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
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.
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J. Heart Lung Transplant. · Mar 2015
ReviewPulmonary hypertension in heart failure with preserved ejection fraction.
In heart failure with preserved ejection fraction (HFpEF), an entity that remains challenging and difficult to treat, the development of pulmonary hypertension (PH), via an increase in left atrial pressure, is the direct consequence of reduced relaxation and enhanced stiffness of the left ventricle and is now viewed as an important contributor to clinical worsening and increased mortality. PH becomes a relevant clinical phenotype in approximately 50% of patients with HFpEF and represents a true challenge in the clinical follow-up and management of these patients. Along with these epidemiologic insights, there has been increasing recognition of the pathophysiology of PH and its consequences on the right ventricle in patients with HFpEF. ⋯ Many theoretical rationales as well as progressively accumulating evidence support the usefulness of nitric oxide pathway-potentiating compounds in targeting the lung vasculature through phosphodiesterase 5 inhibitors or guanylate cyclase stimulators to produce vasodilation and potentially a biologic effect. These pharmacologic strategies may be clinically effective options for the treatment of PH in patients with HFpEF; however, large controlled trials are necessary to address definitively the safety, tolerability, and potential impact on morbidity and mortality. This review details the pathophysiologic process, prevalence, and consequences of HFpEF-associated PH and discusses current and emerging treatment strategies to prevent or treat this deleterious sequela when present.
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J. Heart Lung Transplant. · Mar 2015
Right ventricular remodeling in idiopathic pulmonary arterial hypertension: adaptive versus maladaptive morphology.
Although increased pulmonary pressure is caused by changes in the pulmonary vasculature, prognosis in idiopathic pulmonary arterial hypertension (IPAH) is strongly associated with right ventricular (RV) function. The aim of this study was to describe the best RV adaptive remodeling pattern to increased afterload in IPAH. ⋯ Concentric hypertrophy might represent a more favorable RV adaptive remodeling pattern to increased afterload in IPAH because it is associated with more suitable systolic function and mechanical efficiency.
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J. Heart Lung Transplant. · Mar 2015
S-nitroso human serum albumin attenuates pulmonary hypertension, improves right ventricular-arterial coupling, and reduces oxidative stress in a chronic right ventricle volume overload model.
This study examined the acute effect of intravenous S-nitroso human serum albumin (S-NO-HSA) infusion on overall hemodynamics and oxidative stress in a chronic left-to-right shunt-induced pulmonary arterial hypertension model with right ventricle (RV) failure. ⋯ S-NO-HSA reduces pulmonary hypertension and improves RV systolic and diastolic function and RV-arterial coupling, with a positive effect on ventricular interdependence by increasing energetic reserve and reducing oxidative stress.