Search

Rationale: The characteristics of patients with respiratory complaints and/or lung radiologic abnormalities after hospitalisation for coronavirus disease 2019 (COVID-19) are unknown. The objectives were to determine their characteristics and the relationships between dyspnoea, radiologic abnormalities and functional impairment., Methods: In the COMEBAC (Consultation Multi-Expertise de Bicêtre Après COVID-19) cohort study, 478 hospital survivors were evaluated by telephone 4 months after hospital discharge, and 177 who had been hospitalised in an intensive care unit (ICU) or presented relevant symptoms underwent an ambulatory evaluation. New-onset dyspnoea and cough were evaluated, and the results of pulmonary function tests and high-resolution computed tomography of the chest were collected., Results: Among the 478 patients, 78 (16.3%) reported new-onset dyspnoea, and 23 (4.8%) new-onset cough. The patients with new-onset dyspnoea were younger (56.1±12.3 versus 61.9±16.6 years), had more severe COVID-19 (ICU admission 56.4% versus 24.5%) and more frequent pulmonary embolism (18.0% versus 6.8%) (all p≤0.001) than patients without dyspnoea. Among the patients reassessed at the ambulatory care visit, the prevalence of fibrotic lung lesions was 19.3%, with extent <25% in 97% of the patients. The patients with fibrotic lesions were older (61±11 versus 56±14 years, p=0.03), more frequently managed in an ICU (87.9 versus 47.4%, p<0.001), had lower total lung capacity (74.1±13.7 versus 84.9±14.8% pred, p<0.001) and diffusing capacity of the lung for carbon monoxide ( D LCO ) (73.3±17.9 versus 89.7±22.8% pred, p<0.001). The combination of new-onset dyspnoea, fibrotic lesions and D LCO <70% pred was observed in eight out of 478 patients., Conclusions: New-onset dyspnoea and mild fibrotic lesions were frequent at 4 months, but the association of new-onset dyspnoea, fibrotic lesions and low D LCO was rare., Competing Interests: Conflict of interest: E-M. Jutant has nothing to disclose. Conflict of interest: O. Meyrignac has nothing to disclose. Conflict of interest: A. Beurnier has nothing to disclose. Conflict of interest: X. Jaïs has nothing to disclose. Conflict of interest: T. Pham has nothing to disclose. Conflict of interest: L. Morin has nothing to disclose. Conflict of interest: A. Boucly has nothing to disclose. Conflict of interest: S. Bulifon has nothing to disclose. Conflict of interest: S. Figueiredo has nothing to disclose. Conflict of interest: A. Harrois has nothing to disclose. Conflict of interest: M. Jevnikar has nothing to disclose. Conflict of interest: N. Noël has nothing to disclose. Conflict of interest: J. Pichon has nothing to disclose. Conflict of interest: A. Roche has nothing to disclose. Conflict of interest: A. Seferian has nothing to disclose. Conflict of interest: S. Soliman has nothing to disclose. Conflict of interest: J. Duranteau has nothing to disclose. Conflict of interest: L. Becquemont has nothing to disclose. Conflict of interest: X. Monnet has nothing to disclose. Conflict of interest: O. Sitbon has nothing to disclose. Conflict of interest: M-F. Bellin has nothing to disclose. Conflict of interest: M. Humbert has nothing to disclose. Conflict of interest: L. Savale has nothing to disclose. Conflict of interest: D. Montani has nothing to disclose., (Copyright ©The authors 2022.)

Background: Drugs approved for the treatment of pulmonary arterial hypertension (PAH) improve long-term outcomes. These drugs have pulmonary vasodilator properties which may potentially cause a decrease in arterial oxyhaemoglobin saturation ( S ) in some patients. The present retrospective study of the French Pulmonary Hypertension Registry aimed to describe the clinical characteristics and outcomes of patients showing a ≥3% decrease in aO 2 ) in some patients. The present retrospective study of the French Pulmonary Hypertension Registry aimed to describe the clinical characteristics and outcomes of patients showing a ≥3% decrease in S aO 2 while treated with PAH drugs., Methods: We reviewed 719 PAH patients. The exclusion criteria were PAH associated with congenital heart disease and PAH with overt features of venous/capillaries involvement., Results: 173 (24%) patients had a ≥3% decrease in S . At diagnosis, they were older with a lower diffusing capacity of the lung for carbon monoxide and a shorter 6-min walk distance compared with those who did not display a ≥3% decrease in aO 2 . The percentage of patients meeting the European Society of Cardiology/European Respiratory Society (ESC/ERS) low-risk criteria at re-evaluation was significantly lower in those with a ≥3% decrease in S aO 2 5%; p<0.001). A ≥3% decrease in S was associated with a poorer survival (hazard ratio 1.81, 95% CI 1.43-2.34; p<0.0001). In a multivariate Cox analysis, a ≥3% decrease in aO 2 was a prognostic factor independent of age at diagnosis and ESC/ERS risk stratification at follow-up.versus 5%; p<0.001). A ≥3% decrease in S aO 2 was associated with a poorer survival (hazard ratio 1.81, 95% CI 1.43-2.34; p<0.0001). In a multivariate Cox analysis, a ≥3% decrease in S aO 2 was a prognostic factor independent of age at diagnosis and ESC/ERS risk stratification at follow-up., Conclusions: When treated with PAH drugs, a large subset of patients experience a ≥3% decrease in S aO 2 , which is associated with worse long-term outcomes and reduced survival., Competing Interests: Conflict of interest: S. Valentin has nothing to disclose. Conflict of interest: A. Maurac has nothing to disclose. Conflict of interest: O. Sitbon reports grants, personal fees and non-financial support from Actelion, grants and personal fees from Bayer and MSD, personal fees from Acceleron, Ferrer and Gossamer Bio, grants from GlaxoSmithKline, outside the submitted work. Conflict of interest: A. Beurnier reports personal fees from Sanofi and AstraZeneca, outside the submitted work. Conflict of interest: E. Gomez has nothing to disclose. Conflict of interest: A. Guillaumot reports non-financial support from Actelion, AstraZeneca, Boehringer Ingelheim, MSD and Roche, outside the submitted work. Conflict of interest: L. Textoris has nothing to disclose. Conflict of interest: R. Fay has nothing to disclose. Conflict of interest: L. Savale reports personal fees and non-financial support from Actelion and MSD, grants from Bayer, outside the submitted work. Conflict of interest: X. Jaïs reports grants from Bayer, grants, personal fees and non-financial support from Actelion/Janssen, personal fees from MSD, outside the submitted work. Conflict of interest: D. Montani reports grants and personal fees from Actelion and Bayer, personal fees from GlaxoSmithKline, Pfizer, MSD and Chiesi, outside the submitted work. Conflict of interest: F. Picard reports personal fees from Novartis, outside the submitted work. Conflict of interest: J-F. Mornex reports personal fees and non-financial support from Actelion, grants, personal fees and non-financial support from GlaxoSmithKline, during the conduct of the study; grants, personal fees and non-financial support from LFB and CSL Behring, personal fees from Roche and Chiesi, outside the submitted work. Conflict of interest: G. Prevot has nothing to disclose. Conflict of interest: F. Chabot reports non-financial support from Actelion, AstraZeneca, Boehringer Ingelheim and MSD, outside the submitted work. Conflict of interest: M. Humbert reports grants, personal fees and non-financial support from GlaxoSmithKline, grants and personal fees from Acceleron, Actelion and Bayer, personal fees from AstraZeneca, Novartis, Roche, Sanofi, Teva and Merck, outside the submitted work. Conflict of interest: A. Chaouat has received personal fees for lecturing and/or consulting from Actelion, Boehringer Ingelheim, Novartis, MSD and Chiesi, and research grants from Actelion and GlaxoSmithKline., (Copyright ©The authors 2021. For reproduction rights and permissions contact permissions@ersnet.org.)

Background: Heritable pulmonary arterial hypertension (PAH) is most commonly due to heterozygous mutations of the BMPR2 gene. Based on expert consensus, guidelines recommend annual screening echocardiography in asymptomatic BMPR2 mutation carriers. The main objectives of this study were to evaluate the characteristics of asymptomatic BMPR2 mutation carriers, assess their risk of occurrence of PAH and detect PAH at an early stage in this high-risk population., Methods: Asymptomatic BMPR2 mutation carriers underwent screening at baseline and annually for a minimum of 2 years (DELPHI-2 study; ClinicalTrials.gov: NCT01600898). Annual screening included clinical assessment, ECG, pulmonary function tests, 6-min walk distance, cardiopulmonary exercise testing, chest radiography, echocardiography and brain natriuretic peptide (BNP) or N-terminal (NT)-proBNP level. Right heart catheterisation (RHC) was performed based on predefined criteria. An optional RHC at rest and exercise was proposed at baseline., Results: 55 subjects (26 males; median age 37 years) were included. At baseline, no PAH was suspected based on echocardiography and NT-proBNP levels. All subjects accepted RHC at inclusion, which identified two mild PAH cases (3.6%) and 12 subjects with exercise pulmonary hypertension (21.8%). At long-term follow-up (118.8 patient-years of follow-up), three additional cases were diagnosed, yielding a PAH incidence of 2.3% per year (0.99% per year in males and 3.5% per year in females). All PAH cases remained at low-risk status on oral therapy at last follow-up., Conclusions: Asymptomatic BMPR2 mutation carriers have a significant risk of developing incident PAH. International multicentre studies are needed to confirm that refined multimodal screening programmes with regular follow-up allow early detection of PAH., Competing Interests: Conflict of interest: D. Montani reports grants and personal fees from Actelion and Bayer, personal fees from GlaxoSmithKline, Pfizer, Chiesi, Boehringer and Incyte Biosciences France, grants, personal fees and nonfinancial support from MSD, nonfinancial support from Acceleron, outside the submitted work. Conflict of interest: B. Girerd has nothing to disclose. Conflict of interest: X. Jaïs reports grants from Bayer, grants and personal fees from MSD, grants, personal fees and nonfinancial support from Actelion/Janssen, outside the submitted work. Conflict of interest: P. Laveneziana reports personal fees from Novartis France and Chiesi France, outside the submitted work. Conflict of interest: E.M.T. Lau reports grants and personal fees from Actelion and GlaxoSmithKline, outside the submitted work. Conflict of interest: A. Bouchachi has nothing to disclose. Conflict of interest: S. Hascoët reports grants and personal fees from Abbott, outside the submitted work. Conflict of interest: S. Gunther has nothing to disclose. Conflict of interest: L. Godinas has nothing to disclose. Conflict of interest: F. Parent has nothing to disclose. Conflict of interest: C. Guignabert has nothing to disclose. Conflict of interest: A. Beurnier has nothing to disclose. Conflict of interest: D. Chemla has nothing to disclose. Conflict of interest: P. Hervé has nothing to disclose. Conflict of interest: M. Eyries has nothing to disclose. Conflict of interest: F. Soubrier has nothing to disclose. Conflict of interest: G. Simonneau reports personal fees from Bayer and Acceleron, personal fees and nonfinancial support from MSD, outside the submitted work. Conflict of interest: O. Sitbon reports grants, personal fees and nonfinancial support from Actelion Pharmaceuticals, personal fees from Acceleron Pharmaceuticals, AOP Orphan, Ferrer and Gossamer Bio, grants and personal fees from Bayer HealthCare and MSD, grants from GlaxoSmithKline, outside the submitted work. Conflict of interest: L. Savale reports personal fees and nonfinancial support from Actelion and Bayer, grants, personal fees and nonfinancial support from GlaxoSmithKline, nonfinancial support from MSD, outside the submitted work. Conflict of interest: M. Humbert reports grants, personal fees and nonfinancial support from GlaxoSmithKline, personal fees from AstraZeneca, Novartis, Roche, Sanofi, Teva and Merck, grants and personal fees from Acceleron, Actelion and Bayer, outside the submitted work., (Copyright ©The authors 2021. For reproduction rights and permissions contact permissions@ersnet.org.)

Dyspnoea is a cardinal symptom of asthma and an essential part of assessing control of the disease. Its intensity is variable for the same level of bronchial obstruction, which suggests the involvement of other mechanisms. Therefore, it is extremely important to characterize and measure dyspnoea in asthmatic patients because its profile can be quantitatively and qualitatively modified by disease control, comorbidities and anxiety. Hence the value of using additional tools to ACT and ACQ because the latter do not characterize nor measure specifically dyspnoea in asthma. Different tools can be used in this regard, at rest as the subjective assessment of dyspnoea by scales such as the modified Medical Research Council (mMRC), the New York Heart Association (NYHA) and the Visual Analogue Scale (VAS) or more recently using the Dyspnea-12 and the Multidimensional Dyspnea Profile (MDP) questionnaire, which assesses the sensory and affective dimensions of dyspnoea; and during exercise testing such as the "modified" Borg scale, graduated from 0 to 10, or the VAS. Among the factors contributing to dyspnoea in asthmatic patients, probably bronchial obstruction, increased airway resistance and dynamic hyperinflation play an important role. Despite this, the asthmatic patient's description of dyspnoea may be masked by hyperventilation syndrome or other comorbidities that can easily be detected and treated through educational programs and targeted therapies., (Copyright © 2019 Elsevier Masson SAS. All rights reserved.)