Relevant bibliographies by topics / Pulmonary arterial hypertension (PAH) metabolomics

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Pulmonary arterial hypertension (PAH) metabolomics'

Author: Grafiati
Published: 4 June 2025
Last updated: 1 August 2025

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Journal articles on the topic "Pulmonary arterial hypertension (PAH) metabolomics"

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Zhao, Jun-Han, Yang-Yang He, Shan-Shan Guo, et al. "Circulating Plasma Metabolomic Profiles Differentiate Rodent Models of Pulmonary Hypertension and Idiopathic Pulmonary Arterial Hypertension Patients." American Journal of Hypertension 32, no. 11 (2019): 1109–17. http://dx.doi.org/10.1093/ajh/hpz121.

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Abstract BACKGROUND Pulmonary arterial hypertension (PAH) is a severe progressive disease with systemic metabolic dysregulation. Monocrotaline (MCT)-induced and hypoxia-induced pulmonary hypertension (PH) rodent models are the most widely used preclinical models, however, whether or not these preclinical models recapitulate metabolomic profiles of PAH patients remain unclear. METHODS In this study, a targeted metabolomics panel of 126 small molecule metabolites was conducted. We applied it to the plasma of the 2 preclinical rodent models of PH and 30 idiopathic pulmonary arterial hypertension
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He, Yang-Yang, Yi Yan, Xin Jiang, et al. "Spermine promotes pulmonary vascular remodelling and its synthase is a therapeutic target for pulmonary arterial hypertension." European Respiratory Journal 56, no. 5 (2020): 2000522. http://dx.doi.org/10.1183/13993003.00522-2020.

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Pathological mechanisms of pulmonary arterial hypertension (PAH) remain largely unexplored. Effective treatment of PAH remains a challenge. The aim of this study was to discover the underlying mechanism of PAH through functional metabolomics and to help develop new strategies for prevention and treatment of PAH.Metabolomic profiling of plasma in patients with idiopathic PAH was evaluated through high-performance liquid chromatography mass spectrometry, with spermine identified to be the most significant and validated in another independent cohort. The roles of spermine and spermine synthase we
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Alotaibi, Mona, Yunxian Liu, Gino A. Magalang, et al. "Deriving Convergent and Divergent Metabolomic Correlates of Pulmonary Arterial Hypertension." Metabolites 13, no. 7 (2023): 802. http://dx.doi.org/10.3390/metabo13070802.

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High-dimensional metabolomics analyses may identify convergent and divergent markers, potentially representing aligned or orthogonal disease pathways that underly conditions such as pulmonary arterial hypertension (PAH). Using a comprehensive PAH metabolomics dataset, we applied six different conventional and statistical learning techniques to identify analytes associated with key outcomes and compared the results. We found that certain conventional techniques, such as Bonferroni/FDR correction, prioritized metabolites that tended to be highly intercorrelated. Statistical learning techniques g
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Chen, Yi-Hang, Wen Yuan, Liu-Kun Meng, Jiu-Chang Zhong, and Xiao-Yan Liu. "The Role and Mechanism of Gut Microbiota in Pulmonary Arterial Hypertension." Nutrients 14, no. 20 (2022): 4278. http://dx.doi.org/10.3390/nu14204278.

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Pulmonary arterial hypertension (PAH) is a malignant pulmonary vascular disease characterized by increased pulmonary vascular resistance, pulmonary vasoconstriction, and right ventricular hypertrophy. Recent developments in genomics and metabolomics have gradually revealed the roles of the gut microbiota (GM) and its metabolites in cardiovascular diseases. Accumulating evidence reveals that the GM plays important roles in the occurrence and development of PAH. Gut microbiota dysbiosis directly increases the gut permeability, thereby facilitating pathological bacterial translocation and allowin
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Zhou, Xue-liang, Zhi-bo Liu, Rong-rong Zhu, et al. "NSD2 silencing alleviates pulmonary arterial hypertension by inhibiting trehalose metabolism and autophagy." Clinical Science 133, no. 9 (2019): 1085–96. http://dx.doi.org/10.1042/cs20190142.

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Abstract Nuclear receptor binding SET domain 2 (NSD2)-mediated metabolic reprogramming has been demonstrated to regulate oncogenesis via catalyzing the methylation of histones. The present study aimed to investigate the role of NSD2-mediated metabolic abnormality in pulmonary arterial hypertension (PAH). Monocrotaline (MCT)-induced PAH rat model was established and infected with adeno-associated virus carrying short hairpin RNA (shRNA) targeting NSD2. Hemodynamic parameters, ventricular function, and pathology were evaluated by microcatheter, echocardiography, and histological analysis. Metabo
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Mey, Jacob T., Adithya Hari, Christopher L. Axelrod, et al. "Lipids and ketones dominate metabolism at the expense of glucose control in pulmonary arterial hypertension: a hyperglycaemic clamp and metabolomics study." European Respiratory Journal 55, no. 4 (2020): 1901700. http://dx.doi.org/10.1183/13993003.01700-2019.

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Individuals with idiopathic pulmonary arterial hypertension (PAH) display reduced oral glucose tolerance. This may involve defects in pancreatic function or insulin sensitivity but this hypothesis has not been tested; moreover, fasting nutrient metabolism remains poorly described in PAH. Thus, we aimed to characterise fasting nutrient metabolism and investigated the metabolic response to hyperglycaemia in PAH.12 participants (six PAH, six controls) were administered a hyperglycaemic clamp, while 52 (21 PAH, 31 controls) underwent plasma metabolomic analysis. Glucose, insulin, C-peptide, free f
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Sanders, Jason L., Yuchi Han, Mariana F. Urbina, David M. Systrom, and Aaron B. Waxman. "Metabolomics of exercise pulmonary hypertension are intermediate between controls and patients with pulmonary arterial hypertension." Pulmonary Circulation 9, no. 4 (2019): 204589401988262. http://dx.doi.org/10.1177/2045894019882623.

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Mechanisms underlying pulmonary arterial hypertension (PAH) remain elusive. Pulmonary arterial hypertension and exercise PH share similar physiologic consequences; it is debated whether they share biologic mechanisms and if exercise PH represents an early phase of pulmonary arterial hypertension. We conducted an observational study to test if there is a graded metabolic disturbance along the severity of PH, which may indicate shared or disparate pathophysiology. Individuals referred to an academic medical dyspnea center with unexplained exertional intolerance underwent invasive cardiopulmonary
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Wilkins, Martin R., Jurjan Aman, Lars Harbaum, Anna Ulrich, John Wharton, and Christopher J. Rhodes. "Recent advances in pulmonary arterial hypertension." F1000Research 7 (July 24, 2018): 1128. http://dx.doi.org/10.12688/f1000research.14984.1.

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Pulmonary arterial hypertension (PAH) is a rare disorder with a high mortality rate. Treatment options have improved in the last 20 years, but patients still die prematurely of right heart failure. Though rare, it is heterogeneous at the genetic and molecular level, and understanding and exploiting this is key to the development of more effective treatments. BMPR2, encoding bone morphogenetic receptor type 2, is the most commonly affected gene in both familial and non-familial PAH, but rare mutations have been identified in other genes. Transcriptomic, proteomic, and metabolomic studies lookin
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Bassareo, Pier Paolo, and Michele D’Alto. "Metabolomics in Pulmonary Hypertension—A Useful Tool to Provide Insights into the Dark Side of a Tricky Pathology." International Journal of Molecular Sciences 24, no. 17 (2023): 13227. http://dx.doi.org/10.3390/ijms241713227.

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Pulmonary hypertension (PH) is a multifaceted illness causing clinical manifestations like dyspnea, fatigue, and cyanosis. If left untreated, it often evolves into irreversible pulmonary arterial hypertension (PAH), leading to death. Metabolomics is a laboratory technique capable of providing insights into the metabolic pathways that are responsible for a number of physiologic or pathologic events through the analysis of a biological fluid (such as blood, urine, and sputum) using proton nuclear magnetic resonance spectroscopy or mass spectrometry. A systematic review was finalized according to
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Wawrzyniak, Renata, Tamara Gaillard, Margot Biesemans, et al. "Plasma Multiplatform Metabolomics Towards Evaluation of Gender Differences in Pulmonary Arterial Hypertension—A Pilot Study." Biomedicines 13, no. 7 (2025): 1637. https://doi.org/10.3390/biomedicines13071637.

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Background: Pulmonary arterial hypertension (PAH) is a rare and severe condition characterized by increased pulmonary arterial pressure and vascular resistance. Women are more susceptible to PAH yet have higher survival rates than men, a phenomenon called the “estrogen paradox”. This study aims to investigate the sex-based differences in PAH using plasma untargeted metabolomics. Methods: Plasma samples were collected from 43 PAH patients and 37 healthy controls. The samples were analyzed using two complementary analytical techniques: gas chromatography–mass spectrometry (GC-QqQ/MS) and liquid
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Dissertations / Theses on the topic "Pulmonary arterial hypertension (PAH) metabolomics"

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Assaggaf, Hamza M. "Molecular Risk Factors of Pulmonary Arterial Hypertension." FIU Digital Commons, 2017. https://digitalcommons.fiu.edu/etd/3554.

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The overall objective of the research presented in this dissertation was to investigate molecular risk factors of susceptibility to estrogenic chemicals, polychlorinated biphenyls (PCBs), hormone replacement therapy, and oral contraceptives and how that leads to the development of pulmonary arterial hypertension (PAH). Environmental and molecular risk factors for PAH are not clearly understood. This is a major hurdle for the development of new therapy against PAH as well as understanding individual susceptibility to this disease. Gender has been shown to impact the prevalence of PAH. Although
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Jacher, Joseph E. B. A. "Pulmonary Arterial Hypertension: Specialists’ Knowledge, Practices, and Attitudes of Genetic Testing and Genetic Counseling." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1427797616.

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Cheong, Fei Ying. "Towards the identification of predictors for pulmonary arterial hypertension (PAH) in sclerodermia (SSC) patients." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12325.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.<br>Identification of predictors and biomarkers to monitor disease status and progression in patients with Scleroderma or Systemic Sclerosis (SSc) is of great interest due to its elevated morbidity and mortality of
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Fowler, Robin. "The impact of elevated pulmonary artery pressure on exercise responses." Thesis, Curtin University, 2012. http://hdl.handle.net/20.500.11937/2637.

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Background and research questions. The four studies reported in this thesis investigated the implications of an elevated pulmonary artery pressure (PAP) on the response to an exertional challenge. The level of symptoms and exertion that healthcare professionals consider appropriate for patients with pulmonary arterial hypertension (PAH) was explored in the first study. In studies two, three, and four, exercise responses and exercise testing were evaluated in individuals with an elevated PAP on exercise, but a normal PAP at rest (exercise-induced pulmonary arterial hypertension, [EIPAH]).The fo
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Seifert, Elena. "Metabolic Changes in Pulmonary Arterial Smooth Muscle Cells Exposed to Increased Mechanical Forces from an Ovine Model of Congenital Heart Disease with Increased Pulmonary Blood Flow." Scholarship @ Claremont, 2019. https://scholarship.claremont.edu/cmc_theses/2094.

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An important cause of pulmonary arterial hypertension (PAH) in children with congenital heart disease (CHD) is increased pulmonary blood flow (PBF). To gain a better understanding of the disease process, the changes in biochemical pathways and metabolism of pulmonary arterial smooth muscle cells (PASMCs) were studied using a unique surgical ovine model of increased pulmonary blood flow. PASMCs isolated from 4-week-old lambs with increased PBF (shunt) showed lower oxygen consumption rates and lower extracellular acidification rates linked to glutamine metabolism when compared to controls. Shunt
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Sharmin, Nahid. "Therapeutic Targeting of BMP and TGF-β Signalling Pathways for the Resolution of Pulmonary Arterial Hypertension". Thesis, University of Bradford, 2018. http://hdl.handle.net/10454/17177.

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Vascular remodelling due to excessive proliferation and apoptosis resistance of pulmonary arterial smooth muscle (PASMCs) and endothelial cells (ECs) has been attributed to the pathogenesis of pulmonary arterial hypertension (PAH). It is an incurable cardiovascular disorder, which leads to right heart failure and death, if left untreated. Heterozygous germline mutations in the bone morphogenetic protein receptor type II (BMPR2) have been linked with the majority (~75%) of the familial form of the disease (HPAH). Mutations in the BMPR2 gene impinge upon the BMP signalling which perturbs
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Hassan, Dhiya. "Forced Overexpression of Translationally Controlled Tumor Protein (TCTP/TPT1) Induces a Growth-Dysregulated Phenotype in Endothelial and Smooth Muscle Cells: Role of TCTP Exosomal Export in Paracrine Cell-Cell Signaling Induced by Endothelial Injury." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/38674.

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Background: Pulmonary arterial hypertension (PAH) is a lethal disease for which the fundamental molecular mechanisms are only partially understood. Existing therapies, which primarily focus on endothelial dysfunction, have limited effects on improving outcomes. Increases in pulmonary vascular resistance in PAH may be attributed to complex lung arterial remodeling which result in obliterative “plexiform” lesions, a pathological hallmark of this disease. Recent studies have shown that endothelial cell (ECs) apoptosis may be a central trigger for PAH, resulting in the emergence of growth-dysregul
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Jacquin, Sophie. "Rôle de la protéine p53 dans l’hypertension artérielle pulmonaire humaine et expérimentale." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA114838/document.

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Le terme d’« hypertension artérielle pulmonaire » (HTAP) décrit une maladie vasculaire pulmonaire caractérisée par une augmentation progressive des pressions artérielles pulmonaires (PAP), définie par une PAP moyenne supérieure ou égale à 25 mmHg au repos et dont le principal symptôme est un essoufflement à l’effort. Un remodelage artériel pulmonaire intense conduisant à une obstruction des petits vaisseaux pulmonaires est responsable de la maladie. C’est une maladie rare mais néanmoins grave car pouvant aboutir à une insuffisance ventriculaire droite et entraîner le décès du patient.Le cadre
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Siddiqui, M. A., T. Ogo, and Md Talat Nasim. "Pulmonary arterial hypertension: molecular genetic basis and emerging treatments." 2012. http://hdl.handle.net/10454/7971.

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Yes<br>Pulmonary arterial hypertension (PAH) is a rare cardiovascular disorder caused by narrowing of blood vessels in the lung and in the absence of therapy leads to right heart failure and death. No cure for this devastating disorder is known. The major objective of the current treatments is to improve symptoms and these therapies were developed prior to the discovery that this disease has substantial genetic components. In this review, we discuss molecular genetic basis of PAH together with pathobiology, current and future therapeutic interventions.
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Ferraz, Tiago Guimarães. "MZ-21 (AMP-DNM) as potential treatment of Pulmonary Arterial Hypertension (PAH)." Master's thesis, 2017. https://repositorio-aberto.up.pt/handle/10216/110743.

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Books on the topic "Pulmonary arterial hypertension (PAH) metabolomics"

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Istaphanous, George K., and Andreas W. Loepke. Pulmonary Hypertension. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199764495.003.0035.

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Pediatric pulmonary arterial hypertension (PAH) is characterized by a pathologically elevated pulmonary artery pressure in children. The etiology of PAH is multifactorial, and while its prognosis is closely related to the reversibility of the underlying disease process, much progress has recently been made in its diagnosis and treatment, significantly decreasing the associated morbidity and mortality.
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Thorne, Sara, and Sarah Bowater. Pulmonary hypertension in ACHD. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759959.003.0016.

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Pulmonary arterial hypertension (PAH) is a common complication in ACHD patients, with a prevalence of around 10% in developed countries. It is most commonly due to large, uncorrected left-to-right shunts, although a permissive genotype might explain its development in other, seemingly lower-risk, patients. Histologically, PAH in ACHD is the same as PAH due to other aetiologies, such as idiopathic and connective tissue disease.
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Vigil, Karen J. Non-opportunistic Infections. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0036.

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Lymphocytic interstitial pneumonitis is a common respiratory complication of HIV infection in children but a rare complication in HIV-infected adults. The diagnosis requires histologic confirmation by biopsy. Antiretroviral therapy has been used with success for treatment. Nonspecific interstitial pneumonitis (NSIP) presents with dyspnea, nonproductive cough, and fever in patients with CD4+ T cell counts &gt;200 cells/mm3. The diagnosis of NSIP requires histologic confirmation by biopsy. The optimum treatment remains unclear. The prevalence of pulmonary arterial hypertension (PAH) is higher in
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Book chapters on the topic "Pulmonary arterial hypertension (PAH) metabolomics"

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Garcia, Kristen, Marcus Hock, Vikrant Jaltare, et al. "Investigating the Multiscale Impact of Deoxyadenosine Triphosphate (dATP) on Pulmonary Arterial Hypertension (PAH) Induced Heart Failure." In Computational Physiology. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-05164-7_7.

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Abstract2-deoxy-ATP (dATP) is a myosin activator known to improve cardiac contractile force [1]. In vitro studies have shown that dATP alters the calcium transient profile in addition to the kinetics of the cross-bridge cycle [2]. Furthermore, in vivo studies of transgenic mice with increased production of dATP show elevated left ventricular systolic function [3]. Pulmonary arterial hypertension (PAH) is a rare disease of the pulmonary vasculature in which pressure overload in the right ventricle results in reduced contractile function and right heart failure [4]. We hypothesize that dATP may
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Cui, Jiaxin, Mariluz Rojo Domingo, Ryan Konno, et al. "Impact of Pathological Vascular Remodelling on Right Ventricular Mechanics." In Computational Physiology. Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-25374-4_7.

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AbstractPulmonary arterial hypertension (PAH) is a rare disorder characterized by elevated blood pressure and pulmonary vascular resistance, often followed by right ventricular hypertrophy and heart failure. The effect of PAH and its treatments on the mechanics, function, and remodelling of the right ventricle (RV) is currently not well understood. To study cardiac biomechanics and functionality as PAH progresses, we implemented a computational model of the heart simulating right ventricular maladaptive remodelling. Our Windkessel-based model, which accounts for direct ventricular interaction
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Cicco, S., P. Leone, V. Racanelli, and A. Vacca. "Mucine-1 Is Related to Cell-Mediated Immunoexpression and Blood Pressure in Pulmonary Artery in Pulmonary Arterial Hypertension (PAH): Preliminary Results." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91287-5_44.

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Chakravarty, Eliza. "Pulmonary arterial hypertension." In Practical management of the pregnant patient with rheumatic disease, edited by Karen Schreiber, Eliza Chakravarty, and Monika Østensen. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198845096.003.0004.

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Pulmonary arterial hypertension (PAH) is a recognized manifestation of connective tissue diseases, particularly systemic lupus erythematosus and systemic sclerosis. It is associated with high rates of morbidity and mortality in general, and these risks increase substantially during pregnancy and delivery. Women with systemic sclerosis who wish to conceive should have an evaluation for PAH prior to pregnancy. Women with known PAH should be counselled about the high risks to maternal health associated with pregnancy, and permanent or long acting reversible contraception strongly recommended. Wom
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Elliott, Perry, Pier D. Lambiase, and Dhavendra Kumar. "Pulmonary arterial hypertension." In Inherited Cardiac Disease. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198829126.003.0014.

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This chapter covers pulmonary hypertension (PH), including its definitions and classifications. Pulmonary arterial hypertension (PAH) is a pre-capillary form of PH, and its clinical features and signs are described. The 2019 updated clinical classification of PH is included, along with hereditable PAH, associated genetic mutations, and clinical screenings.
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"Pulmonary Arterial Hypertension (PAH)." In Thoracic Pathology. Elsevier, 2012. http://dx.doi.org/10.1016/b978-1-4377-2380-9.00067-x.

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"Pulmonary Arterial Hypertension (PAH)." In Encyclopedia of Trauma Care. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-29613-0_101237.

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Hadinnapola, Charaka, and Nicholas Morrell. "Heritable pulmonary arterial hypertension." In ESC CardioMed, edited by Marc Humbert. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0590.

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Heritable pulmonary arterial hypertension (PAH) is diagnosed in patients presenting with PAH who have a family history of the disease or carry a mutation in a gene known to be associated with PAH. Heterozygous mutations in the gene encoding the bone morphogenetic protein receptor type 2 (BMPR2) are the most common genetic defects seen in heritable PAH. Mutations in BMPR2 are found in 82% of patients with a family history of PAH and 17% of patients presenting with no family history of the disease. Other causal genes include members of the transforming growth factor beta pathway, including activ
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Mar, Hugo Paz y., and Neal F. Chaisson. "Pulmonary Arterial Hypertension." In Sleep Disorders. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190671099.003.0052.

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The high prevalence of pulmonary arterial hypertension (PAH) in patients with obstructive sleep apnea (OSA) and the putative pathophysiologic connections have been extensively documented. Conversely, patients with established PAH are at risk for sleep-related ventilatory instability, including OSA, central sleep apnea, and nocturnal desaturations. This chapter reviews the prevalence and pathophysiologic interactions of these conditions, the interplay with associated disorders, and the effects of continuous positive airway pressure therapy on pulmonary hemodynamics. In patients with OSA, chroni
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Moledina, Shahin, and Bejal Pandya. "Pulmonary hypertension." In ESC CardioMed. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0181.

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Congenital heart disease is a major cause of pulmonary arterial hypertension (PAH) and this can largely be prevented by early repair. PAH in the presence of systemic-to-pulmonary communication, leads to shunt reversal and cyanosis, with multiple systemic consequences (Eisenmenger syndrome). Congenital heart disease patients with PAH are vulnerable and are at high risk from non-cardiac surgery, pregnancy, and inappropriate medical treatment (e.g. excessive venesection). Survival is reduced, but is better than in idiopathic PAH. Recommendations for surgery should be based on careful assessment b
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Conference papers on the topic "Pulmonary arterial hypertension (PAH) metabolomics"

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Oliveira, Talita, Daniela Calderaro, Bruna Piloto, et al. "Platelets and pulmonary arterial hypertension (PAH)." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4756.

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Winkler, T., P. Kohli, V. J. Kelly, et al. "Regional Pulmonary Vascular Resistance in Pulmonary Arterial Hypertension (PAH)." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4513.

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Higton, AM, CI Whale, NA Fernandez, et al. "Similarities between Pulmonary Hypertension (PHT) Complicating Lung Disease and Pulmonary Arterial Hypertension (PAH)." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4913.

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Yahiaoui, Rachida, Zakia Bennoui, Djenette Hakem, Rabah Amrane, and Rafika Boughrarou. "Epidemiological and Clinical aspects of pulmonary arterial hypertension (PAH)." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa3095.

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Strange, Geoff, Anne Keogh, Simon stewart, et al. "Symptoms To Definitive Diagnosis Of Pulmonary Arterial Hypertension (PAH)." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1923.

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Barbera, Joan Albert, Nazzareno Galie, Adaani Frost, et al. "Pulmonary Function and response to treatment in pulmonary arterial hypertension (PAH)." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2411.

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Batson, M., J. Minhas, O. A. Shlobin, et al. "Physical Activity Characteristics in Pulmonary Arterial Hypertension (PAH): The Pulmonary Hypertension Association Registry (PHAR)." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a3748.

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Man, D. K. W., W. M. Kuebler, and O. T. Guenat. "Advanced 3D Arterial Microvessel-on-Chip to Model Pulmonary Arterial Hypertension (PAH)." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a7135.

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Zapata Ortega, M., E. Revilla López, B. Sáez Gimenez, et al. "Lung transplantation in pulmonary arterial hypertension (PAH): survival analysis according to PAH risk." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1747.

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Jais, X., L. Savale, O. Sitbon, et al. "Hemoptysis in Pulmonary Arterial Hypertension (PAH): A Life-Threatening Complication." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2667.

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