Active clinical trials for "Hypertension, Pulmonary"

ADAMTSL4 (A disintegrin and metalloproteinase with thrombospondin motifs like) is a member of the ADAMTSL family. ADAMTSL4 is one of the family of 7 ADAMTS-Like proteins, themselves part of the Thrombospondin type 1 repeat (TSR) superfamily of proteins. These 7 proteins are divided into two distinct clades, of which ADAMTSL4 and ADAMTS-Like 6 form part of one clade, differing from ADAMTS-Like 1, ADAMTS-Like 3 and ADAMTS-Like 7 by lacking immunoglobulin repeat regions. ADAMTSL4 is widely expressed in brain, colon, heart, kidney, liver, lung, pancreas and spleen, yet, its precise role is unclear. in addition, ADAMTSL4 protein high expression to the medial layer of the arterial wall, and medial vascular smooth muscle cells specifically.

This single center study will monitor the developmental progress of PPHN patients who received iv sildenafil in study A1481276. Two visits will be conducted, at 12 and 24 months following the end of study drug infusion.

Prospective multicenter registry including incident patients and prevalent patients which pretends to identify clinical characteristics, treatment trends in-hospital and four years follow-up outcome through major adverse cardiovascular events (MACE) in a Mexican population with well characterized Pulmonary Hypertension.

This is a prospective, international, multicenter outcome cohort study. This study starts at the moment patients visit the outpatient clinic 3 to 6 months after a diagnosis of acute PE as part of routine medical care. If patients consent to study participation, the CTEPH clinical prediction score will be calculated. CTEPH is considered to be not present in patients with a low probability (≤6 points) and no symptoms suggestive of CTEPH, i.e. dyspnea on exertion, edema, newly developed palpitations, syncope or chest pains.The remaining patients with either high probability (>6 points) or who report symptoms that may be associated with CTEPH will be subjected to the 'rule-out criteria'. CTEPH will be assumed not present in patients with an age- and gender dependent normal NT-proBNP level (as defined by the assay's manufacturer), in the absence of any of the 3 ECG criteria. Patients who have an abnormal result from the 'rule-out criteria' will be referred for transthoracic echocardiography. All echocardiograms will be performed according to a predefined standardized protocol. In case of echocardiographic intermediate or high probability of PH, patients will be referred for further diagnostic work-up of suspected CTEPH starting with perfusion lung scan or VQ-scan and right heart catheterization, of which the results will be discussed by an independent interdisciplinary working group of PH specialists, to ensure optimal diagnostic management. This latter diagnostic work-up of an abnormal echocardiograph lies within the setting of standard medical care. All patients who were not diagnosed with pulmonary hypertension of any origin, or with NYHA class III or IV heart failure due to left ventricular systolic dysfunction, left ventricular diastolic dysfunction or significant valvular lesions, will be followed for a total of 2 years from the index PE diagnosis. During that period, the study protocol will not interfere with standard patient care, allowing diagnostic tests as deemed indicated by the treating physician including echocardiography in case of new respiratory symptoms. At the end of the follow-up period, all patients will be subjected to a second echocardiography that will be handled according to the above stated procedures to evaluate the presence of CTEPH.

Pulmonary embolism, or clots blocking the blood vessels of the lungs, is a common clinical condition requiring treatment with blood thinners. In most patients, recovery is complete. A small proportion of patients, however, develop complications (high blood pressure in the lung circulation, i.e. pulmonary hypertension). Persisting breathlessness during activity is a common symptom in many of these patients and leads to a reduced ability to engage in daily physical activity. The reason for this activity-related breathlessness remains uncertain and is the main question of the proposed study. Using new sophisticated technology, the investigators will determine the root causes of perceived breathing difficulty. The investigators will test the idea that breathlessness is fundamentally the result of increased drive to breathe from control centers in the brain. The investigators will measure drive to breathe by measuring the electrical activity descending from the brain to the main muscle of breathing - the diaphragm. The investigators will discover if the increased drive to breathe is due to accumulation of carbon dioxide in the blood as a result of poor blood perfusion of areas of the lung due to the effects of blockage by clots. The investigators also will investigate whether weakness and fatigue of the muscles of breathing, as a result of the high breathing demands that are present in patients with blood clots in the lungs, contribute to breathlessness. With this information it is hopeful that better treatment options will be developed to relieve this distressing symptom.

Poor function of the right side of the heart and rise in pressure of the blood vessels leading to the lungs are two main heart-related factors that are associated with worsening of airway disease. A relatively new method which uses magnetic field to create images of the heart called cardiac magnetic resonance (CMR) imaging shows immense promise in detailed and accurate assessment of the heart in patients with airway diseases. This project aims to assess the heart in patients with asthma and chronic obstructive pulmonary disease (COPD) as well as healthy participants using CMR to help us determine features on CMR that are different is patients with asthma and COPD compared to healthy participants. This may help with early identification of patients who are at risk of episodes of acute worsening of airway disease, called exacerbation, and potentially halt the progression of the heart dysfunction with currently available or new treatments. Study involves one visit at Glenfiled Hospital, Leicester, lasting approximately 4 hours. The visit will include following assessments: clinical history, health status, physical examination, electrocardiogram (ECG), blood tests, lung function testing, echocardiogram and CMR. Part of the study will involve a participant questionnaire in which the participants will rate their CMR experience. The results will potentially change the way CMR is undertaken. A sub-set of the participants will also be invited back to do a one off focus group discussing the CMR experience further.

Physical activity is an important factor in understanding how diseases can affect a child. Decreases in physical activity are sometimes the first thing that happens before a child is diagnosed with a disease. When a child sees their doctor, that visit reflects a single point in time. It does not capture how a child feels during the days in between visits to their doctor. This study plans to use special monitors called actigraphs to collect information about physical activity in children with a type of disease called pulmonary hypertension. This study will measure how active these children are and compare their activity to clinical information and to actigraphy measurements in children without pulmonary hypertension.

Comparison of standard 6 minute walk test with 6 minute walk test smartphone app.

Background: Prostacyclin analogues (epoprostenol, treprostinil and iloprost) induce vasodilation in advanced pulmonary arterial hypertension (PAH) but also inhibit platelets, increasing patients' bleeding risk. The antiplatelet effects of different prostacyclin analogues have never been compared head-to-head. The goal of the PAPAYA (Platelet Reactivity and Treatment With Prostacyclin Analogues in Pulmonary Arterial Hypertension) trial is(i) to compare platelet function (platelet reactivity, extracellular vesicles concentration and thrombus formation) in patients with PAH treated with prostacyclin analogues on top of endothelin receptor antagonists (ERA) and/or phosphodiesterase type 5 inhibitors (PDE5i) and patients treated only with ERA and PDE5i, and (ii) to compare the antiplatelet effect of different prostacyclin analogues. Venous blood will be collected from patients treated with prostacyclin analogues (study group; n=40) and patients treated with ERA or PDE5i (control group; n=40). Platelet reactivity will be analysed in whole blood by impedance aggregometry using arachidonic acid, adenosine diphosphate and thrombin receptor-activating peptide as agonists. Concentrations of extracellular vesicles from all platelets (CD61+), activated platelets (CD62P+), leukocytes (CD45+) and endothelial cells (CD146+) will be analysed in platelet-depleted plasma using flow cytometry (A-60 Micro). Platelet-rich thrombus formation will be measured using whole blood perfusion system. The study will determine the antiplatelet effect of prostacyclin analogues and compare different prostacyclin analogues head-to-head to identify the best drugs to use in case of thrombosis or bleeding.

Myelodysplastic and myeloproliferative Disease represent conditions with increased risk for pulmonary hypertension. However, the exact prevalence of pulmonary hypertension in these conditions is not known. The effects of pulmonary hypertension on the clinical picture and the symptoms of patients in these conditions needs also further exploration. This exploratory study is designed to describe the prevalence of pulmonary hypertension in the population with such hematologic diseases, and the stages of pulmonary hypertension as well its effect on exercise capacity at time of diagnosis.