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Aims We aim to evaluate the clinical relevance and the prognostic value of arterial and venous renal Doppler in acute decompensated precapillary pulmonary hypertension (PH). Methods and results The renal resistance index (RRI) and the Doppler-derived renal venous stasis index (RVSI) were monitored at admission and on Day 3 in a prospective cohort of precapillary PH patients managed in intensive care unit for acute right heart failure (RHF). The primary composite endpoint included death, circulatory assistance, urgent transplantation, or rehospitalization for acute RHF within 90 days following inclusion. Ninety-one patients were enrolled (58% female, age 58 ± 16 years). The primary endpoint event occurred in 32 patients (33%). In univariate logistic regression analysis, variables associated with RRI higher than the median value were non-variable parameters (age and history of hypertension), congestion (right atrial pressure and renal pulse pressure), cardiac function [tricuspid annular plane systolic excursion (TAPSE) and left ventricular outflow tract- velocity time integral], systemic pressures and NT-proBNP. Variables associated with RVSI higher than the median value were congestion (high central venous pressure, right atrial pressure, and renal pulse pressure), right cardiac function (TAPSE), severe tricuspid regurgitation, and systemic pressures. Inotropic support was more frequently required in patients with high RRI (P = 0.01) or high RVSI (P = 0.003) at the time of admission. At Day 3, a RRI value Conclusion Renal Doppler provides additional information to assess the severity of patients admitted to the intensive care unit for acute decompensated precapillary PH.

BACKGROUND: Activins are novel therapeutic targets in pulmonary arterial hypertension (PAH). We therefore studied whether key members of the activin pathway could be used as PAH biomarkers. METHODS: Serum levels of activin A, activin B, α-subunit of inhibin A and B proteins, and the antagonists follistatin and follistatin-like 3 (FSTL3) were measured in controls and in patients with newly diagnosed idiopathic, heritable, or anorexigen-associated PAH (n=80) at baseline and 3 to 4 months after treatment initiation. The primary outcome was death or lung transplantation. Expression patterns of the inhibin subunits, follistatin, FSTL3, Bambi, Cripto, and the activin receptors type I (ALK), type II (ACTRII), and betaglycan were analyzed in PAH and control lung tissues. RESULTS: Death or lung transplantation occurred in 26 of 80 patients (32.5%) over a median follow-up of 69 (interquartile range, 50–81) months. Both baseline (hazard ratio, 1.001 [95% CI, 1.000–1.001]; P =0.037 and 1.263 [95% CI, 1.049–1.520]; P =0.014, respectively) and follow-up (hazard ratio, 1.003 [95% CI, 1.001–1.005]; P =0.001 and 1.365 [95% CI, 1.185–1.573]; P P =0.009) and 0.17 (95% CI, 0.06–0.45; P P =0.019) and 0.27 (95% CI, 0.09–0.78, P =0.015), respectively. Prognostic values of activin A and FSTL3 were confirmed in an independent external validation cohort. Histological analyses showed a nuclear accumulation of the phosphorylated form of Smad2/3, higher immunoreactivities for ACTRIIB, ALK2, ALK4, ALK5, ALK7, Cripto, and FSTL3 in vascular endothelial and smooth muscle layers, and lower immunostaining for inhibin-α and follistatin. CONCLUSIONS: These findings offer new insights into the activin signaling system in PAH and show that activin A and FSTL3 are prognostic biomarkers for PAH.

International audience; Rationale: The relationship between the initial treatment strategy and survival in pulmonary arterial hypertension (PAH) remains uncertain. Objectives: To evaluate the long-term survival of patients with PAH categorized according to the initial treatment strategy. Methods: A retrospective analysis of incident patients with idiopathic, heritable, or anorexigen-induced PAH enrolled in the French Pulmonary Hypertension Registry (January 2006 to December 2018) was conducted. Survival was assessed according to the initial strategy: monotherapy, dual therapy, or triple-combination therapy (two oral medications and a parenteral prostacyclin). Measurements and Main Results: Among 1,611 enrolled patients, 984 were initiated on monotherapy, 551 were initiated on dual therapy, and 76 were initiated on triple therapy. The triple-combination group was younger and had fewer comorbidities but had a higher mortality risk. The survival rate was higher with the use of triple therapy (91% at 5 yr) as compared with dual therapy or monotherapy (both 61% at 5 yr) (P < 0.001). Propensity score matching of age, sex, and pulmonary vascular resistance also showed significant differences between triple therapy and dual therapy (10-yr survival, 85% vs. 65%). In high-risk patients (n = 243), the survival rate was higher with triple therapy than with monotherapy or dual therapy, whereas there was no difference between monotherapy and double therapy. In intermediate-risk patients (n = 1,134), survival improved with an increasing number of therapies. In multivariable Cox regression, triple therapy was independently associated with a lower risk of death (hazard ratio, 0.29; 95% confidence interval, 0.11-0.80; P = 0.017). Among the 148 patients initiated on a parenteral prostacyclin, those on triple therapy had a higher survival rate than those on monotherapy or dual therapy. Conclusions: Initial triple-combination therapy that includes parenteral prostacyclin seems to be associated with a higher survival rate in PAH, particularly in the youngest high-risk patients.

Pulmonary hypertension is associated with stiffening of pulmonary arteries which increases right ventricular pulsatile loading. High pulmonary artery wedge pressure (PAWP) in postcapillary pulmonary hypertension (Pc-PH) further decreases pulmonary arterial compliance (PAC) at a given pulmonary vascular resistance (PVR) compared with precapillary pulmonary hypertension, thus responsible for a higher total arterial load. In all other vascular beds, arterial compliance is considered as mainly determined by the distending pressure, due to non-linear stress-strain behaviour of arteries. We tested the applicability, advantages and drawbacks of two comparison methods of PAC depending on the level of mean pulmonary arterial pressure (mPAP; isobaric PAC) or PVR. Right heart catheterisation data including PAC (stroke volume/pulse pressure) were obtained in 112 Pc-PH (of whom 61 had combined postcapillary and precapillary pulmonary hypertension) and 719 idiopathic pulmonary arterial hypertension (iPAH). PAC could be compared over the same mPAP range (25–66 mmHg) in 792 (95.3%) out of 831 patients and over the same PVR range (3–10.7 WU) in only 520 (62.6%) out of 831 patients. The main assumption underlying comparisons at a given PVR was not verified as the PVR×PAC product (RC-time) was not constant but on the contrary more variable than mPAP. In the 788/831 (94.8%) patients studied over the same PAC range (0.62–6.5 mL·mmHg−1), PVR and thus total arterial load tended to be higher in iPAH. Our study favours comparing PAC at fixed mPAP level (isobaric PAC) rather than at fixed PVR. A reappraisal of the effects of PAWP on the pulsatile and total arterial load put on the right heart is needed, and this point deserves further studies., In postcapillary and precapillary pulmonary hypertension patients, this study favours comparing pulmonary arterial compliance (PAC) at fixed mean pulmonary artery pressure level (isobaric PAC) rather than at fixed pulmonary vascular resistance level https://bit.ly/3aTLYdS

It is unknown whether pulmonary arterial hypertension (PAH) risk stratification instruments could be helpful to support the decision to list a patient for lung transplantation (LT). Our aim was to evaluate contemporary risk assessment tools in a cohort of PAH patients listed for LT.Consecutive PAH patients (without pulmonary veno-occlusive disease or unrepaired congenital heart disease) listed for LT at the French Pulmonary Hypertension Reference Center between January 2006 and December 2018 were included. At the time of listing, risk stratification was assessed using the ESC/ERS criteria, the REVEAL Lite 2 score and the COMPERA 2.0 method. The primary end point was overall survival after LT listing. Secondary outcome measures were mortality on waiting list and posttransplant survival.One hundred and two patients were enrolled (mean age 38 ± 13 years, 69% females). Overall survival after listing was 72%, 58% and 46% at 1, 3 and 5 years respectively. Survival after LT listing was lower in "high-risk" patients according to the ESC/ERS criteria (p = 0.0001) and the REVEAL Lite 2 score (p = 0.04). The COMPERA 2.0 method discriminated post-listing survival of patients at high-risk, intermediate-high and intermediate-low risk (p = 0.04). The proportion of patients requiring urgent transplantation and extracorporeal life support as a bridge to transplantation was higher in the "high-risk" patients. Posttransplant survival was significantly lower in "high-risk" patients according to the ESC/ERS criteria (p = 0.0004).High-risk PAH patients at the time of LT listing have poor outcomes, suggesting that LT should be considered earlier in the course of PAH remaining refractory to triple combination therapy with a parenteral prostacyclin.

BackgroundRisk stratification and assessment of disease progression in patients with pulmonary arterial hypertension (PAH) are challenged by the lack of accurate disease-specific and prognostic biomarkers. To date, brain natriuretic peptide (BNP) and/or its N-terminal fragment (NT-proBNP) are the only markers for right ventricular dysfunction used in clinical practice, in association with echocardiographic and invasive haemodynamic variables to predict outcome in patients with PAH.MethodsThis study was designed to identify an easily measurable biomarker panel in the serum of 80 well-phenotyped PAH patients with idiopathic, heritable or drug-induced PAH at baseline and at first follow-up. The prognostic value of identified cytokines of interest was secondly analysed in an external validation cohort of 125 PAH patients.ResultsAmong the 20 biomarkers studied with the multiplex Ella platform, we identified a three-biomarker panel composed of β-NGF, CXCL9 and TRAIL that were independently associated with prognosis both at the time of PAH diagnosis and at the first follow-up after initiation of PAH therapy. β-NGF and CXCL9 were predictors of death or transplantation, whereas high levels of TRAIL were associated with a better prognosis. Furthermore, the prognostic value of the three cytokines was more powerful for predicting survival than usual non-invasive variables (New York Heart Association Functional Class, 6-min walk distance and BNP/NT-proBNP). The results were validated in a fully independent external validation cohort.ConclusionThe monitoring of β-NGF, CXCL9 and TRAIL levels in serum should be considered in the management and treatment of patients with PAH to objectively guide therapeutic options.

BackgroundDrugs 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 (SaO2) 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 inSaO2while treated with PAH drugs.MethodsWe reviewed 719 PAH patients. The exclusion criteria were PAH associated with congenital heart disease and PAH with overt features of venous/capillaries involvement.Results173 (24%) patients had a ≥3% decrease inSaO2. 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 inSaO2. 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 inSaO2and more patients started long-term oxygen therapy in this group (16%versus5%; pSaO2was associated with a poorer survival (hazard ratio 1.81, 95% CI 1.43–2.34; pSaO2was a prognostic factor independent of age at diagnosis and ESC/ERS risk stratification at follow-up.ConclusionsWhen treated with PAH drugs, a large subset of patients experience a ≥3% decrease inSaO2, which is associated with worse long-term outcomes and reduced survival.

Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the coronavirus disease 2019 (COVID-19) pandemic that has resulted in millions of deaths and a major strain on health systems worldwide. Medical treatments for COVID-19 (anticoagulants, corticosteroids, anti-inflammatory drugs, oxygenation therapy and ventilation) and vaccination have improved patient outcomes. The majority of patients will recover spontaneously or after acute-phase management, but clinicians are now faced with long-term complications of COVID-19 including a large variety of symptoms, defined as “post-acute COVID-19 syndrome”. Most studies have focused on patients hospitalised for severe COVID-19, but acute COVID-19 syndrome is not restricted to these patients and exists in outpatients. Given the diversity of symptoms and the high prevalence of persistent symptoms, the management of these patients requires a multidisciplinary team approach, which will result in the consumption of large amounts of health resources in the coming months. In this review, we discuss the presentation, prevalence, pathophysiology and evolution of respiratory complications and other organ-related injuries associated with post-acute COVID-19 syndrome.

RationaleThe 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.MethodsIn 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.ResultsAmong 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 versus 56±14 years, p=0.03), more frequently managed in an ICU (87.9 versus 47.4%, pversus 84.9±14.8% pred, pDLCO) (73.3±17.9 versus 89.7±22.8% pred, pDLCO ConclusionsNew-onset dyspnoea and mild fibrotic lesions were frequent at 4 months, but the association of new-onset dyspnoea, fibrotic lesions and low DLCO was rare.

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., Asymptomatic BMPR2 mutation carriers have a 2.3% per year risk of developing PAH. DELPHI-2 provides the platform for future international multicentre studies to refine multimodal screening algorithms in BMPR2 mutation carriers. http://bit.ly/3oi2KJ1

The level of knowledge about a direct link between sleep-related breathing disorders and pre-capillary pulmonary hypertension (PH) is low and there is a chicken and egg question to know which disease causes the other. On one hand, sleep-related breathing disorders are considered as a cause of group 3 PH, in the subgroup of patients with hypoxemia without lung disease. Indeed, isolated sleep-related breathing disorders can lead to mild pre-capillary PH on their own, although this is rare for obstructive sleep apnea and difficult to establish for obesity-hypoventilation syndrome, the evolution towards PH being observed especially in the presence of respiratory comorbidities. The hemodynamic improvement under treatment with continuous positive airway pressure or non-invasive ventilation also argues for a causal link between pre-capillary PH and sleep-related breathing disorders. On the other hand, patients followed for pre-capillary PH, particularly pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension, develop more sleep-related breathing disorders than the general population, especially sleep hypoxemia, central sleep apnea in patients with severe PH and obstructive sleep apnea in older patients with higher body mass index. The main objective of this article is therefore to answer two main questions, which will then lead us to discuss the bilateral link between these diseases: are sleep-related breathing disorders independent risk factors for pre-capillary PH and does pre-capillary PH induce sleep-related breathing disorders? In other words, who is the chicken and who is the egg?

Background Viral respiratory infections are the main causes of asthma exacerbation. The susceptibility of asthmatics to develop an exacerbation when they present with severe pneumonia due to SARS-CoV-2 infection is unknown. The objective of this study was to investigate the characteristics and outcomes of asthmatic patients with COVID-19 pneumonia who required hospitalisation during the spring 2020 outbreak in Paris, France. Methods A prospective cohort follow-up was carried out from March 15 to April 15, 2020 in Bicêtre Hospital, University Paris-Saclay, France. All hospitalised patients with a SARS-CoV-2 infection who reported a history of asthma were included. Results Among 768 hospitalised patients, 37 (4.8%) reported a history of asthma, which had been previously confirmed by a pulmonologist in 85% of cases. Patients were mainly female (70%), non-smokers (85%), with a median age of 54 years (interquartile range, IQR 42–67). None of them presented with an asthma exacerbation. Twenty-two (59%) had major comorbidities and 31 (84%) had a body mass index ≥25 kg·m−2. The most common comorbidities were obesity (36%), hypertension (27%) and diabetes (19%). All patients had a confirmed diagnosis of COVID-19 pneumonia on computed tomography of the chest. Eosinopenia was a typical biologic feature with a median count of 0/mm3 (IQR 0–0). Eleven patients (30%) were admitted in intensive care unit with three death (8.1%) occurring in the context of comorbidities. Conclusion Asthmatics were not overrepresented among patients with severe pneumonia due to SARS-CoV-2 infection who required hospitalisation. Worst outcomes were observed mainly in patients with major comorbidities., Asthmatics were not overrepresented among patients with severe pneumonia due to SARS-CoV-2 infection who require hospitalisation. None of them presented with an asthma exacerbation. Worst outcomes were observed mainly in patients with major comorbidities.

IntroductionContemporary risk assessment tools categorise patients with pulmonary arterial hypertension (PAH) as low, intermediate or high risk. A minority of patients achieve low risk status with most remaining intermediate risk. Our aim was to validate a four-stratum risk assessment approach categorising patients as low, intermediate-low, intermediate-high or high risk, as proposed by the Comparative, Prospective Registry of Newly Initiated Therapies for Pulmonary Hypertension (COMPERA) investigators.MethodsWe evaluated incident patients from the French PAH Registry and applied a four-stratum risk method at baseline and at first reassessment. We applied refined cut-points for three variables: World Health Organization functional class, 6-min walk distance and N-terminal pro-brain natriuretic peptide. We used Kaplan–Meier survival analyses and Cox proportional hazards regression to assess survival according to three-stratum and four-stratum risk approaches.ResultsAt baseline (n=2879), the four-stratum approach identified four distinct risk groups and performed slightly better than a three-stratum method for predicting mortality. Four-stratum model discrimination was significantly higher than the three-stratum method when applied during follow-up and refined risk categories among subgroups with idiopathic PAH, connective tissue disease-associated PAH, congenital heart disease and portopulmonary hypertension. Using the four-stratum approach, 53% of patients changed risk category from baseline compared to 39% of patients when applying the three-stratum approach. Those who achieved or maintained a low risk status had the best survival, whereas there were more nuanced differences in survival for patients who were intermediate-low and intermediate-high risk.ConclusionsThe four-stratum risk assessment method refined risk prediction, especially within the intermediate risk category of patients, performed better at predicting survival and was more sensitive to change than the three-stratum approach.

Points essentiels La dyspnee est un symptome cardinal de l’asthme et constitue un element essentiel d’evaluation du controle de la maladie. Son intensite est variable pour un meme niveau d’obstruction bronchique, ce qui suggere l’implication d’autres mecanismes. Il est donc extremement important de caracteriser et mesurer la dyspnee de l’asthmatique car son profil peut etre modifie de maniere quantitative et qualitative par le controle de la maladie, les comorbidites et l’anxiete. D’ou l’interet d’utiliser des outils supplementaires a l’ACT et ACQ car ces deux questionnaires ne caracterisent ni ne mesurent la dyspnee de l’asthmatique de facon specifique. Differents outils peuvent etre utilises dans cet objectif. Au repos il s’agit des echelles telles que le modified Medical Research Council (mMRC), la New York Heart Association (NYHA) et l’echelle visuelle analogique (EVA) ou plus recemment lequestionnaire Dyspnea-12 et le questionnaire Multidimensional Dyspnea Profile (MDP) qui evalue les dimensions sensorielles et affectives de la dyspnee ; au cours d’une epreuve d’effort, on peut utiliser l’echelle de Borg « modifiee », graduee de 0 a 10, ou l’echelle visuelle analogique (EVA ou VAS en anglais). Parmi les facteurs qui contribuent a la dyspnee chez l’asthmatique, sans doute l’obstruction bronchique, l’augmentation de resistances des voies aeriennes et la distension dynamique jouent un role important. Malgre cela, la description de la sensation de dyspnee par le patient asthmatique peut etre parasitee par le syndrome d’hyperventilation ou autres comorbidites qui peuvent aisement etre decelees et traitees par des programmes educationnels et des therapies ciblees.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has provoked an ongoing global pandemic of coronavirus disease 2019 (COVID-19), which has affected 130 million people worldwide and caused nearly 3 million deaths in just over 1 year [1]. In 2020, COVID-19 has represented the third highest cause of death in the US after heart disease and cancer [2], and this outbreak has led to the largest drop in life expectancy since World War II [2]. Evidence-based medical treatment of COVID-19 (anticoagulants, corticosteroids, anti-inflammatory drugs, oxygenation therapy and ventilation) [3] seems to have improved patients’ outcomes, and the vast majority will recover spontaneously or after acute phase management. Acknowledgement: We thank the patients, relatives, healthcare providers, administrative hospital teams and the writing committee of the COMEBAC study.

Importance Little is known about long-term sequelae of COVID-19. Objective To describe the consequences at 4 months in patients hospitalized for COVID-19. Design, setting, and participants In a prospective uncontrolled cohort study, survivors of COVID-19 who had been hospitalized in a university hospital in France between March 1 and May 29, 2020, underwent a telephone assessment 4 months after discharge, between July 15 and September 18, 2020. Patients with relevant symptoms and all patients hospitalized in an intensive care unit (ICU) were invited for further assessment at an ambulatory care visit. Exposures Survival of hospitalization for COVID-19. Main outcomes and measures Respiratory, cognitive, and functional symptoms were assessed by telephone with the Q3PC cognitive screening questionnaire and a checklist of symptoms. At the ambulatory care visit, patients underwent pulmonary function tests, lung computed tomographic scan, psychometric and cognitive tests (including the 36-Item Short-Form Health Survey and 20-item Multidimensional Fatigue Inventory), and, for patients who had been hospitalized in the ICU or reported ongoing symptoms, echocardiography. Results Among 834 eligible patients, 478 were evaluated by telephone (mean age, 61 years [SD, 16 years]; 201 men, 277 women). During the telephone interview, 244 patients (51%) declared at least 1 symptom that did not exist before COVID-19: fatigue in 31%, cognitive symptoms in 21%, and new-onset dyspnea in 16%. There was further evaluation in 177 patients (37%), including 97 of 142 former ICU patients. The median 20-item Multidimensional Fatigue Inventory score (n = 130) was 4.5 (interquartile range, 3.0-5.0) for reduced motivation and 3.7 (interquartile range, 3.0-4.5) for mental fatigue (possible range, 1 [best] to 5 [worst]). The median 36-Item Short-Form Health Survey score (n = 145) was 25 (interquartile range, 25.0-75.0) for the subscale "role limited owing to physical problems" (possible range, 0 [best] to 100 [worst]). Computed tomographic lung-scan abnormalities were found in 108 of 171 patients (63%), mainly subtle ground-glass opacities. Fibrotic lesions were observed in 33 of 171 patients (19%), involving less than 25% of parenchyma in all but 1 patient. Fibrotic lesions were observed in 19 of 49 survivors (39%) with acute respiratory distress syndrome. Among 94 former ICU patients, anxiety, depression, and posttraumatic symptoms were observed in 23%, 18%, and 7%, respectively. The left ventricular ejection fraction was less than 50% in 8 of 83 ICU patients (10%). New-onset chronic kidney disease was observed in 2 ICU patients. Serology was positive in 172 of 177 outpatients (97%). Conclusions and relevance Four months after hospitalization for COVID-19, a cohort of patients frequently reported symptoms not previously present, and lung-scan abnormalities were common among those who were tested. These findings are limited by the absence of a control group and of pre-COVID assessments in this cohort. Further research is needed to understand longer-term outcomes and whether these findings reflect associations with the disease.

We thank Porfidia and colleagues for their interest in our study describing the prevalence of pulmonary embolism (PE) in patients with coronavirus disease (COVID-19) at the time of hospital admission [1]. We fully agree on the need to consider a PE diagnostic algorithm in COVID-19 at the time of hospital admission, because indiscriminate execution of computed tomography pulmonary angiography (CTPA) cannot be a doable routine approach in such patients., High prevalence of pulmonary embolisme in patients with COVID-19 at the time of hospital admission despite a low level of clinical suspicion.

Introduction Il est frequent d’observer des comorbidites respiratoires chez les patients cirrhotiques; certaines peuvent representer des contre-indications a la transplantation hepatique (TH), ou plus rarement une indication a la TH (syndrome hepatopulmonaire, SHP). Leur prevalence et leur impact pronostique chez les candidats a une TH sont peu connus. L’objectif de notre etude etait de determiner la prevalence des comorbidites respiratoires sur une cohorte de patients consecutifs candidats a une transplantation hepatique (PHRC LUNGOLT). Methodes Au moment de l’inscription sur liste d’attente de TH, ont ete realises une evaluation de la classe fonctionnelle NYHA (CF), un test de marche de 6 minutes (TM6), une mesure des gaz du sang arteriel, un catheterisme cardiaque droit et une recherche de SHP par echocardiographie avec epreuve de contraste et/ou scintigraphie corps entier. L’impact pronostique des parametres respiratoires a ete etudie sur une duree de suivi de 10 ans. Resultats Population etudiee: âge moyen 52 ± 8 ans, 78 % d’hommes, 72 % avec cirrhose Child-Pugh (CP) B ou C. Une CF NYHA II ou plus etait rapportee par 36 % des patients et 47 % avaient une hypoxemie definie par une difference alveolo-arterielle en oxygene (DAaO 2) elargie. La prevalence d’un trouble ventilatoire obstructif etait de 15 % avec un VEMS Conclusion Les comorbidites respiratoires sont frequentes chez les candidats a une TH et associees a un plus grand risque de mortalite sur liste d’attente sans impact sur la mortalite post transplantation.

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.