UCLA lung transplant program performs landmark 1000th surgery
TheUCLA Lung Transplant program performed its 1,000th transplant surgery in mid-September, becoming the first program on the West Coast, and one of only seven centers nationwide, to achieve this milestone.The recipient of the donor lungs was Elba De Contreras, 59, from Goleta, California, who suffered from idiopathic pulmonary fibrosis and pulmonary hypertension. The six-hour surgery took place at Ronald Reagan UCLA Medical Center, led by Dr. Abbas Ardehali, surgical director of the lung and heart transplant programs.De Contreras, who relied on an oxygen tank prior to her surgery, is recuperating well and said she feels happy and energetic. With three sons and four grandkids, De Contreras said she looks forward to resuming her social life. Her husband, Willy, said that the donor lungs have given his wife “new life” and she looks 20 years younger.“This is a big milestone for UCLA’s lung transplant program” said Ardehali, a professor of cardiothoracic surgery. “Achieving 1,000 lung transplants is a reflection of the experience and dedication of our team.”Lung transplantation has come a long way since UCLA performed its first operation in 1988. While the procedure used to have a significant morbidity rate, as new techniques were developed the 30-day survival rate improved dramatically, reaching 98 percent at UCLA currently, compared to the national average of 96.5 percent.These advances in patient outcomes are attributable to several fac...
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.
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.
Chronic thromboembolic pulmonary hypertension (CTEPH), is a progressive condition characterized by persistent occlusion of the pulmonary arteries by organized thrombus and a pulmonary arteriopahty. CTEPH is potentially curable with pulmonary thrombo-endarterectomy (PTE). The pathophysiological mechanisms that lead to the development of CTEPH and progressive arteriopathy has not been fully elucidated. We hypothesize that Endothelin-1(ET1), a potent endogenous vasoconstrictor and smooth muscle mitogen may contribute to the development of CTEPH.
Endothelial to Mesenchymal Transition (EndMT) is a complex biological process in which endothelial cells transdifferentiate to collagen producing mesenchymal cells. The phenomenon of EndMT has been associated with development of vascular remodeling in monocrotaline rat model of pulmonary arterial hypertension (PAH). However, data on its role in pulmonary vascular remodeling in heart failure (HF) leading to pulmonary hypertension (PH) is lacking. The presence of End MT in lungs in association with pulmonary vascular remodeling could indicate its role in development of PH.
Chronic thrombo-embolic pulmonary hypertension (CTEPH) results in right ventricular (RV) dysfunction, primary cause of death in CTEPH. Previous studies described a continuum from an adaptive heart with modified metabolism, angiogenesis and structure, to a maladaptive heart with RV failure. We sought to describe relationships between histological features of RV remodeling and functional and metabolic imaging of the right ventricle in CTEPH.
We present a case of vasculitis-associated PH initially diagnosed as CTEPH.