Active clinical trials for "Hypertension, Pulmonary"

The mechanism governing how blood flows from the heart to the lungs depends on many factors including the pumping function of the right ventricle, properties of the arteries that carry the blood from the right ventricle to the lungs (pulmonary arteries), and the lungs themselves. Under normal conditions the pressure in the pulmonary arteries is well controlled and significantly lower than in the systemic circulation, however there are a number of conditions that lead to abnormally high pressures and significant morbidity and mortality. However different patients respond differently to similarly elevated pressures, leading doctors to believe that there must be differences in either the right ventricles, the properties of the arteries, or the lungs themselves. It can be difficult to determine the relative contributions of each of these factors on blood flow because their effects are superimposed on each other. One approach that has been used to look at this in other parts of the circulation (including in the systemic circulation and the coronary arteries) is to measure simultaneous pressure and flow, and apply a technique called wave intensity analysis (WIA). This technique can amongst other things, quantify the separate effects of wave reflection and the 'reservoir function' (or compliance) of the arteries, and in the systemic circulation WIA has increased the understanding of the mechanisms behind hypertension and the physiological changes of ageing. The pulmonary arteries are accepted to be very different from the systemic circulation and the mechanisms behind pulmonary hypertension are thought to be very different to those of systemic hypertension. This protocol aims to determine the major influences on blood flow in the pulmonary arteries in health and disease, to help to understand why some patients are affected more than others by elevated pulmonary pressures.

The most frequent access site for veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is the common femoral artery (CFA), using either an open or percutaneous technique. Currently, percutaneous closure devices for femoral arterial access sites are approved for use only when a 10-F or smaller sheath has been used. However, the availability of the Perclose ProGlide (Abbott Laboratories, Chicago, IL) device has now made it possible to perform percutaneous vessel closure after using larger sheaths.The preclose technique using Perclose ProGlide, has been widely used in endovascular procedures. In a prospective randomized study, complication rates at the access site were similar in patients who underwent total percutaneous access (including percutaneous arteriotomy closure) than in those who underwent surgical cutdown and subsequent surgical closure. Total percutaneous closure of femoral arterial access sites increases patient comfort and decreases the rate of wound infections and lymphatic fistulas.[6,7] Furthermore, patients are mobilized and discharged earlier following the use of closure devices than with compression alone. Despite the above observations, no data have been published regarding percutaneous closure of femoral artery access sites in patients who have undergone VA-ECMO. In this study, we evaluated the safety and feasibility of a percutaneous closure technique using Perclose ProGlide to close the CFA access site after VA-ECMO.

The purpose of the study is to determine whether the excretion of renal water- and salt-channels in the urine reflects the handling of water and salt in the kidneys, and whether the excretion can be used to monitor and/or predict the effects of treatment of certain heart or lung diseases.

Background Flexible bronchoscopy (FB) is one of the most common invasive procedures performed by pulmonologists (1) . Typically performed under topical anesthesia and conscious sedation, the procedure is considered to be safe, effective and well tolerated in patients with a wide variety of pulmonary diseases (2). Complications associated with the procedure are rare and studies have estimated an incidence of 0.5-4% (3) The most commonly recognized complications include hypoxia, bleeding, bronchospasm, cardiac dysrhythmias, pneumothorax, and vagal reactions (4). Several conditions increase the risk of complications including pre-existent hypoxemia, use of mechanical ventilation, uremia, profound thrombocytopenia, coagulopathy and pulmonary hypertension (PH) (5). Although previous reports suggest that transbronchial biopsies increase the risk for hemorrhage in this population, data are is limited to survey analyses and isolated reports. Recently Guzman et al. reported a retrospective analysis about the safety of FB in PH. (6) They found that FB can be performed safely in patients with mild and moderate PH. However, the study was small and retrospective analysis. Furthermore, there is no consensus regarding levels of pulmonary artery pressure (PAP) considered to be safe for invasive diagnostic interventions such as TBLB or transbronchial needle aspiration. Objective To assess the safety of FB in patients with PH and to study the occurrence of complications associated with different diagnostic bronchoscopic procedures.

Patients with pulmonary hypertension will be randomized into two groups. One group will receive telerehabilitation sessions including upper and lower extremity strengthening exercises and breathing exercises. The other will me monitored routinely. Patients will be assessed by 6 minute walk test, emphasis-10 questionnaire for quality of life and muscle strength with hand-held dynamometer.

The HOKUSAI post VTE study contains of two different research questions; one on the long term outcomes of deep vein thrombosis and one on the long term effects of pulmonary embolism, post thrombotic syndrome (PTS) and chronic thromboembolic pulmonary hypertension (CTEPH) respectively. Our aim of the study is to compare the long term outcomes along with the quality of life assessment of VTE in a group treated with heparin+VKA versus a group treated with heparin+edoxaban in the acute setting.

Research design: This is a controled prospective study. Methodology: Patients with newly diagnosed and untreated OSA with total apnea-hypopnea index (AHI) >5/h, and control (AHI<5/h) will be recruited from the Long Beach VA sleep center. Controls are subjects without OSA or other sleep disorders and no sign of pulmonary hypertension based on echo. The investigators also measure pulmonary artery pressure by 2D Echo and exclude patient with any sign of left heart dysfunction. PH will be defined as RVSP > 35 mmHg or mean PA pressure>25 mmHg. The investigators will recruit subjects with and without PH and OSA in three separate groups: group one : OSA+ PH, group two: normal individual with no OSA and no PH, group three: OSA with no PH Pulmonary function test will be done to exclude patients with underlying lung disease. The inclusion criteria is: Age >20, AHI >5, AHI <5 (as control), RVSP > 35 mmHg OR Mean PA pressure>25 mmHg, RVSP < 35 mmHg OR Mean PA pressure < 25 mmHg (as control). Subjects will be excluded if they had known peripheral vascular disease, liver disease, hemolytic anemia, inflammatory disease, active infection, or if they were pregnant, on therapy for OSA, on chronic steroid treatment, or younger than 20 years of age, patients with left heart failure (systolic or diastolic), patients are on PH medications including sildenafil, active smokers, COPD and asthma, active infection or inflammatory disease and collagen vascular disease. Nocturnal polysomnography will be performed and scored according to the American Academy of Sleep Medicine. Exhaled Carbon monoxide (CO) will be measured with a calibrated fuel cell type electrochemical device with sensor sensitivity of 1 ppm. The mean of three reproducible measurements will be recorded and corrected for ambient CO. Exhaled Nitric Oxide (NO) will be measured. At each testing session, at least three flow-regulated FENO measurements will be performed. The investigators will repeat 2D Echo and measurements of above factors after 3 months of CPAP treatment. The investigators also check patient's compliance with the treatment by downloading data off of their CPAP device. Each subject will be informed of the experimental procedures, which is approved by the Human Investigation Committee of the VA-Long Beach. Finding: The investigators hypothesize that HO pathway causing perturbation of pulmonary endothelial function by inhibition of nitric oxide. Clinical significance: OSA is associated with PH, but exact mechanism is not well known. In the past, I have shown that increased endogenous CO in the setting of elevated NO concentration is associated with endothelial dysfunction in patient with OSA. Therefore, the investigators sought to investigate the roles of HO and NO pathways in patients with OSA associated with PH. Impact/significance: It addresses a fundamental gap in our understanding of how OSA results in increase the pulmonary artery pressure and if substantiated, will provide the basis for the design and testing of new approaches to prevention and treatment of OSA.

This prospective observational follow-up study is designed to assess the long-term outcomes after Venous thromboembolism (VTE) and to assess the effect of the new oral anticoagulant (NOAC) rivaroxaban on the prevalence of post-thrombotic syndrome (PTS). The study will not be testing any formal hypothesis.

The clinical study aims to investigate the numbers of predefined complications in the first six month after implantation of the implantable LENUS Pro® medications pump for intravenous application of treprostinil sodium in patients with PAH. The manufacturer is Tricumed GmbH, Germany; exclusive marketing rights: OMT GmbH & Co KG 78665 Frittlingen, Germany.

To characterize the demographics and clinical course of the patient population diagnosed as having WHO group I pulmonary arterial hypertension and WHO group IV pulmonary hypertension due to chronic thromboembolic pulmonary hypertension To describe real-world outcome of Chinese patients with WHO group I pulmonary arterial hypertension and WHO group IV pulmonary hypertension due to chronic thromboembolic pulmonary hypertension To evaluate differences in patient outcomes according to classification subgroup To identify clinical predictors of long-term survival To assess the relationship between targeted therapies for pulmonary arterial hypertension and patient outcomes