Genes on Y chromosome protect against pulmonary hypertension, study suggests
This study is the first to examine the involvement of sex chromosomes in the disease's development in the absence of sex hormones. In humans, females typically have two copies of the X chromosome, while males typically have one X and one Y chromosome.METHODIn the lab, the researchers engineered mice with different chromosomal makeups and measured their development of pulmonary hypertension in an environment with 10 percent oxygen, which is a well-established setting for inducing the disease.One group of mice was engineered with sex chromosomes that were independent of their gonadal sex, or sex based on their genitalia, so that the researchers could isolate the impact of sex chromosomes. The other group of mice in the experiment had different variants of sex chromosomes in order for the researchers to determine the impact of the presence of a Y chromosome versus varying numbers of X chromosomes. All the mice had their gonads removed so that the researchers could eliminate the potential effects of sex hormones.The researchers then placed the mice in the 10 percent oxygen environment for three weeks. At the end of the experiment, the researchers examined the hearts and lungs of the mice. Mice with a Y chromosome experienced significantly less severe pulmonary hypertension and were protected against the development of the disease.IMPACTThese findings identify a new avenue for research into effective ways to treat pulmonary hypertension. In the future, determining which genes on t...
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
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.
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