The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation
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J. Heart Lung Transplant. · Mar 2015
Assessment of right ventricular adaptability to loading conditions can improve the timing of listing to transplantation in patients with pulmonary arterial hypertension.
Right ventricle (RV) performance is load dependent, and right-sided heart failure (RHF) is the main cause of death in pulmonary arterial hypertension (PAH). Prediction of RV worsening for timely identification of patients needing transplantation (Tx) is paramount. Assessment of RV adaptability to load has proved useful in certain clinical circumstances. This study assessed its predictive value for RHF-free and Tx-free outcome with PAH. ⋯ Assessment of RV adaptability to load allows prediction of RV function and Tx-free survival with severe PAH during the next 1 to 3 years. This can improve the timing of listing for Tx.
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J. Heart Lung Transplant. · Mar 2015
Right ventricular dyssynchrony in idiopathic pulmonary arterial hypertension: determinants and impact on pump function.
Right ventricular (RV) dyssynchrony has been described in pulmonary arterial hypertension (PAH), but no evidence is available on its morphologic determinants and its effect on systolic function. The aim of this study was to evaluate the morphologic determinants of RV dyssynchrony by echocardiographic and cardiac magnetic resonance imaging and its effect on systolic function. ⋯ In IPAH with narrow QRS, RV dyssynchrony is associated with RV dilation and eccentric hypertrophy pattern, suggesting a role of segmental wall stress heterogeneity as the major determinant of mechanical delay. Post-systolic shortening, as inefficient contraction, contributes to pump dysfunction.
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J. Heart Lung Transplant. · Mar 2015
Pulmonary endarterectomy in severe chronic thromboembolic pulmonary hypertension.
The outcome of patients with chronic thromboembolic pulmonary hypertension (CTEPH) undergoing pulmonary endarterectomy (PEA) after urgent hospitalization for decompensated right heart failure (DRHF) remains unclear. ⋯ DRHF occurs more frequently in patients with TPR > 1,200 dynes · sec · cm(-5), increasing the operative risk in these patients. The outcome of patients with high TPR in the absence of DRHF is excellent. However, patients with residual mean pulmonary artery pressure ≥35 mm Hg frequently receive pulmonary hypertension therapy after PEA.
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J. Heart Lung Transplant. · Mar 2015
Pulmonary hypertension is associated with increased post-lung transplant mortality risk in patients with chronic obstructive pulmonary disease.
Pulmonary hypertension associated with lung disease (PHLD) has been shown to be a predictor of disease severity and survival in patients awaiting lung transplantation. Little is known about the relationship of PHLD and survival after lung transplantation or how this may vary by disease. This study evaluated the effect of PHLD on 1-year survival after lung transplantation for patients with the 3 most common indications for transplantation: chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and cystic fibrosis (CF). ⋯ COPD patients with PHLD have increased post-transplant 1-year mortality. No significant difference was seen in patients with IPF or CF. Further studies to evaluate the potential mechanisms for this difference between diagnoses are needed.
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J. Heart Lung Transplant. · Mar 2015
Endothelin-Bone morphogenetic protein type 2 receptor interaction induces pulmonary artery smooth muscle cell hyperplasia in pulmonary arterial hypertension.
Endothelin receptor antagonists improve pulmonary arterial hypertension (PAH). Mutations in the bone morphogenetic protein (BMP) type 2 receptor (BMPR2) predispose to PAH. Here, we sought to determine whether there might exist interactions between these 2 signaling pathways and their effect on the acquisition of the altered phenotype of pulmonary artery smooth muscle cells (PA-SMCs) observed in PAH. ⋯ Endothelin-1 downregulates canonical BMPR2 signaling. This is related to decreased BMPR2 and increased anti-BMP gremlin expression associated with increased activation of p38(MAPK) and results in PA-SMC proliferation.