Pulmonary hypertension reversed by blocking molecular pathway in rats
Pulmonary hypertension, a deadly form of high blood pressure that develops in the lungs, may be caused by an inflammation-producing molecular pathway that damages the inner lining of blood vessels, according to a new study by researchers at the Stanford University School of Medicine. The results, published in Science Translational Medicine, suggest that using medications to block this pathway could lead to the first-known cure for the disease, apart from lung transplantation...
AbstractA 27-year-old female patient had presented progressing exertional dyspnea due to pulmonary hypertension. Chest CT revealed diffusely spread patchy ground-glass opacities sparing subpleural parenchymal areas suggesting the diagnosis of pulmonary veno-occlusive disease (PVOD). Despite the diagnosis of PVOD, she was somehow managed by a repetitive escalation of the epoprostenol dose and oxygen supply during the 12-month waiting period until successful bilateral lung transplantation was performed. Pathology demonstrated capillary proliferation in alveolar septae with scarce lesions of narrowed and/or occluded postcapil...
Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare but severe complication of acute pulmonary embolism leading to right heart failure and premature mortality. Its cumulative incidence ranges from 0.1 –9.1% within the first 2 years after symptomatic acute pulmonary embolism, although probably underestimated due to the lack of systematic follow-up and screening in clinical routine.1–3
Clinical Transplantation, EarlyView.
Chronic thromboembolic pulmonary hypertension (CTEPH) results from persistent pulmonary vascular obstructions, presumably due to inflammatory thrombosis. Because estimates of thrombus volume at diagnosis have no predictive value, we investigated the role of the thrombosis marker D-dimer and the inflammation marker C-reactive protein (CRP) for predicting outcomes in CTEPH.
We report a very rare case of pulmonary chromomycosis caused by Scedosporium prolificans that developed after lung transplantation and was successfully treated with endobronchial topical amphotericin B instillation. The subject was a woman in her 50s with a history of bilateral lobar lung transplantation from living donors for idiopathic pulmonary hypertension. Eight years after the lung transplantation, chest radiography X-ray and computed tomography showed an abnormal shadow in the right lung.
The pathobiology of chronic thromboembolic pulmonary hypertension (CTEPH) is poorly understood. Metabolic dysregulation is prominent in idiopathic pulmonary arterial hypertension (IPAH). Using an “omics” approach, we sought to determine the metabolic fingerprint of CTEPH patients compared to IPAH and healthy controls.
We hypothesized that dynamic measures of pulmonary arterial compliance (Cpa), and elastance (Epa), RV elastance (Ees), and RV-PA coupling would improve prediction of post-op mean PA pressure (PAP), Length of Stay (LOS), ICU duration (ICUd) and need for inotropes (NFI) compared to prediction based solely on pre-op PAP, CO and PVR in patients with chronic thromboembolic pulmonary hypertension (CTEPH) undergoing pulmonary thromboendaterectomy (PTE).
Exercise right heart catheterization (RHC), currently used to identify occult pulmonary hypertension (PH), may have additional applications. An elevated total pulmonary resistance (TPR), the change in mean pulmonary arterial pressure (mPAP) divided by the change in cardiac output during exercise, has been associated with worse clinical outcomes. We hypothesize that the combination of the TPR and the PCWP during exercise ( ∆TPRex) reflects pulmonary arterial disease and is a marker of outcomes.
LVAD therapy in patients with pulmonary hypertension (PH) has shown improvements in pulmonary vascular resistance (PVR) but benefits of this strategy of mechanical unloading pre heart transplantation (HTx) remains uncertain. Here, we determine if patients with PH who are bridge to transplant (BTT) with an LVAD have improved outcomes after HTx.
Right ventricular (RV) dysfunction in patients with pulmonary hypertension due to chronic lung disease (Group 3 PH) is not well described. We compared RV function in Group 3 and Group 1 PH patients, and investigated the correlates of RV function in Group 3 PH patients.