
Role of the Nitric Oxide (NO) in Pre-oxygenation Before Anesthetic Induction in Patients With a...
Pulmonary HypertensionThe pulmonary hypertension (HTP) due to a left heart disease or a hypoxemiant lung disease is frequent in cardiac surgery. The HTP represents an independent risk factor of morbidity and mortality in cardiac surgery, entering to the criteria of Euroscore evaluation (European System for Cardiac Operative Risk Evaluation). An acute perioperative hemodynamic decompensation of these patients is frequent. Perioperative hemodynamic modifications, hypoxemia, hypercapnia, sympathetic stimulation, increase pulmonary vascular resistances (RVP) and might provoke right ventricular failure. The anesthetic induction and the beginning of mechanical ventilation are the most sensible times due to the risk of hemodynamic decompensation. The suppression of the sympathetic tonus which is consequence of the anesthetic induction, decrease the systemic vascular resistances and lead to decrease of blood pressure. In return, the anesthetic induction is associated with an increase of pulmonary vascular resistances, resulting in increase of the postcharge and the work of the right ventricle (VD). These systemic and pulmonary hemodynamic modifications can lead to equalization, or even an inversion of the systemic and pulmonary pressures. As consequence, a hemodynamic collapse or even a heart arrest can arise. The patients suffering from HTP are hypoxemic. They have very limited oxygen reserves due to decrease of the functional residual capacity (CRF). The apnea period, which follows the anesthetic induction, is often associated with a fast desaturation, even if a good pre-oxygenation was performed before. This desaturation causes an increase of the pulmonary vascular resistances with the hemodynamic consequences previously mentioned. A risk of hypoxic heart arrest is also present. Nitric Oxide (NO) is an endogenous mediator produced from the vascular endothelium. The NO is a powerful vasodilator and is used in intensive care in inhaled way as selective pulmonary vasodilator (iNO). NO decreases the RVP, the shunt effect and improves the oxygenation by optimization of ventilation-perfusion ratio. The short lifetime of iNO (6sec approximately) allows a fast metabolism without inducing any undesirable effects such as the systemic hypotension. No studies, until now, have investigated the use of iNO in pre-oxygenation before anesthetic induction in cardiac surgery. We hope to demonstrate that iNO used in oxygenation before anesthetic induction will have a beneficial effect on the respiratory and cardiovascular parameters. Our objective is to estimate the feasibility and the tolerance of iNO before anesthetic induction of the patients with a moderate or severe HTP programmed for cardiac surgery with extracorporeal circulation. The effect will be estimated in terms of efficiency (hemodynamic and respiratory optimization).

Sildenafil in Hemodialysis Patients With Pulmonary Hypertension
Pulmonary HypertensionHemodialysis ComplicationSildenafil is a phosphodiesterase inhibitor that can exert a nitric oxide-mediated vasodilation effect, so it's considered one of the preferred agents especially in hypoxia induced pulmonary hypertension, can achieve pulmonary vasodilation by enhancing sustained levels of cyclic guanosine monophosphate (cGMP) and nitric oxide. Despite the potential burden of pulmonary hypertension in hemodialysis patients, such agent like sildenafil has limited studies about optimum dose, safety and long term efficacy in End stage renal disease patients on hemodialysis with pulmonary hypertension

Upfront Combination Pulmonary Arterial Hypertension Therapy
Pulmonary HypertensionTo evaluate the safety and efficacy of first-line combination therapy using riociguat with ambrisentan in patients with Pulmonary Arterial Hypertension (PAH).

Clinical Study of Adipose Derived Mesenchymal Stem Cells for Treatment of Pulmonary Arterial Hypertension...
Pulmonary HypertensionPulmonary arterial hypertension is a disease characterised by pathological changes in the pulmonary arteries leading to a progressive increase in pulmonary vascular resistance and pulmonary artery pressure. Right ventricular failure is the main cause of death in patients with pulmonary arterial hypertension, and the ability of the right ventricle to adapt to the progressive increase in pulmonary vascular resistance associated with changes to the pulmonary vasculature in pulmonary arterial hypertension is the main determinant of a patient's functional capacity and survival.Mesenchymal stem cells (MSCs)are a subset of adult stem cells residing in many tissues, including bone marrow(BM), adipose tissue, umbilical cord blood. Recent experimental findings have shown the ability of MSCs to home to damaged tissues and to produce paracrine factors with anti-inflammatory properties, potentially resulting in reduction of inflammation and functional recovery of the damaged tissues.It was found that MSCs can significantly improve the pulmonary hemodynamics, lung tissue gross and decrease the pulmonary artery pressure, middle artery thickness and right cardiac hypertrophy by intravenous injection.

A Randomized Trial of Udenafil Therapy in Patients With Mild Pulmonary Hypertension [ULTIMATE-Mild...
Mild Pulmonary HypertensionThe investigators hypothesized that udenafil, a newly developed phosphodiesterase type 5 inhibitor, would improve symptom, exercise capacity and hemodynamic status in patients with mild pulmonary hypertension.

Sildenafil Versus Placebo in Chronic Heart Failure
Heart FailurePulmonary HypertensionThis protocol describes a 2-arm randomised controlled pilot study assessing the tolerance, safety and efficacy of sildenafil compared to control. The hypothesis is that sildenafil will be well tolerated and efficacious in patients with chronic heart failure (NYHA class II and III) with evidence of systolic dysfunction (EF ≤40 %) and secondary pulmonary hypertension (SPAP >40mmHg). Patients that satisfy the inclusion criteria will be randomized to sildenafil (40mg x 3) or placebo therapy for 6 months in a 2:1 blinded fashion. The placebo group will be compared to the active therapy group and analysed for differences in the main study end-points Patient Global Assessment and 6-Minute Walk Test. The study will also assess safety, tolerability, symptoms and quality of life.

Bosentan for Severe Mitral Valve Dysfunction
SECONDARY PULMONARY HYPERTENSIONMITRAL STENOSIS2 moreVasoconstrictive signaling via endothelin receptors is not limited to primary pulmonary arterial hypertension, but has also been documented in secondary pulmonary hypertension due to congestive heart failure, including cardiac valve disease. The investigators aim to examine the clinical and physiologic effects of bosentan therapy in patients with secondary pulmonary hypertension due to severe, inoperable cardiac valve disease, using a single-center, prospective, open-label, non-randomized study of oral bosentan in outpatients with severe mitral stenosis due to childhood rheumatoid fever. Primary end-point will be exercise capacity at six months determined by six-minute walking distance and cardiopulmonary exercise testing. Secondary end-points will be symptomatic relief, echocardiographic left ventricular function and pulmonary pressure, serum pro-brain natriuretic peptide, and adverse events at six months.

N-Terminal Pro-brain Natriuretic Peptide Hormone and Persistent Pulmonary Hypertension
Persistent Pulmonary Hypertension of NewbornBabies who are suspected of having persistent pulmonary hypertension (PPHN) will be included in this study. PPHN is a condition in which the blood is restricted from flowing to the lungs in a normal way making it hard for babies to breath and placing strain on the heart. This study will observe whether certain hormones that measure stress (N-terminal pro-brain natriuretic peptide) can help determine how well a baby will do when they have PPHN.

Trial of Iloprost in Pulmonary Hypertension Secondary to Pulmonary Fibrosis
Pulmonary FibrosisPulmonary HypertensionIdiopathic pulmonary fibrosis(IPF) is chronic progressive fibrosing lung disease of unknown cause. There is no effective therapy yet for this disease and the mean survival in most reports is about 3 years after the diagnosis. Because of the stiff fibrosis of the lung, pulmonary hypertension is the late complication of IPF and its development heralds a very poor outcome of the patients. For the primary pulmonary hypertension, recently the effective drugs have been available. However, there is no study about the efficacy of these drugs in the patients with pulmonary hypertension secondary to pulmnary fibrosis, and the aim of this trial is to study the safty and efficacy of "Iloprost," one of the safe and effective drugs in primary pulmonary hypertension.

Nitro Oxide Inhalation Continued With Sildenafil on Neonatal Persistent Pulmonary Hypertension
Persistent Pulmonary Hypertension of NewbornNitro Oxide (NO) inhalation was recognized as an effect treatment of Neonatal Persistent Pulmonary Hypertension (PPHN), while the safety of NO long term application was under investigation. Several research suggested too much NO2 was generated in the lung after long term (> 72h) use of NO inhalation, which cause bad effects on PS production. Sildenafil was proved to be effective to PPHN as NO. This medication has a similar clinical effect but need monitoring of blood pressure. The possible hypotension effect restrict the dosage of sildenafil, which limit the usage of sildenafil in severe PPHN. But we recommend sildenafil to The purpose of the study was to establish if NO continued with sildenafil has the same effect as single NO inhalation.