 month and 3 months after initiation of therapy.
The objective of this surveillance is to collect information about 1) adverse drug reaction not expected from the LPD (unknown adverse drug reaction), 2) the incidence of adverse drug reactions in this surveillance, and 3)factors considered to affect the safety and/or efficacy of this drug.
Current standard of the diagnosis and monitoring of PHNT requiring combination of invasive and non-invasive tests. The goal of the study is to correlate data from CT scans, echocardiograms, right heart catheterization, PFTs, sleep studies, and perfusion scans. The ultimate goal is to determine patterns of the PAH disease processes.
The prevalence of an increased pulmonary blood pressure amongst patients with chronic obstructive pulmonary disease (COPD)is unclear. So is the impact of abnormal pulmonary blood pressure on symptoms. The aim of this study is to determine the prevalence of an increased pulmonary blood pressure in 200 patients with COPD. Furthermore we will investigate if lung function test results and blood tests can predict an increased pulmonary blood pressure, and explore whether COPD patients with a high pulmonary blood pressure have more symptoms that their co-patients.