Active clinical trials for "Hypertension, Pulmonary"

Monocentric cohort study, prospective, evaluating the variability of cardiac output measurement by resting and stress impedancemetry as a prognostic factor for Pulmonary Hypertension

Adult patients with suspected or confirmed Connective Tissue Disease Patients (CTD)With Pulmonary Hypertension(PH)will be recruited. Patients will be approached, consented, have baseline demographics, diagnostics and disease activity measures recorded, and blood taken. The collection of data and biological material will mirror usual clinical practice as far as possible. Subjects will ideally attend further visits at 3, 6 and 12 months to have bloods taken, outcome measures recorded and questionnaires completed.

to detect the incidence of CTEPH patients. Primary outcome To predict CETHP in symptomatic patients after pulmonary embolism episode. Secondary outcome: On Echocardiography revealed RV dysfunction which are peak TR Velocity , the RV/LV basal diameter ratio, flattening of the IVS, RV acceleration time and/or midsystolic notching, IVC diameter with decreased inspiratory collapse and RA area.

In this trial the effects of the inhaled drug BAY1237592 will be studied in patients with high blood pressure in the pulmonary blood vessels due to Pulmonary Arterial Hypertension (PAH) and due to Chronic Thromboembolic Pulmonary Hypertension (CTEPH). Pulmonary hypertension is characterized by the elevation of pressure in the pulmonary arteries (PAP) and of the pulmonary vascular resistance (PVR) leading to increased workload of the right chamber of the heart to eject blood against this elevated resistance. The goal of this study is to measure the safety and tolerability of the drug as well as the reduction of the PVR at different doses In Part A patients without specific treatment for PH (untreated patients) will be tested. In Part B also patients stably pre-treated with specific PH drugs will be studied in combination with the new inhaled drug

The purpose of this study is to learn more about the safety and dosing of sildenafil in infants.

Chronic thromboembolic Pulmonary hypertension(CTEPH) is characterized by obstruction of the pulmonary vasculature, leading to increased pulmonary vascular resistance, progressive pulmonary hypertension (PH) and right ventricular failure- most common cause of death for patients with PH. Riociguat, (ADEMPAS) is a member of a new class of drug recently approved in Canada for the treatment of CTEPH. This pilot study is designed to assess if at least 24 weeks of treatment with riociguat will show changes in glucose metabolism and improved resting myocardial blood flow using positron emission tomography ( PET ) imaging to measure myocardial function. The response between both treatment naive patients as well as patients on maximally tolerated dose of riociguat with tratment duration of at least 3 months will be included.

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: Elevated Parathyroid hormone Metastatic Calcification due to the increase of the calcium-phosphor multiple High cardiac output Nitric oxide-endothelin metabolism 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.

OBJECTIVES: I. Describe the psychosocial response of parents and caretakers who learn cardiopulmonary resuscitation (CPR) techniques for infants at high risk for respiratory or cardiac arrest. II. Compare the effect of 4 methods of CPR instruction on psychosocial response. III. Evaluate a psychological intervention based on social support theory designed to offset the potential adverse psychological outcomes of CPR instruction. IV. Evaluate a self-paced CPR learning module using the principles of adult learning theory. V. Document the level of CPR knowledge and skill retention over time. VI. Document the frequency of CPR and its outcome following a witnessed respiratory or cardiac arrest.

Patients with severe Chronic Obstructive Pulmonary Disease (COPD) and low oxygen levels in the blood are at risk of developing pulmonary hypertension and strain on the right side of the heart, both of which are known to increase symptoms and worsen prognosis It is not fully established whether interval exercise training in patients with severe COPD and concomitant low oxygen levels is beneficial. This study aims to evaluate the effects of aerobic interval exercise training in patients with severe COPD and low oxygen levels in the blood, with a particular emphasis on such effects on the cardiovascular system and pulmonary circulation.

To study hemodynamic effects of Sildenafil during exercise in patients with pulmonary hypertension.