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These findings document a much higher local pulmonary arterial hypertension incidence and prevalence than previously reported in REVEAL. While population ethnicity differed markedly from REVEAL, the disease burden was not driven by these differences. The possible association of moderately increased residential altitude with pulmonary arterial hypertension warrants further evaluation. © The Author(s) 2020.Pulmonary hypertension is a complex, multifactorial disease that results in right heart failure and premature death. Since the initial reports of pulmonary hypertension in the late 1800s, the diagnosis of pulmonary hypertension has evolved with respect to its definition, screening tools, and diagnostic techniques. This historical perspective traces the earliest roots of pulmonary hypertension detection and diagnosis through to the current recommendations for classification. We highlight the diagnostic tools used in the past and present, and end with a focus on the future directions of early detection. Early detection of pulmonary hypertension and pulmonary arterial hypertension and the proper determination of etiology are vital for the early therapeutic intervention that can prolong life expectancy and improve quality of life. The search for a non-invasive screening tool for the identification and classification of pulmonary hypertension is ongoing, and we discuss the role of animal models of the disease in this search. © The Author(s) 2020.We aimed to characterize the plasma metabolome of chronic thromboembolic pulmonary hypertension patients using a high-throughput unbiased omics approach. We collected fasting plasma from a peripheral vein in 33 operable chronic thromboembolic pulmonary hypertension patients, 31 healthy controls, and 21 idiopathic pulmonary arterial hypertension patients matched for age, gender, and body mass index. Metabolomic analysis was performed using an untargeted approach (Metabolon Inc. Durham, NC). Of the total of 862 metabolites identified, 362 were different in chronic thromboembolic pulmonary hypertension compared to controls 178 were higher and 184 were lower. Compared to idiopathic pulmonary arterial hypertension, 147 metabolites were different in chronic thromboembolic pulmonary hypertension 45 were higher and 102 were lower. The plasma metabolome allowed us to distinguish subjects with chronic thromboembolic pulmonary hypertension and healthy controls with a predictive accuracy of 89%, and chronic thromboembolic pulmonary hypertension versus idiopathic pulmonary arterial hypertension with 80% accuracy. Compared to idiopathic pulmonary arterial hypertension and healthy controls, chronic thromboembolic pulmonary hypertension patients had higher fatty acids and glycerol; while acyl cholines and lysophospholipids were lower. Compared to healthy controls, both idiopathic pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension patients had increased acyl carnitines, beta-hydroxybutyrate, amino sugars and modified amino acids and nucleosides. The plasma global metabolomic profile of chronic thromboembolic pulmonary hypertension suggests aberrant lipid metabolism characterized by increased lipolysis, fatty acid oxidation, and ketogenesis, concomitant with reduced acyl choline and phospholipid moieties. Future research should investigate the pathogenetic and therapeutic potential of modulating lipid metabolism in chronic thromboembolic pulmonary hypertension. © The Author(s) 2020.Selexipag is an oral prostacyclin receptor agonist; it was recently approved for use in adults with pulmonary arterial hypertension. The safety and efficacy of selexipag has not yet been determined in the pediatric population. We describe short-term hemodynamic and clinical data with selexipag therapy in four pediatric patients with pulmonary hypertension. We reviewed clinical, echocardiographic, and hemodynamic data. One patient was transitioned from subcutaneous treprostinil to selexipag, and in three patients, selexipag was added as a third agent. Drug dosing was attained empirically based on patient body size. A follow-up catheterization was performed 12-18 months after initiation of selexipag therapy. All four patients tolerated selexipag well, without significant side effects. One patient transitioned successfully from subcutaneous treprostinil to selexipag. None of the four patients had clinical deterioration. In three patients who were able to perform a 6-minute walk test, pre and post selexipag distances were 350 and 400, 409 and 390, and 300 and 360 m, respectively. Echocardiograms showed no significant changes. Catheterization showed a variable change in pulmonary vascular resistance (small decrease in three patients and increase in one patient). Brain natriuretic peptide levels before and after selexipag in the four patients were 38 and 49, 33 and 54, 29 and 25, and 12 and 14 pg/mL, respectively. Selexipag use for 16-28 months was safe in four pediatric patients; none of them had clinical deterioration. Larger number of patients and longer follow-up intervals are necessary before further recommendations can be made. learn more © The Author(s) 2020.Background Rhinitis is a common problem within the population. Many subjects with rhinitis also have atopic multimorbidity, such as asthma and eczema. The purpose of this investigation was to compare subjects with only rhinitis to those that have rhinitis, asthma and/or eczema in relation to immunoglobulin E (IgE) sensitization, inflammatory markers, family history, lung function and body mass index (BMI). Methods A total of 216 adult subjects with rhinitis from the European Community Respiratory Health Survey II were investigated with multiplex component allergen analysis (103 allergen components), total IgE, C-reactive protein, eosinophilic cationic protein, fractional exhaled nitric oxide and spirometry. Rhinitis, eczema, asthma and parental allergy were questionnaire-assessed. Results Of the 216 participants with rhinitis, 89 also had asthma and/or eczema. Participants with rhinitis that also had asthma or eczema were more likely to be IgE-sensitized (3.44, odds ratio, OR 95% CI 1.62-7.30, adjusted for sex, age, mother’s allergy, total IgE and forced expiratory volume (FEV1)).