Active clinical trials for "Hypertension, Pulmonary"

The purpose of this study is to demonstrate the safety and efficacy of inhaled Iloprost (Ventavis®) among adult Chinese patients with primary pulmonary hypertension, which is in compliance with Chinese SFDA regulation.

It has been shown, that subjects susceptible to high altitude pulmonary edema (HAPE)are characterized by an abnormal increase of pulmonary artery pressure at rest in hypoxia and during exercise in normoxia. This abnormal rise of pulmonary artery pressure has also been observed in about 10 % of otherwise healthy subjects without prior altitude exposure. The aim of the study is to investigate the susceptibility to HAPE in unacclimatized subjects with abnormal increase of pulmonary artery pressure at rest in hypoxia and during exercise in normoxia after rapid ascent to high altitude (4559 m).

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.

Primary pulmonary hypertension (PPH) is a rare lung disorder in which the blood pressure in the pulmonary artery rises far above normal levels for no apparent reason. The pulmonary artery is a blood vessel carrying oxygen-poor blood from the right ventricle (one of the heart's pumping chambers) to the lungs. In the lungs, the blood picks up oxygen, then flows to the heart's left side, where the left ventricle pumps it to the rest of the body through the aorta. In the United States, an estimated 500 to 1,000 new cases of primary pulmonary hypertension are diagnosed each year. The greatest number is reported in women between ages 20 and 40. However, men and women in all age ranges as well as very young children can develop PPH. Researchers have identified more than 40 BMPR2 mutations that can cause primary pulmonary hypertension. Many of these mutations introduce a stop signal that halts protein production prematurely, decreasing the amount of functional BMPR2 protein. Other mutations prevent the BMPR2 protein from reaching the cell surface, or alter its structure so it cannot form a complex with other proteins. It remains unclear how BMPR2 mutations cause primary pulmonary hypertension. Researchers suggest that a mutation in this gene prevents cell death or promotes cell proliferation, resulting in an overgrowth of cells in the blood vessels of the lungs. Cell overgrowth can narrow the diameter of the vessels, restricting blood flow and resulting in elevated blood pressure. However, it has not yet been reported regarding the genetic variants in Taiwan. Further details have been described in this project proposal.

The purpose of the TCRN is to accelerate research in the management of thalassemia, standardize existing treatments, and evaluate new ones in a network of clinical centers in North America. The emphasis will be on clinical trials that help identify optimal therapy. Therapeutic trials may involve investigational drugs, drugs already approved but not currently used, and drugs currently used.

Chronic thromboembolic pulmonary hypertension (CTEPH) is caused by scarred blood clots in the blood vessels supplying the lungs. This in turn leads to failure of the right side of the heart. The reason why these scarred clots form is unknown. An operation to remove the scarred clots, known as pulmonary endarterectomy, is a potential cure. However, some patients have persistent obstructions within the blood vessels and heart failure even after surgery. It is thought that abnormal levels of proteins, found in the blood stream and responsible for inflammation and the development of new blood vessels may have role in causing the disease. In this study, these proteins were measured to assess whether they provide clues as to the cause of the disease and whether they could be used for the risk stratification of patients.

This is an observational study of Neuregulin-1 (NRG-1) plasma levels in patients with different forms of cardiovascular disease including microvascular angina (MVA), heart failure with preserved ejection fraction (HFpEF), as well as, heart failure with reduced ejection fraction (HFrEF) and pulmonary hypertension (PH). Investigators intend to identify cardiovascular diseases which are characterized by increased circulating NRG-1, considered to be a biomarker of therapeutic potential of NRG-1. Participants will undergo blood sampling over 3 days following randomisation. Patients demographics and clinical characteristics will be recorded and their associations with NRG-1 will be analysed.

Pulmonary Arterial Hypertension is a progressive disease that has no cure. Patients die young and are limited in their daily activity. Current treatments only treat the symptoms of the disease rather than the underlying cause. At least 1 in 5 patients has a change in a gene called the bone morphogenetic type 2 protein (or BMPR2). Extensive evidence supports the concept of addressing the reduced levels of the BMPR2 protein to reverse disease. Through work already undertaken by this group, two potential therapies which increase BMPR2 have been identified for use in a future randomised control trial. In order for a clinical trial to be informative we need an accurate way of measuring the protein or the effects of the protein (known as a biomarker). This study will use blood samples taken from 17 patients and 30 healthy participants over various time-points (2-5 visits over 5 weeks for healthy controls; 2 visits, approximately four months apart for patients). Laboratory work will help identify the best biomarkers for subsequent therapy studies. By defining the best biomarkers we can speed up the drug development in this rare disease.

The aim of this investigation is to determine the incidence of silent interstitial pulmonary edema by chest ultrasound at moderate altitude (3905m). Secondary endpoints are to detect a suspected association with acute mountain sickness (AMS), co-morbidities and endothelial dysfunction (marker of hypoxia responses, endothelial damage and inflammation).

Systemic sclerosis (SSc, also known as scleroderma) is a disease characterized by fibrosis of the skin and organs, inflammation, and an abnormal endothelial cell lining inside of vessels. A common and deadly complication of SSc is pulmonary hypertension (PH), which is an abnormal elevation in the blood pressure within the lung blood vessels. Early identification and treatment of PH is important in SSc, and no clinical factors can predict which patients will develop PH with acceptable accuracy. A potential marker of PH in SSc is the presence of increased amounts of endothelial microparticles (EMPs), which are substances circulating in the blood that were released from damaged vessel wall endothelial lining. A main goal of this study is to investigate if there is a difference in EMP levels between SSc patients with and without PH. The investigators will also use human endothelial cells in a lab environment to test whether these EMPs isolated from SSc patients are actually causing damage to the vessel lining. Lastly, the investigators will investigate the potential benefit of a medication used after transplant, mycophenolate mofetil (MMF). This will be done by causing damage to isolated human endothelial cells and treating them with MMF. The main goal of this portion of our study is to see if EMP levels are reduced when cells are treated with MMF. Overall, the investigators anticipate the following outcomes of this study: 1) use EMP levels to differentiation patients with SSc who have PH from those without PH, 2) use EMPs to understand how endothelial damage occurs in SSc, and 3) use EMPs to help us develop new treatments for patients with vascular diseases.