Pub Date : 2019-03-01DOI: 10.21693/1933-088X-18.1.37
Traci Housten, E. Jackson, A. Davis
Children with Down syndrome and pulmonary hypertension (PH) are a unique and challenging group of patients. Down syndrome, or Trisomy 21, affects approximately one in every 600 to 800 live births. PH, currently defined as a resting mean pulmonary artery pressure of ≥25 mm Hg, is known to increase morbidity and mortality significantly in this group of patients and has been identified in as many as 28% of all patients with Down syndrome. Furthermore, specific risk factors and comorbidities have been shown to increase the chance of developing PH in this population. Careful screening and proper treatment is imperative in children with Down syndrome to prevent the development, recurrence, or progression of PH in this population. Recent findings from Bush et al demonstrate clear clinical characteristics and risk factors for development of PH in children with Down syndrome. Prior to this study, data regarding the incidence of PH throughout the Down syndrome lifespan, associations with comorbidities, exacerbating factors, and overall impact of PH in the Down syndrome population were lacking. Most notably, perhaps, was their finding that a vast majority (87%) of patients who suffered from recurrent PH after a previous resolution were classified as World Health Organization (WHO) Group 3 or associated with lung disease. The study also demonstrated that obstructive sleep apnea (OSA), recurrent hypoxia, and aspiration are clear risk factors for development or recurrence of PH. Given these findings, we as providers must take an organized approach in screening for potentially preventable lung insults that contribute to the development and further progression of PH.
患有唐氏综合征和肺动脉高压(PH)的儿童是一个独特且具有挑战性的患者群体。唐氏综合症，或21三体，大约每600到800个活产婴儿中就有一个患有唐氏综合症。PH，目前定义为静息平均肺动脉压≥25 mm Hg，已知会显著增加这组患者的发病率和死亡率，并已在多达28%的唐氏综合征患者中被发现。此外，特定的危险因素和合并症已被证明会增加这一人群发生PH的机会。仔细的筛查和适当的治疗对于患有唐氏综合症的儿童至关重要，以防止该人群中PH的发生、复发或进展。Bush等人最近的研究结果明确了唐氏综合征儿童PH发展的临床特征和危险因素。在这项研究之前，缺乏关于唐氏综合征人群中PH在整个唐氏综合征生命周期中的发病率、与合共病的关系、加剧因素以及PH总体影响的数据。也许最值得注意的是，他们发现绝大多数(87%)在先前的解决后再次遭受PH的患者被世界卫生组织(who)分类为第3组或与肺部疾病相关。该研究还表明，阻塞性睡眠呼吸暂停(OSA)、复发性缺氧和误吸是PH发生或复发的明显危险因素。鉴于这些发现，我们作为提供者必须采取有组织的方法筛查可能导致PH发生和进一步进展的可预防的肺损伤。
{"title":"PH Professional Network: Comprehensive Evaluation and Ongoing Approach to Children With Down Syndrome Who Have Pulmonary Hypertension or Are at Risk of Developing Pulmonary Hypertension","authors":"Traci Housten, E. Jackson, A. Davis","doi":"10.21693/1933-088X-18.1.37","DOIUrl":"https://doi.org/10.21693/1933-088X-18.1.37","url":null,"abstract":"Children with Down syndrome and pulmonary hypertension (PH) are a unique and challenging group of patients. Down syndrome, or Trisomy 21, affects approximately one in every 600 to 800 live births. PH, currently defined as a resting mean pulmonary artery pressure of ≥25 mm Hg, is known to increase morbidity and mortality significantly in this group of patients and has been identified in as many as 28% of all patients with Down syndrome. Furthermore, specific risk factors and comorbidities have been shown to increase the chance of developing PH in this population. Careful screening and proper treatment is imperative in children with Down syndrome to prevent the development, recurrence, or progression of PH in this population. Recent findings from Bush et al demonstrate clear clinical characteristics and risk factors for development of PH in children with Down syndrome. Prior to this study, data regarding the incidence of PH throughout the Down syndrome lifespan, associations with comorbidities, exacerbating factors, and overall impact of PH in the Down syndrome population were lacking. Most notably, perhaps, was their finding that a vast majority (87%) of patients who suffered from recurrent PH after a previous resolution were classified as World Health Organization (WHO) Group 3 or associated with lung disease. The study also demonstrated that obstructive sleep apnea (OSA), recurrent hypoxia, and aspiration are clear risk factors for development or recurrence of PH. Given these findings, we as providers must take an organized approach in screening for potentially preventable lung insults that contribute to the development and further progression of PH.","PeriodicalId":92747,"journal":{"name":"Advances in pulmonary hypertension","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48040568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-03-01DOI: 10.21693/1933-088x-18.1.25
Guest editor Dunbar Ivy, MD, Chief of Pediatric Cardiology and Director of the Pediatric Pulmonary Hypertension Program at the University of Colorado School of Medicine and Children's Hospital of Colorado led a discussion among Editor-in-Chief Harrison (Hap) Farber, MD, then Professor of Medicine and Director of the Pulmonary Hypertension Center at Boston University/Boston Medical Center; Mary P. Mullen, MD, PhD, Assistant Professor of Pediatrics at Harvard Medical School, associate cardiologist at Boston Children's Hospital and Associate Director of the Pulmonary Hypertension Service as well as a member of the adult congenital heart program; Jeffrey R. Fineman, MD, Professor and Vice Chair of Pediatrics, Director of Pediatric Critical Care Medicine and Pulmonary Hypertension, University of California, San Francisco, Benioff Children's Hospital; and Gareth Morgan, MD, Associate Professor of Pediatrics-Cardiology at the University of Colorado School of Medicine and Director of the Cardiac Catheterization Lab at Children's Hospital of Colorado.
{"title":"Pulmonary Hypertension Roundtable: The Crossover From Child to Adult With PH and Congenital Heart Disease","authors":"","doi":"10.21693/1933-088x-18.1.25","DOIUrl":"https://doi.org/10.21693/1933-088x-18.1.25","url":null,"abstract":"Guest editor Dunbar Ivy, MD, Chief of Pediatric Cardiology and Director of the Pediatric Pulmonary Hypertension Program at the University of Colorado School of Medicine and Children's Hospital of Colorado led a discussion among Editor-in-Chief Harrison (Hap) Farber, MD, then Professor of Medicine and Director of the Pulmonary Hypertension Center at Boston University/Boston Medical Center; Mary P. Mullen, MD, PhD, Assistant Professor of Pediatrics at Harvard Medical School, associate cardiologist at Boston Children's Hospital and Associate Director of the Pulmonary Hypertension Service as well as a member of the adult congenital heart program; Jeffrey R. Fineman, MD, Professor and Vice Chair of Pediatrics, Director of Pediatric Critical Care Medicine and Pulmonary Hypertension, University of California, San Francisco, Benioff Children's Hospital; and Gareth Morgan, MD, Associate Professor of Pediatrics-Cardiology at the University of Colorado School of Medicine and Director of the Cardiac Catheterization Lab at Children's Hospital of Colorado.","PeriodicalId":92747,"journal":{"name":"Advances in pulmonary hypertension","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48750940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-03-01DOI: 10.21693/1933-088X-18.1.19
J. Fineman, S. Black
The pathophysiology of pulmonary hypertension (PH) is multifactorial, complex, and incompletely understood. However, it is known that abnormal mechanical forces within the pulmonary vasculature participate in the disease process. The pulmonary vasculature is continually exposed to hemodynamic forces that include: (1) shear stress, the tangential friction force acting on the vessel wall due to blood flow; (2) hydrostatic pressure, the perpendicular force acting on the vascular wall; and (3) cyclic strain, the circumferential stretch of the vessel wall. Mechanosensors on pulmonary vascular endothelial cells detect these forces and transduce them into biochemical signals that trigger vascular responses (Figure 1). Among the various force-induced signaling molecules, nitric oxide (NO), reactive oxygen species (ROS), and endothelin-1 (ET-1) have been implicated in vascular health and disease. For example, increases in physiologic shear stress associated with increased cardiac output (ie, during exercise) result in induction of NO production with decreased ROS and ET-1, facilitating pulmonary vasodilation and increased flow. However, the pathologic pulmonary vasculature may induce supraphysiologic levels of shear stress, pressure, and cyclic strain resulting in decreased NO with increased ROS and ET-1. Thus, abnormal hemodynamic forces develop in and participate in the disease progression of most forms of pulmonary vascular disease (PVD). However, the influence of hemodynamic forces in the pathobiology of PVD is most clearly demonstrated in patients with PH secondary to congenital heart disease (CHD).
{"title":"Pressure vs Flow-Induced Pulmonary Hypertension","authors":"J. Fineman, S. Black","doi":"10.21693/1933-088X-18.1.19","DOIUrl":"https://doi.org/10.21693/1933-088X-18.1.19","url":null,"abstract":"The pathophysiology of pulmonary hypertension (PH) is multifactorial, complex, and incompletely understood. However, it is known that abnormal mechanical forces within the pulmonary vasculature participate in the disease process. The pulmonary vasculature is continually exposed to hemodynamic forces that include: (1) shear stress, the tangential friction force acting on the vessel wall due to blood flow; (2) hydrostatic pressure, the perpendicular force acting on the vascular wall; and (3) cyclic strain, the circumferential stretch of the vessel wall. Mechanosensors on pulmonary vascular endothelial cells detect these forces and transduce them into biochemical signals that trigger vascular responses (Figure 1). Among the various force-induced signaling molecules, nitric oxide (NO), reactive oxygen species (ROS), and endothelin-1 (ET-1) have been implicated in vascular health and disease. For example, increases in physiologic shear stress associated with increased cardiac output (ie, during exercise) result in induction of NO production with decreased ROS and ET-1, facilitating pulmonary vasodilation and increased flow. However, the pathologic pulmonary vasculature may induce supraphysiologic levels of shear stress, pressure, and cyclic strain resulting in decreased NO with increased ROS and ET-1. Thus, abnormal hemodynamic forces develop in and participate in the disease progression of most forms of pulmonary vascular disease (PVD). However, the influence of hemodynamic forces in the pathobiology of PVD is most clearly demonstrated in patients with PH secondary to congenital heart disease (CHD).","PeriodicalId":92747,"journal":{"name":"Advances in pulmonary hypertension","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43406948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-03-01DOI: 10.21693/1933-088X-18.1.14
Stephanie S. Handler, J. Feinstein
Despite significant improvements in the surgical and postoperative care for patients with single-ventricle physiology culminating in the Fontan circulation, significant late morbidity and mortality remains. In the setting of passive (ie, non-“pump” driven) pulmonary blood flow, pulmonary vascular resistance (PVR) plays a key role in determining cardiac output, and even slight elevations in PVR may result in significant morbidity. There is now great interest to treat Fontan patients with pulmonary vasodilators in an attempt to “optimize” PVR (and by extension, quality of life) and/or improve an elevated PVR. This review discusses the hemodynamic implications of the Fontan circulation, the evidence for use of pulmonary vasodilator therapy, and possible target physiologic mechanisms.
{"title":"Pulmonary Vascular Disease in the Single-Ventricle Patient: Is it Really Pulmonary Hypertension and if So, How and When Should We Treat it?","authors":"Stephanie S. Handler, J. Feinstein","doi":"10.21693/1933-088X-18.1.14","DOIUrl":"https://doi.org/10.21693/1933-088X-18.1.14","url":null,"abstract":"Despite significant improvements in the surgical and postoperative care for patients with single-ventricle physiology culminating in the Fontan circulation, significant late morbidity and mortality remains. In the setting of passive (ie, non-“pump” driven) pulmonary blood flow, pulmonary vascular resistance (PVR) plays a key role in determining cardiac output, and even slight elevations in PVR may result in significant morbidity. There is now great interest to treat Fontan patients with pulmonary vasodilators in an attempt to “optimize” PVR (and by extension, quality of life) and/or improve an elevated PVR. This review discusses the hemodynamic implications of the Fontan circulation, the evidence for use of pulmonary vasodilator therapy, and possible target physiologic mechanisms.","PeriodicalId":92747,"journal":{"name":"Advances in pulmonary hypertension","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46908984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-11-01DOI: 10.21693/1933-088X-17.3.123
F. Shah, A. Duarte
{"title":"PH Grand Rounds: Interferon-Associated Pulmonary Arterial Hypertension","authors":"F. Shah, A. Duarte","doi":"10.21693/1933-088X-17.3.123","DOIUrl":"https://doi.org/10.21693/1933-088X-17.3.123","url":null,"abstract":"","PeriodicalId":92747,"journal":{"name":"Advances in pulmonary hypertension","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41971745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-11-01DOI: 10.21693/1933-088X-17.3.121
S. Studer, C. King, O. Shlobin
{"title":"Ask the Expert: What Is the Association Between Thyroid Disease and Pulmonary Hypertension: Do Pulmonary Arterial Hypertension Patients Need a Closer Look?","authors":"S. Studer, C. King, O. Shlobin","doi":"10.21693/1933-088X-17.3.121","DOIUrl":"https://doi.org/10.21693/1933-088X-17.3.121","url":null,"abstract":"","PeriodicalId":92747,"journal":{"name":"Advances in pulmonary hypertension","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42787388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-11-01DOI: 10.21693/1933-088X-17.3.103
C. Rhodes, J. Wharton, M. Wilkins
Christopher J. Rhodes, PhD Centre for Pharmacology & Therapeutics Department of Medicine Hammersmith Campus, Imperial College London London, UK John Wharton, PhD Centre for Pharmacology & Therapeutics Department of Medicine Hammersmith Campus, Imperial College London London, UK Martin R. Wilkins, MD, FRCP Centre for Pharmacology & Therapeutics Department of Medicine Hammersmith Campus, Imperial College London London, UK
Christopher J. Rhodes，英国伦敦帝国理工学院哈默史密斯校区药理学与治疗学博士中心John Wharton，英国伦敦帝国理工学院哈默史密斯校区药理学与治疗学博士中心Martin R. Wilkins，医学博士，英国伦敦帝国理工学院哈默史密斯校区药理学与治疗学FRCP中心
{"title":"Metabolomic Insights in Pulmonary Arterial Hypertension","authors":"C. Rhodes, J. Wharton, M. Wilkins","doi":"10.21693/1933-088X-17.3.103","DOIUrl":"https://doi.org/10.21693/1933-088X-17.3.103","url":null,"abstract":"Christopher J. Rhodes, PhD Centre for Pharmacology & Therapeutics Department of Medicine Hammersmith Campus, Imperial College London London, UK John Wharton, PhD Centre for Pharmacology & Therapeutics Department of Medicine Hammersmith Campus, Imperial College London London, UK Martin R. Wilkins, MD, FRCP Centre for Pharmacology & Therapeutics Department of Medicine Hammersmith Campus, Imperial College London London, UK","PeriodicalId":92747,"journal":{"name":"Advances in pulmonary hypertension","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42454475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-11-01DOI: 10.21693/1933-088X-17.3.126
Traci Housten, Anna M. Brown
Medications for pulmonary hypertension (PH) are expensive and often require prior authorization from insurance payers. The task of submitting prior authorization requests and appealing denials can burden PH practices with a heavy workload and delay or interrupt medical treatment. However, it is possible to reduce this burden, improve success rates, and reduce waiting times by implementing a standard office workflow for managing the prior authorization process. Such a system involves several key components: assessment of existing staff and level of expertise; dedicated office staff to oversee the process from start to finish; streamlined gathering, storage, and transmittal of patient documents; direct communication with pharmacies and Risk Evaluation Mitigation Strategy programs; and careful documentation of PH diagnosis and treatment plans for a given patient, aimed at reducing the necessity for appeals. This article reviews prior authorization strategies and systems used at PH clinics, and case studies in other therapeutic areas that demonstrate how such systems can reduce staff time and waiting time for initiation of medications while improving the rate of success. The article also describes the special challenges of requesting prior authorization for PH medications prescribed to pediatric patients.
{"title":"PH Professional Network: The Burden of Prior Authorization for Pulmonary Hypertension Medications: A Practical Guide for Managing the Process","authors":"Traci Housten, Anna M. Brown","doi":"10.21693/1933-088X-17.3.126","DOIUrl":"https://doi.org/10.21693/1933-088X-17.3.126","url":null,"abstract":"Medications for pulmonary hypertension (PH) are expensive and often require prior authorization from insurance payers. The task of submitting prior authorization requests and appealing denials can burden PH practices with a heavy workload and delay or interrupt medical treatment. However, it is possible to reduce this burden, improve success rates, and reduce waiting times by implementing a standard office workflow for managing the prior authorization process. Such a system involves several key components: assessment of existing staff and level of expertise; dedicated office staff to oversee the process from start to finish; streamlined gathering, storage, and transmittal of patient documents; direct communication with pharmacies and Risk Evaluation Mitigation Strategy programs; and careful documentation of PH diagnosis and treatment plans for a given patient, aimed at reducing the necessity for appeals. This article reviews prior authorization strategies and systems used at PH clinics, and case studies in other therapeutic areas that demonstrate how such systems can reduce staff time and waiting time for initiation of medications while improving the rate of success. The article also describes the special challenges of requesting prior authorization for PH medications prescribed to pediatric patients.","PeriodicalId":92747,"journal":{"name":"Advances in pulmonary hypertension","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42289955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-11-01DOI: 10.21693/1933-088X-17.3.110
E. Brittain
Metabolic derangement is a pathologic feature of pulmonary arterial hypertension (PAH).1 Metabolic abnormalities such as aerobic glycolysis and impaired fatty acid oxidation are consistently observed across different animal models of PAH. Importantly, altered metabolism in human PAH and experimental models is not restricted to the pulmonary vasculature, raising the possibility that PAH is a systemic metabolic disease.2 For example, lipid accumulation is present in the myocardium and skeletal muscle of humans with PAH and the right ventricle exhibits increased glucose uptake compared with matched controls. As a result of these observations, targeting metabolic dysfunction has emerged as an important therapeutic approach for patients with PAH.3 This article will review key aspects of metabolism in PAH, existing metabolic data in humans, and will describe completed and ongoing clinical trials targeting metabolic dysfunction in patients with PAH.
{"title":"Clinical Trials Targeting Metabolism in Pulmonary Arterial Hypertension","authors":"E. Brittain","doi":"10.21693/1933-088X-17.3.110","DOIUrl":"https://doi.org/10.21693/1933-088X-17.3.110","url":null,"abstract":"Metabolic derangement is a pathologic feature of pulmonary arterial hypertension (PAH).1 Metabolic abnormalities such as aerobic glycolysis and impaired fatty acid oxidation are consistently observed across different animal models of PAH. Importantly, altered metabolism in human PAH and experimental models is not restricted to the pulmonary vasculature, raising the possibility that PAH is a systemic metabolic disease.2 For example, lipid accumulation is present in the myocardium and skeletal muscle of humans with PAH and the right ventricle exhibits increased glucose uptake compared with matched controls. As a result of these observations, targeting metabolic dysfunction has emerged as an important therapeutic approach for patients with PAH.3 This article will review key aspects of metabolism in PAH, existing metabolic data in humans, and will describe completed and ongoing clinical trials targeting metabolic dysfunction in patients with PAH.","PeriodicalId":92747,"journal":{"name":"Advances in pulmonary hypertension","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46955600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-11-01DOI: 10.21693/1933-088x-17.3.115
A. Hemnes, R. Zamanian
On June 20, 2018, Guest Editor Anna Ryan Hemnes, MD, gathered a group of pulmonary hypertension specialists by telephone to talk about the role of metabolic disease in PH. Among the participants in the animated discussion was Roham Zamanian, MD, Director of the Adult Pulmonary Hypertension Program at Stanford University Medical Center. He directs the Vera Moulton Wall Center clinical database and biobank and focuses his research on clinical characterization and impact of novel risk factors such as methamphetamine use, and biomarkers such as insulin resistance in pulmonary arterial hypertension. Readers will recall his participation in the previous issue's roundtable on drug-induced PH. Joining Dr Zamanian were Ioana Preston, MD, Pulmonary Function Lab Director; Director, Pulmonary Hypertension Center; and Associate Professor, Tufts University School of Medicine; and Advances in Pulmonary Hypertension editor-in-chief Harrison W. Farber, MD.
2018年6月20日，客座编辑Anna Ryan Hemnes医学博士通过电话召集了一群肺动脉高压专家，讨论代谢性疾病在ph中的作用。斯坦福大学医学中心成人肺动脉高压项目主任Roham Zamanian医学博士参与了热烈的讨论。他指导维拉莫尔顿沃尔中心临床数据库和生物库，并专注于临床特征和新风险因素的影响，如甲基苯丙胺的使用，以及肺动脉高压中的胰岛素抵抗等生物标志物。读者还记得他参加了上期关于药物诱导博士的圆桌会议。与Zamanian博士一起参加会议的有肺功能实验室主任Ioana Preston医学博士;肺动脉高压中心主任;塔夫茨大学医学院副教授;《肺动脉高压进展》杂志主编Harrison W. Farber，医学博士。
{"title":"Pulmonary Hypertension Roundtable: Metabolic Disease and PH","authors":"A. Hemnes, R. Zamanian","doi":"10.21693/1933-088x-17.3.115","DOIUrl":"https://doi.org/10.21693/1933-088x-17.3.115","url":null,"abstract":"On June 20, 2018, Guest Editor Anna Ryan Hemnes, MD, gathered a group of pulmonary hypertension specialists by telephone to talk about the role of metabolic disease in PH. Among the participants in the animated discussion was Roham Zamanian, MD, Director of the Adult Pulmonary Hypertension Program at Stanford University Medical Center. He directs the Vera Moulton Wall Center clinical database and biobank and focuses his research on clinical characterization and impact of novel risk factors such as methamphetamine use, and biomarkers such as insulin resistance in pulmonary arterial hypertension. Readers will recall his participation in the previous issue's roundtable on drug-induced PH. Joining Dr Zamanian were Ioana Preston, MD, Pulmonary Function Lab Director; Director, Pulmonary Hypertension Center; and Associate Professor, Tufts University School of Medicine; and Advances in Pulmonary Hypertension editor-in-chief Harrison W. Farber, MD.","PeriodicalId":92747,"journal":{"name":"Advances in pulmonary hypertension","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68108539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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