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Background: The "Baveno classification" replaced the apnoea-hypopnoea index (AHI) with symptoms and comorbidities for treatment indication in obstructive sleep apnoea (OSA). This study evaluates a modified Baveno classification which adds a validated cardiovascular disease (CVD) risk score and acknowledges severe breathing disturbances., Method: OSA patients from the European Sleep Apnoea Database (ESADA) were retrospectively allocated into CVD risk groups 1-3 based on the SCORE2 risk prediction model and European Society of Cardiology guidelines. AHI ≥30 events·h -1 conferred strong treatment indication. When AHI was <30 events·h -1 , symptoms and CVD risk dictated allocation to the weak, intermediate or strong treatment indication group. Changes in Epworth Sleepiness Scale (ESS) score and office systolic blood pressure (SBP) at follow-up (12-24 months) under positive airway pressure (PAP) were assessed., Results: 8625 patients were analysed (29% female; median (interquartile range) age 56 (49-64) years and body mass index 31.9 (28.4-36.3) kg·m -2 ). Treatment indication was weak in 501 (6%), intermediate in 2085 (24%) and strong in 6039 (70%). There was a continuous increase in age, SBP, C-reactive protein and glycosylated haemoglobin from weak to strong (p<0.001). PAP prescription increased from 52% to 64% to 93% (weak to strong; p<0.001). The change in ESS score was -2, -4 and -5, respectively (p<0.001). Reductions of ≥3 mmHg median SBP occurred when AHI was ≥30 events·h -1 and in symptomatic patients with CVD risk levels >1 when AHI was <30 events·h -1 ., Conclusion: This analysis provides supporting evidence for the key role of CVD risk assessment and severe breathing disturbances in the identification of OSA patients most likely to benefit from treatment., Competing Interests: Conflict of interest: S. Matthes reports travel grants from Chiesi and Boehringer. L. Grote has performed educational activities for AstraZeneca, Lundbeck, ResMed, Philipps and Itamar, has interests in two patents licensed to Desitin GMBH, and provides medical advice to Onera BV. J. Hedner has provided scientific advice to SomnoMed and is a part owner of two patents, outside the submitted work. J-L. Pépin is funded by the French National Research Agency in the framework of the “Investissements d'avenir” programme (ANR-15-IDEX-02) and “e-health and integrated care and trajectories medicine and MIAI artificial intelligence” (ANR-19-P3IA-0003) Chairs of excellence from the Grenoble Alpes University; and reports income related to medical education from ResMed, Bioprojet, Jazz and Zoll. W.T. McNicholas reports participation in the Horizon 2020 research and innovation programme under grant agreement number 965417: Sleep Revolution, and is a board member at ESRS. J. Verbraecken reports grants and fees from SomnoMed, AirLiquide, Atos Medical, Vivisol, Mediq Tefa, Medidis, Micromed OSG, Bioprojet, Desitin, Epilog, Idorsia, Inspire Medical Systems, Löwenstein Medical, Ectosense, Philips, ProSomnus, ResMed, Sefam, SD Worx, SOS Oxygène, Tilman, Total Care, Vlaamse Gemeenschap, Vlerick and Zoll Itamar, outside the submitted work, and consultancy for Bioprojet and Epilog. G. Parati reports honoraria for lectures from Omron, SOMNOmedics, Merck and ReCor. W.J. Randerath reports grants and personal fees from Philips Respironics, Loewenstein Medical, ResMed, Bayer Vital, Bioprojet and Vanda Pharma, outside the submitted work. The remaining authors have no potential conflicts of interest to disclose., (Copyright ©The authors 2024. For reproduction rights and permissions contact permissions@ersnet.org.)

Medication-induced central sleep apnea (CSA) is one of the eight categories of causes of CSA but in the absence of awareness and careful history may be misclassified as primary CSA. While opioids are a well-known cause of respiratory depression and CSA, non-opioid medications including sodium oxybate, baclofen, valproic acid, gabapentin, and ticagrelor are less well-recognized. Opioids-induced respiratory depression and CSA are mediated primarily by µ-opioid receptors, which are abundant in the pontomedullary centers involved in breathing. The non-opioid medications, sodium oxybate, baclofen, valproic acid, and gabapentin, act upon brainstem gamma-aminobutyric acid (GABA) receptors, which co-colonize with µ-opioid receptors and mediate CSA. The pattern of ataxic breathing associated with these medications is like that induced by opioids on polysomnogram. Finally, ticagrelor also causes periodic breathing and CSA by increasing central chemosensitivity and ventilatory response to carbon dioxide. Given the potential consequences of CSA and the association between some of these medications with mortality, it is critical to recognize these adverse drug reactions, particularly because discontinuation of the offending agents has been shown to eliminate CSA., (© The Author(s) 2024. Published by Oxford University Press on behalf of Sleep Research Society. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Introduction: Advanced chronic obstructive pulmonary disease (COPD) is associated with chronic hypercapnic failure. The present work aimed to comprehensively investigate inspiratory muscle function as a potential key determinant of hypercapnic respiratory failure in patients with COPD., Methods: Prospective patient recruitment encompassed 61 stable subjects with COPD across different stages of respiratory failure, ranging from normocapnia to isolated nighttime hypercapnia and daytime hypercapnia. Arterialized blood gas analyses and overnight transcutaneous capnometry were used for patient stratification. Assessment of respiratory muscle function encompassed body plethysmography, maximum inspiratory pressure (MIP), diaphragm ultrasound, and transdiaphragmatic pressure recordings following cervical magnetic stimulation of the phrenic nerves (twPdi) and a maximum sniff manoeuvre (Sniff Pdi)., Results: Twenty patients showed no hypercapnia, 10 had isolated nocturnal hypercapnia, and 31 had daytime hypercapnia. Body plethysmography clearly distinguished patients with and without hypercapnia but did not discriminate patients with isolated nocturnal hypercapnia from those with daytime hypercapnia. In contrast to ultrasound parameters and transdiaphragmatic pressures, only MIP reflected the extent of hypercapnia across all three stages. MIP values below -48 cmH2O predicted nocturnal hypercapnia (area under the curve = 0.733, p = 0.052)., Conclusion: In COPD, inspiratory muscle dysfunction contributes to progressive hypercapnic failure. In contrast to invasive tests of diaphragm strength only MIP fully reflects the pathophysiological continuum of hypercapnic failure and predicts isolated nocturnal hypercapnia., (© 2024 S. Karger AG, Basel.)

Study Objective: Excessive daytime sleepiness is common with obstructive sleep apnoea and can persist despite efforts to optimise primary airway therapy. The literature lacks recommendations regarding differential diagnosis and management of excessive daytime sleepiness in obstructive sleep apnoea. This study sought to develop expert consensus statements to bridge the gap between existing literature/guidelines and clinical practice., Methods: A panel of 10 international experts was convened to undertake a modified Delphi process. Statements were developed based on available evidence identified through a scoping literature review, and expert opinion. Consensus was achieved through 3 rounds of iterative, blinded survey voting and revision to statements until a predetermined level of agreement was met (≥80 % voting "strongly agree" or "agree with reservation")., Results: Consensus was achieved for 32 final statements. The panel agreed excessive daytime sleepiness is a patient-reported symptom. The importance of subjective/objective evaluation of excessive daytime sleepiness in the initial evaluation and serial management of obstructive sleep apnoea was recognised. The differential diagnosis of residual excessive daytime sleepiness in obstructive sleep apnoea was discussed. Optimizing airway therapy (eg, troubleshooting issues affecting effectiveness) was addressed. The panel recognised occurrence of residual excessive daytime sleepiness in obstructive sleep apnoea despite optimal airway therapy and the need to evaluate patients for underlying causes., Conclusions: Excessive daytime sleepiness in patients with obstructive sleep apnoea is a public health issue requiring increased awareness, recognition, and attention. Implementation of these statements may improve patient care, long-term management, and clinical outcomes in patients with obstructive sleep apnoea., Competing Interests: Declaration of competing interest J. Steier has received consultancy fees from Jazz Pharmaceuticals. R. Bogan is a shareholder of WaterMark Medical and Healthy Humming, LLC; serves on the board of directors for WaterMark Medical; receives consultancy fees from Jazz Pharmaceuticals, Harmony Biosciences, Avadel Pharmaceuticals, Takeda, and Oventus; performs industry-funded research for Avadel, Axsome, Bresotec, Bayer, Idorsia, Suven, Jazz, Balance, NLS, Vanda, Merck, Eisai, Philips, Fresca, Takeda, Liva Nova, Roche, Sanofi, Sommetrics, and Noctrix; and serves on the speakers bureau for Jazz, Eisai, and Harmony. I. Cano-Pumarega has received consultancy fees from Jazz Pharmaceuticals and Bioprojet, as well as fees for speaking activities from Jazz Pharmaceuticals. J. Fleetham has received consultancy fees and fees for speaking activities from Jazz Pharmaceuticals. G. Insalaco has received consultancy fees and fees for speaking activities from Jazz Pharmaceuticals and Bioprojet. C. Lal has received consultancy fees from Jazz Pharmaceuticals and Chest/GSK. J.-L. Pepin has received lecture fees or conference traveling grants from Resmed, Perimetre, Philips, Fisher and Paykel, AstraZeneca, Jazz Pharmaceuticals, Agiradom, and Bioprojet, and has received unrestricted research funding from ResMed, Philips, GlaxoSmithKline, Bioprojet, Fondation de la Recherche Medicale (Foundation for Medical Research), Direction de la Recherche Clinique du CHU de Grenoble (Research Branch Clinic CHU de Grenoble), and fond de dotation “Agir pour les Maladies Chroniques” (endowment fund “Acting for Chronic Diseases”). W. Randerath is a member of the advisory board and receives consultancy fees, personal fees, and travel grants from Jazz Pharmaceuticals and Bioprojet and (outside this topic) from Philips Respironics (ended 2021) and Desitin (ended 2020). S. Redline received grants from Jazz and NIH and consultancy fees from Jazz, Eli Lilly, Apnimed Inc, and Eisai Inc. A. Malhotra receives funding from NIH; receives income related to medical education from Livanova, Jazz, Equillium, and Corvus; and reports that ResMed provided a philanthropic donation to UC San Diego., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is of high clinical relevance. It not only affects the quality of life but also makes a significant contribution to the mortality rate of patients with rheumatoid arthritis. RA-ILD can present with all known radiological and histopathological patterns seen in other interstitial pneumonias. Among these pneumonias, diffuse alveolar damage (DAD), followed by usual interstitial pneumonia (UIP) has the worst prognosis. In addition, acute exacerbation of RA-ILD, which can occur at any time during the disease, is highly lethal. An algorithm for the diagnosis and treatment of RA-ILD is pending and will be addressed in the following article. In addition to immunosuppressants and disease-modifying antirheumatic drugs (DMARD), antifibrotics have recently gained importance in the therapy of RA-ILD., Competing Interests: Tina Schreiber, David M. Kofler und Torsten Kubacki geben an, dass keine Interessenkonflikte bestehen. Lars Hagmeyer erhielt Beratungs- und Vortragshonorare von Boehringer Ingelheim und Roche. Konrad F. Frank hat Beratungs-und Vortragshonorare von Astra Zeneca, Bayer, Boehringer Ingelheim, GSK und Roche erhalten. Winfried J. Randerath erhielt Honorare von Boehringer Ingelheim., (Thieme. All rights reserved.)

Rationale: Diaphragm dysfunction is frequently observed in critically ill patients with difficult weaning from mechanical ventilation. Objectives: To evaluate the effects of temporary transvenous diaphragm neurostimulation on weaning outcome and maximal inspiratory pressure. Methods: Multicenter, open-label, randomized, controlled study. Patients aged ⩾18 years on invasive mechanical ventilation for ⩾4 days and having failed at least two weaning attempts received temporary transvenous diaphragm neurostimulation using a multielectrode stimulating central venous catheter (bilateral phrenic stimulation) and standard of care (treatment) ( n  = 57) or standard of care (control) ( n  = 55). In seven patients, the catheter could not be inserted, and in seven others, pacing therapy could not be delivered; consequently, data were available for 43 patients. The primary outcome was the proportion of patients successfully weaned. Other endpoints were mechanical ventilation duration, 30-day survival, maximal inspiratory pressure, diaphragm-thickening fraction, adverse events, and stimulation-related pain. Measurements and Main Results: The incidences of successful weaning were 82% (treatment) and 74% (control) (absolute difference [95% confidence interval (CI)], 7% [-10 to 25]), P  = 0.59. Mechanical ventilation duration (mean ± SD) was 12.7 ± 9.9 days and 14.1 ± 10.8 days, respectively, P  = 0.50; maximal inspiratory pressure increased by 16.6 cm H 2 O and 4.8 cm H 2 O, respectively (difference [95% CI], 11.8 [5 to 19]), P  = 0.001; and right hemidiaphragm thickening fraction during unassisted spontaneous breathing was +17% and -14%, respectively, P  = 0.006, without correlation with changes in maximal inspiratory pressure. Serious adverse event frequency was similar in both groups. Median stimulation-related pain in the treatment group was 0 (no pain). Conclusions: Temporary transvenous diaphragm neurostimulation did not increase the proportion of successful weaning from mechanical ventilation. It was associated with a significant increase in maximal inspiratory pressure, suggesting reversal of the course of diaphragm dysfunction. Clinical trial registered with www.clinicaltrials.gov (NCT03096639) and the European Database on Medical Devices (CIV-17-06-020004).

Rationale: Several mutational variants of SARS-CoV-2 have been identified in the past months with increasing prevalence worldwide. Some variants, such as B.1.1.7, are of high relevance due to increased transmissibility, facilitating virus spread and calling for stricter containment measures., Objectives: The aim of this study was to examine proportion and dynamic of B.1.1.7 in SARS-CoV-2-positive samples in a large city in the west of Germany., Methods: Consecutive SARS-CoV-2-positive samples from a local outpatient clinic, obtained over a period of 4 weeks (mid-January to mid-February 2021), were examined for the presence of the variant B.1.1.7. The size of B.1.1.7 infection clusters was compared with non-B.1.1.7 clusters. The transmissibility of SARS-CoV-2 variant B.1.1.7 was described based on corresponding cases of an infection cluster in a local child daycare centre., Results: Among 226 SARS-CoV-2-positive cases, B.1.1.7 was detected in 74 subjects (33%). The 7-day moving mean of the B.1.1.7 proportion started at 20% and reached 50% only 3 weeks later. B.1.1.7 clusters comprised 10.7 ± 12.1 persons per cluster, while non-B.1.1.7 clusters were considerably smaller (5.1 ± 5.8). One specific B.1.1.7 infection cluster in a 40-children daycare centre started with one teacher leading to 11 infected children and 8 infections among teachers. The infection spread to 6 families and one other daycare centre, with a total 43 SARS-CoV-2-positive subjects., Conclusions: We found a rapid increase in the SARS-CoV-2 variant B.1.1.7 with larger infection clusters than non-B.1.1.7. These results suggested a rapid increase in the B.1.1.7 proportion and a renewed increase in the total number of SARS-CoV-2 infections for the time following the analysed period. Considering the rapid emergence and spread of viral variants, close monitoring of mutation events is essential. Therefore, routine whole-genome sequencing appears to be useful in addition to searching for known mutations., Competing Interests: All authors declare no conflict of interest., (Copyright © 2022 by S. Karger AG, Basel.)

Introduction: There is a general underappreciation of the spectrum of obesity-related breathing disorders and their consequences. We therefore compared characteristics of obese patients with eucapnic obstructive sleep apnea (OSA), OSA with obesity-related sleep hypoventilation (ORSH) or obesity hypoventilation syndrome (OHS) to identify the major determinants of hypoventilation., Patients and Methods: In this prospective, diagnostic study (NCT04570540), obese patients with OSA, ORSH or OHS were characterized applying polysomnography with transcutaneous capnometry, blood gas analyses, bodyplethysmography and measurement of hypercapnic ventilatory response (HCVR). Pathophysiological variables known to contribute to hypoventilation and differing significantly between the groups were specified as potential independent variables in a multivariable logistic regression to identify major determinants of hypoventilation., Results: Twenty, 43 and 19 patients were in the OSA, ORSH and OHS group, respectively. BMI was significantly lower in OSA as compared to OHS. The extent of SRBD was significantly higher in OHS as compared to OSA or ORSH. Patients with ORSH or OHS showed a significantly decreased forced expiratory volume in 1 s and forced vital capacity compared to OSA. HCVR was significantly lower in OHS and identified as the major determinant of hypoventilation in a multivariable logistic regression (Nagelkerke R 2  = 0.346, p = 0.050, odds ratio (95%-confidence interval) 0.129 (0.017-1.004))., Conclusion: Although there were differences in BMI, respiratory mechanics and severity of upper airway obstruction between groups, our data support HCVR as the major determinant of obesity-associated hypoventilation., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Rationale: Determining whether an individual has obstructive or central sleep apnea is fundamental to selecting the appropriate treatment. Objectives: Here we derive an automated breath-by-breath probability of obstruction, as a surrogate of gold-standard upper airway resistance, using hallmarks of upper airway obstruction visible on clinical sleep studies. Methods: From five nocturnal polysomnography signals (airflow, thoracic and abdominal effort, oxygen saturation, and snore), nine features were extracted and weighted to derive the breath-by-breath probability of obstruction (P obs ). A development and initial test set of 29 subjects (development = 6, test = 23) (New York, NY) and a second test set of 39 subjects (Solingen, Germany), both with esophageal manometry, were used to develop P obs and validate it against gold-standard upper airway resistance. A separate dataset of 114 subjects with 2 consecutive nocturnal polysomnographies (New York, NY) without esophageal manometry was used to assess the night-to-night variability of P obs . Measurements and Main Results: A total of 1,962,229 breaths were analyzed. On a breath-by-breath level, P obs was strongly correlated with normalized upper airway resistance in both test sets (set 1: cubic adjusted [adj.] R 2  = 0.87, P  < 0.001, area under the receiver operating characteristic curve = 0.74; set 2: cubic adj. R 2  = 0.83, P  < 0.001, area under the receiver operating characteristic curve = 0.7). On a subject level, median P obs was associated with the median normalized upper airway resistance (set 1: linear adj. R 2  = 0.59, P  < 0.001; set 2: linear adj. R 2  = 0.45, P  < 0.001). Median P obs exhibited low night-to-night variability [intraclass correlation(2, 1) = 0.93]. Conclusions: Using nearly 2 million breaths from 182 subjects, we show that breath-by-breath probability of obstruction can reliably predict the overall burden of obstructed breaths in individual subjects and can aid in determining the type of sleep apnea.

Hypersensitivity pneumonitis (HP) is an inflammatory and/or fibrotic disease of the lung parenchyma and terminal bronchioles caused by an allergic reaction to inhaled antigens. The immune response following antigen exposure results in lymphocytic inflammation as well as granuloma formation.The typical histologic pattern of HP consists of cellular interstitial pneumonia, cellular bronchiolitis, and epithelioid cell granulomas. The additional presence of fibrosis has a significant impact on the course as well as the prognosis of the disease and represents a therapeutic approach. Therefore, a classification into a non-fibrotic and a fibrotic phenotype is proposed.The diagnosis of HP is made by high-resolution computed tomography (HRCT) of the lung, evaluation of possible antigen exposure, and bronchoscopy with bronchoalveolar lavage and, if necessary, forceps biopsy. If the diagnosis is inconclusive, transbronchial cryobiopsy or surgical lung biopsy may need to follow. A multidisciplinary board is critical in making the diagnosis., Competing Interests: Tina Schreiber gibt keine Interessenkonflikte an. Lars Hagmeyer ist für Böhringer Ingelheim und Roche tätig. Winfried J. Randerath gibt Honorare von Böhringer Ingelheim an., (Thieme. All rights reserved.)

Background: Central sleep apnea (CSA) is common among patients with heart failure and has been strongly linked to adverse outcomes. However, progress toward improving outcomes for such patients has been limited. The purpose of this official statement from the American Thoracic Society is to identify key areas to prioritize for future research regarding CSA in heart failure. Methods: An international multidisciplinary group with expertise in sleep medicine, pulmonary medicine, heart failure, clinical research, and health outcomes was convened. The group met at the American Thoracic Society 2019 International Conference to determine research priority areas. A statement summarizing the findings of the group was subsequently authored using input from all members. Results : The workgroup identified 11 specific research priorities in several key areas: 1 ) control of breathing and pathophysiology leading to CSA, 2 ) variability across individuals and over time, 3 ) techniques to examine CSA pathogenesis and outcomes, 4 ) impact of device and pharmacological treatment, and 5 ) implementing CSA treatment for all individuals Conclusions: Advancing care for patients with CSA in the context of heart failure will require progress in the arenas of translational (basic through clinical), epidemiological, and patient-centered outcome research. Given the increasing prevalence of heart failure and its associated substantial burden to individuals, society, and the healthcare system, targeted research to improve knowledge of CSA pathogenesis and treatment is a priority.

New findings on pathophysiology, epidemiology, and outcome have raised concerns on the relevance of the apnoea-hypopnoea index (AHI) in the classification of obstructive sleep apnoea (OSA) severity. Recently, a multicomponent grading system decision integrating symptomatology and comorbidities (Baveno classification), was proposed to characterise OSA and to guide therapeutic decisions. We evaluated whether this system reflects the OSA population, whether it translates into differences in outcomes, and whether the addition of AHI improves the scheme. A total of 14 499 OSA patients from the European Sleep Apnoea Database cohort were analysed. The groups were homogeneously distributed and were found to clearly stratify the population with respect to baseline parameters. Differences in sleepiness and blood pressure between the groups were analysed in a subgroup of patients after 24-36 months of treatment. Group A (minor symptoms and comorbidities) did not demonstrate any effect of treatment on outcome. However, groups B (severe symptoms, minor comorbidities), C (minor symptoms, severe comorbidities) and D (severe symptoms and comorbidities) were associated with improvement in either or both parameters with treatment. The AHI is an essential prerequisite of the diagnosis; however, adding the AHI did not improve the classification. Rather, it was inferior with respect to guiding the treatment decision. Thus, the Baveno classification allows a better stratification of the OSA population and may provide a better guidance for therapeutic decisions in OSA., Competing Interests: Conflict of interest: W.J. Randerath reports speaking fees and travel grants from Philips Respironics, Heinen und Löwenstein, ResMed, Bioprojet, Bayer Vital and Vanda Pharma outside the submitted work. Conflict of interest: S. Herkenrath has nothing to disclose. Conflict of interest: M. Treml has nothing to disclose. Conflict of interest: L. Grote reports grants from Bayer, the Philips Respironics Foundation and the ResMed Foundation for the ESADA network during the conduct of the study; and nonfinancial and other support from Itamar Medical, ResMed, Philips, AstraZeneca and Breas outside the submitted work. In addition, L. Grote has a patent on sleep apnoea therapy licensed. Conflict of interest: J. Hedner reports grants from Bayer AG, the European Respiratory Society (for database maintenance) and Desitin GmbH outside the submitted work; in addition, J. Hedner has a patent issued on pharmacological therapy of OSA. Conflict of interest: M.R. Bonsignore has nothing to disclose. Conflict of interest: J.L. Pépin grants and research funds from the Air Liquide Foundation, Agiradom, AstraZeneca, Fisher and Paykel, Mutualia, Philips, ResMed, and Vitalaire; and fees from Agiradom, AstraZeneca, Boehringer Ingelheim, Jazz Pharmaceutical, Night Balance, Philips and ResMed. Conflict of interest: S. Ryan has nothing to disclose. Conflict of interest: S. Schiza has nothing to disclose. Conflict of interest: J. Verbraecken reports an educational grant and an advisory board fee from ResMed; a consultancy fee from Philips; lecture fees from Sanofi and Agfa-Gevaert; an educational grant and an advisory board fee from Bioprojet; an educational grant from and study participation for Jazz Pharmaceutics; an educational grant from AirLiquide; a lecture fee from Springer; an educational grant from Westfalen Medical; an educational grant and a lecture fee from SomnoMed; educational grants from Vivisol, Total Care, Medidis, Fisher & Paykel, Wave Medical, OSG, Mediq Tefa, NightBalance and Heinen & Löwenstein; lecture fees from AstraZeneca; and educational grants from Accuramed, Bekaert Deslee Academy and UCB Pharma, all outside the submitted work. Conflict of interest: W.T. McNicholas has nothing to disclose. Conflict of interest: A. Pataka has nothing to disclose. Conflict of interest: P. Sliwinski has nothing to disclose. Conflict of interest: Ö.K. Basoglu has nothing to disclose., (Copyright ©The authors 2021.)

At the 2020 "Luftschlösser" (castles in the air) conference, experts from a wide range of pneumological fields discussed technical innovations in pneumology, which can be seen in many different areas of the field, including e-health, screening, diagnostics, and therapy. They contribute to substantial advancements ranging from the innovative use of diagnostic tools to novel treatments for chronic lung diseases. Artificial intelligence enables broader screening, which can be expected to have beneficial effects on disease progression and overall prognosis. There is still a high demand for clinical trials to investigate the usefulness and risk-benefit ratio. Open questions remain especially about the quality and utility of medical apps in an inadequately regulated market. This article weighs the pros and cons of technical innovations in specific subspecialties of pneumology based on the lively exchange of ideas among various pneumological experts., (© 2021 S. Karger AG, Basel.)

Background: Exercise intolerance in heart failure with reduced ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF) results from both cardiac dysfunction and skeletal muscle weakness. Respiratory muscle dysfunction with restrictive ventilation disorder may be present irrespective of left ventricular ejection fraction and might be mediated by circulating pro-inflammatory cytokines., Objective: To determine lung and respiratory muscle function in patients with HFrEF/HFpEF and to determine its associations with exercise intolerance and markers of systemic inflammation., Methods: Adult patients with HFrEF (n = 22, 19 male, 61 ± 14 years) and HFpEF (n = 8, 7 male, 68 ± 8 years) and 19 matched healthy control subjects underwent spirometry, measurement of maximum mouth occlusion pressures, diaphragm ultrasound, and recording of transdiaphragmatic and gastric pressures following magnetic stimulation of the phrenic nerves and the lower thoracic nerve roots. New York Heart Association (NYHA) class and 6-min walking distance (6MWD) were used to quantify exercise intolerance. Levels of circulating interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured using ELISAs., Results: Compared with controls, both patient groups showed lower forced vital capacity (FVC) (p < 0.05), maximum inspiratory pressure (PImax), maximum expiratory pressure (PEmax) (p < 0.05), diaphragm thickening ratio (p = 0.01), and diaphragm strength (twitch transdiaphragmatic pressure in response to supramaximal cervical magnetic phrenic nerve stimulation) (p = 0.01). In patients with HFrEF, NYHA class and 6MWD were both inversely correlated with FVC, PImax, and PEmax. In those with HFpEF, there was an inverse correlation between amino terminal pro B-type natriuretic peptide levels and FVC (r = -0.77, p = 0.04). In all HF patients, IL-6 and TNF-α were statistically related to FVC., Conclusions: Irrespective of left ventricular ejection fraction, HF is associated with respiratory muscle dysfunction, which is associated with increased levels of circulating IL-6 and TNF-α., (© 2020 S. Karger AG, Basel.)