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BackgroundDespite considerable progress, it remains unclear why some patients admitted for COVID-19 develop adverse outcomes while others recover spontaneously. Clues may lie with the predisposition to hypoxemia or unexpected absence of dyspnea ('silent hypoxemia') in some patients who later develop respiratory failure. Using a recently-validated breath-holding technique, we sought to test the hypothesis that gas exchange and ventilatory control deficits observed at admission are associated with subsequent adverse COVID-19 outcomes (composite primary outcome: non-invasive ventilatory support, intensive care admission, or death).MethodsPatients with COVID-19 (N = 50) performed breath-holds to obtain measurements reflecting the predisposition to oxygen desaturation (mean desaturation after 20-s) and reduced chemosensitivity to hypoxic-hypercapnia (including maximal breath-hold duration). Associations with the primary composite outcome were modeled adjusting for baseline oxygen saturation, obesity, sex, age, and prior cardiovascular disease. Healthy controls (N = 23) provided a normative comparison.ResultsThe adverse composite outcome (observed in N = 11/50) was associated with breath-holding measures at admission (likelihood ratio test, p = 0.020); specifically, greater mean desaturation (12-fold greater odds of adverse composite outcome with 4% compared with 2% desaturation, p = 0.002) and greater maximal breath-holding duration (2.7-fold greater odds per 10-s increase, p = 0.036). COVID-19 patients who did not develop the adverse composite outcome had similar mean desaturation to healthy controls.ConclusionsBreath-holding offers a novel method to identify patients with high risk of respiratory failure in COVID-19. Greater breath-hold induced desaturation (gas exchange deficit) and greater breath-holding tolerance (ventilatory control deficit) may be independent harbingers of progression to severe disease.

Background and objectiveUpper airway collapsibility predicts the response to several non-continuous positive airway pressure (CPAP) interventions for obstructive sleep apnoea (OSA). Measures of upper airway collapsibility cannot be easily performed in a clinical context; however, a patient's therapeutic CPAP requirement may serve as a surrogate measure of collapsibility. The present work aimed to compare the predictive use of CPAP level with detailed physiological measures of collapsibility.MethodsTherapeutic CPAP levels and gold-standard pharyngeal collapsibility measures (passive pharyngeal critical closing pressure (Pcrit ) and ventilation at CPAP level of 0 cmH2 O (Vpassive )) were retrospectively analysed from a randomized controlled trial (n = 20) comparing the combination of oxygen and eszopiclone (treatment) versus placebo/air control. Responders (9/20) to treatment were defined as those who exhibited a 50% reduction in apnoea/hypopnoea index (AHI) plus an AHI

Study objectivesUpper airway collapsibility is a key determinant of obstructive sleep apnea (OSA) which can influence the efficacy of certain non-continuous positive airway pressure (CPAP) treatments for OSA. However, there is no simple way to measure this variable clinically. The present study aimed to develop a clinically implementable tool to evaluate the collapsibility of a patient's upper airway.MethodsCollapsibility, as characterized by the passive pharyngeal critical closing pressure (Pcrit), was measured in 46 patients with OSA. Associations were investigated between Pcrit and data extracted from patient history and routine polysomnography, including CPAP titration.ResultsTherapeutic CPAP level, demonstrated the strongest relationship to Pcrit (r2=0.51, p < .001) of all the variables investigated including apnea-hypopnea index, body mass index, sex, and age. Patients with a mildly collapsible upper airway (Pcrit ≤ -2 cmH2O) had a lower therapeutic CPAP level (6.2 ± 0.6 vs. 10.3 ± 0.4 cmH2O, p < .001) compared to patients with more severe collapsibility (Pcrit > -2 cmH2O). A therapeutic CPAP level ≤8.0 cmH2O was sensitive (89%) and specific (84%) for detecting a mildly collapsible upper airway. When applied to the independent validation data set (n = 74), this threshold maintained high specificity (91%) but reduced sensitivity (75%).ConclusionsOur data demonstrate that a patient's therapeutic CPAP requirement shares a strong predictive relationship with their Pcrit and may be used to accurately differentiate OSA patients with mild airway collapsibility from those with moderate-to-severe collapsibility. Although this relationship needs to be confirmed prospectively, our findings may provide clinicians with better understanding of an individual patient's OSA phenotype, which ultimately could assist in determining which patients are most likely to respond to non-CPAP therapies.

Objective: To compare clinical characteristics and outcomes of hospitalized acute exacerbations of COPD (AECOPD)s secondary to SARS-CoV-2 versus other respiratory viruses amongst a highly vaccinated population in the Omicron era., Design: Retrospective cohort study; analysis of hospital medical records and linked pathology and radiology reports., Setting: Tertiary health network in Victoria, Australia; January 2022-August 2022., Main Outcome Measures: Key clinical information including comorbidities, vaccination status, treatments administered and outcomes such as hospital length of stay, ICU admission, non-invasive ventilation usage and inpatient mortality., Results: One hundred ninety-nine viral AECOPDs - 125 SARS-CoV-2 and 74 other viruses were identified. Of the SARS-CoV-2 group. 13.6% were unvaccinated, 17.6% partially and 68.0% fully vaccinated. The SARS-CoV-2 group were older (77.2 vs 68.9, p < 0.00001) with more comorbidities (1[1-2] vs 1[0-2], p = 0.008) and lower candidacy for full resuscitation (25.6% vs 56.8%, p < 0.0001). Mortality tended to be higher among SARS-CoV2 admission (9.6% v 2.7%, p = 0.066) but rates of ICU admission (10.4% v 13.5%, p = 0.507), length of hospitalisation (5[3-8] vs 5[3-9], p = 0.9) and readmission within 30 days (25% vs 33.3%, p = 0.184) were similar., Conclusion: In a highly vaccinated population in the Omicron era, COPD patients requiring hospitalisation with SARS-CoV-2 are older with more comorbidities than those admitted with other respiratory viruses. Length of hospitalisation and ICU utilisation was similar. Inpatient mortality may be higher., Competing Interests: The authors report no conflicts of interest in this work., (© 2024 Chhor et al.)

Background: Obstructive sleep apnoea (OSA) is associated with increased coronary artery disease (CAD) plaque burden, but the role of vascular inflammation in this relationship is unclear. Coronary computed tomography angiography (CTA) enables surrogate assessment of systemic inflammation via subcutaneous adipose tissue attenuation (SCAT-a), and of coronary inflammation via epicardial adipose tissue volume and attenuation (EAT-v and EAT-a) and pericoronary adipose tissue attenuation (PCAT-a). We investigated whether patients with severe OSA and high plaque burden have increased vascular inflammation., Methods: Patients with overnight polysomnography within ≤12 months of coronary CTA were included. Severe OSA was classified as apnoea/hypopnoea index (AHI) >30. High plaque burden was defined as a CT-adapted Leaman score (CT-LeSc) ≥8.3. Patients with both severe OSA and high plaque burden were defined as 'Group 1', all other patients were classified as 'Group 2'. ScAT, PCAT and EAT attenuation and volume were assessed on semi-automated software., Results: A total of 91 patients were studied (59.3±11.1 years). Severe OSA was associated with high plaque burden (P=0.02). AHI correlated with CT-LeSc (r=0.24, P=0.023). Group 1 had lower EAT-a and PCAT-a compared to Group 2 (EAT-a: -87.6 vs. -84.0 HU, P=0.011; PCAT-a: -90.4 vs. -83.4 HU, P<0.01). However, among patients with low plaque burden, EAT-a was higher in the presence of severe OSA versus mild-moderate OSA (-80.3 vs. -84.0 HU, P=0.020). On multivariable analysis, severe OSA and high plaque burden associated with EAT-a (P<0.02), and severe OSA and high plaque burden (P<0.01) and hypertension (P<0.01) associated with PCAT-a., Conclusions: EAT and PCAT attenuation are decreased in patients with severe OSA and high plaque burden, but EAT attenuation was increased in patients with severe OSA and low plaque burden. These divergent results suggest vascular inflammation may be increased in OSA independent of CAD, but larger studies are required to validate these findings., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cdt.amegroups.com/article/view/10.21037/cdt-21-338/coif). SJN received research support from Amgen, Anthera, AstraZeneca, Cerenis, Eli Lilly, Esperion, InfraReDx, Liposcience, Novartis, The Medicines Company, Resverlogix, Roche, Sanofi-Regeneron, The Medicines Company, and consulting fees from Akcea, Anthera, AstraZeneca, Boehringer Ingelheim, CSL Behring, Eli Lilly, Esperion, Merck, Omthera, Resverlogix, Sanofi-Regeneron and Takeda. GSH received equipment to support research from ResMed, Philips Respironics and Air Liquide Healthcare. DW received honoraria for lectures from Eli-Lilly, Pfizer and Boehringer. DTLW serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from February 2021 to January 2023. The other authors have no conflicts of interest to declare., (2022 Cardiovascular Diagnosis and Therapy. All rights reserved.)

Introduction: Nosocomial transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been a major feature of the COVID-19 pandemic. Evidence suggests patients can auto-emit aerosols containing viable viruses; these aerosols could be further propagated when patients undergo certain treatments, including continuous positive airway pressure (PAP) therapy. Our aim was to assess 1) the degree of viable virus propagated from PAP circuit mask leak and 2) the efficacy of a ventilated plastic canopy to mitigate virus propagation., Methods: Bacteriophage phiX174 (10 8  copies·mL -1 ) was nebulised into a custom PAP circuit. Mask leak was systematically varied at the mask interface. Plates containing Escherichia coli host quantified viable virus ( via plaque forming unit) settling on surfaces around the room. The efficacy of a low-cost ventilated headboard created from a tarpaulin hood and a high-efficiency particulate air (HEPA) filter was tested., Results: Mask leak was associated with virus contamination in a dose-dependent manner (χ 2 =58.24, df=4, p<0.001). Moderate mask leak (≥21 L·min -1 ) was associated with virus counts equivalent to using PAP with a vented mask. The highest frequency of viruses was detected on surfaces <1 m away; however, viable viruses were recorded up to 3.86 m from the source. A plastic hood with HEPA filtration significantly reduced viable viruses on all plates. HEPA exchange rates ≥170 m 3 ·h -1 eradicated all evidence of virus contamination., Conclusions: Mask leak from PAP may be a major source of environmental contamination and nosocomial spread of infectious respiratory diseases. Subclinical mask leak levels should be treated as an infectious risk. Low-cost patient hoods with HEPA filtration are an effective countermeasure., Competing Interests: Conflict of interest: S.A. Landry has nothing to disclose. Conflict of interest: J.J. Barr has nothing to disclose. Conflict of interest: M.I. MacDonald has nothing to disclose. Conflict of interest: D. Subedi has nothing to disclose. Conflict of interest: D. Mansfield has nothing to disclose. Conflict of interest: G.S. Hamilton reports nonfinancial support (provision of research equipment) from ResMed, Philips Respironics and Air Liquide Healthcare, outside the submitted work. Conflict of interest: B.A. Edwards reports grants from Monash Partners and Heart Foundation, during the conduct of the study; grants from Apnimed Australia, personal fees from Signifier Medical, outside the submitted work. Conflict of interest: S.A. Joosten has nothing to disclose., (Copyright ©ERS 2021. For reproduction rights and permissions contact permissions@ersnet.org.)

Introduction: We investigated if long-term household air pollution (HAP) is associated with asthma and lung function decline in middle-aged adults, and whether these associations were modified by glutathione S -transferase (GST) gene variants, ventilation and atopy., Materials and Methods: Prospective data on HAP (heating, cooking, mould and smoking) and asthma were collected in the Tasmanian Longitudinal Health Study (TAHS) at mean ages 43 and 53 years (n=3314). Subsamples had data on lung function (n=897) and GST gene polymorphisms (n=928). Latent class analysis was used to characterise longitudinal patterns of exposure. Regression models assessed associations and interactions., Results: We identified seven longitudinal HAP profiles. Of these, three were associated with persistent asthma, greater lung function decline and % reversibility by age 53 years compared with the "Least exposed" reference profile for those who used reverse-cycle air conditioning, electric cooking and no smoking. The "All gas" (OR 2.64, 95% CI 1.22-5.70), "Wood heating/smoking" (OR 2.71, 95% CI 1.21-6.05) and "Wood heating/gas cooking" (OR 2.60, 95% CI 1.11-6.11) profiles were associated with persistent asthma, as well as greater lung function decline and % reversibility. Participants with the GSTP1 Ile/Ile genotype were at a higher risk of asthma or greater lung function decline when exposed compared with other genotypes. Exhaust fan use and opening windows frequently may reduce the adverse effects of HAP produced by combustion heating and cooking on current asthma, presumably through increasing ventilation., Conclusions: Exposures to wood heating, gas cooking and heating, and tobacco smoke over 10 years increased the risks of persistent asthma, lung function decline and % reversibility, with evidence of interaction by GST genes and ventilation., Competing Interests: Conflict of interest: X. Dai has nothing to disclose. Conflict of interest: D.S. Bui has nothing to disclose. Conflict of interest: J.L. Perret reports grants from the National Health and Medical Research Council of Australia and Asthma Foundation, during the conduct of the study; grants from Boehringer Ingelheim, outside the submitted work. Conflict of interest: A.J. Lowe reports grants from the National Health and Medical Research Council of Australia, during the conduct of the study. Conflict of interest: P.A. Frith has nothing to disclose. Conflict of interest: G. Bowatte has nothing to disclose. Conflict of interest: P.S. Thomas has nothing to disclose. Conflict of interest: G.G. Giles has nothing to disclose. Conflict of interest: G.S. Hamilton has nothing to disclose. Conflict of interest: H. Tsimiklis has nothing to disclose. Conflict of interest: J. Hui has nothing to disclose. Conflict of interest: J. Burgess has nothing to disclose. Conflict of interest: A.K. Win has nothing to disclose. Conflict of interest: M.J. Abramson reports grants from Pfizer and Boehringer Ingelheim, personal fees for consultancy from Sanofi, outside the submitted work. Conflict of interest: E.H. Walters has nothing to disclose. Conflict of interest: S.C. Dharmage has nothing to disclose. Conflict of interest: C.J. Lodge has nothing to disclose., (Copyright ©ERS 2021.)

Objective: Evaluate the concordance between overall and positional oxygen desaturation indices (ODI) and apnea-hypopnea indices (AHI) according to two different definitions for positional obstructive sleep apnea (POSA)., Methods: A total of 184 in-home polysomnograms were edited to simulate Level III home sleep apnea tests (HSAT) with the auto-scored AHI and ODI based on recording time. POSA was determined using 132 records with an AHI≥5 and at least 20 mins of recording time in both supine and non-supine positions. POSA was defined independently for the AHI and ODI based on ratios of overall/non-supine event/h ≥1.4 (O/NS) and supine/non-supine event/h≥2.0 (S/NS)., Results: Correlation between the AHI and ODI was 0.97 overall, 0.94 for supine, and 0.96 for non-supine recording times (all p <0.001). For most records, differences between the AHI and ODI were small, with only 14% of the records having a AHI-ODI difference exceeding >5/hr, and 6% exceeding >10 events/hr. The positive and negative percent agreements were uniformly good to excellent across varying clinical POSA cutoffs; percent agreements (positive, negative) were: AHI≥5=0.99, 0.78; AHI≥10=0.96, 0.89; and AHI≥15=0.96, 0.89. Cohen's Kappa scores also showed substantial agreement for overall as well as supine and non-supine positions across varying clinical cutoffs of the AHI. Frequency of POSA was reproducibly uniform between 59% and 61% for both POSA criteria. When the O/NS and S/NS definitions conflicted in POSA characterization, O/NS was superior for identifying patients who might exhibit a greater response to supine restriction positional therapy., Conclusions: Auto-scored positional oximetry is a clinically viable alternative to an auto-scored Level III HSAT AHI in the characterization of POSA based on a 3% desaturation., Competing Interests: Mr Levendowski and Dr Westbrook are shareholders in Advanced Brain Monitoring, Inc. and would benefit financially if the intellectual property for the Sleep Profiler, Night Shift, and/or Positional Sleep Assessment System was acquired by a third party. Mr Levendowski and Dr. Westbrook have the following patents issued to Advanced Brain Monitoring: US 8783264, US 9198615, US 9855006, US 8355769 and US 8639313. Dr Hamilton reports they have received equipment to support research projects from Resmed, Philips Respironics and Air Liquide Healthcare. Dr St. Louis report grants from NIH NHLBI, NIA, NINDS, Michael J. Fox Foundation and Sunovion, Inc., outside the submitted work.  Dr St. Louis is on the Adverse Events Adjudication and Data Safety Monitoring Board for Clinical Trial for Inspire, Inc. Dr Penzel report grants from Itamar, Cidelec, Resmed, Löwenstein Medical and grants and personal fees from Philips/Respironics, during the conduct of the study; grants from Cidelec, Itamar, Resmed, Löwenstein Medical and grants and personal fees from Philis/Respironics, outside the submitted work. Dr Dawson reports personal fees from consultancy with Philips Respironics, personal fees from Managing Director of OSA Risk Management Ltd and personal fees from being a shareholder in Sleep Doctor Ltd, outside the submitted work. The authors report no other conflicts of interest in this work.

Cheyne-Stokes respiration (CSR) foretells deleterious outcomes in patients with heart failure. Currently, the size of therapeutic intervention is not guided by the patient's underlying pathophysiology. In theory, the intervention needed to resolve CSR, as a control system instability (loop gain >1), can be predicted knowing the baseline loop gain and how much it falls with therapy.In 12 patients with heart failure, we administered an inspiratory carbon dioxide fraction of 1-3% during CSR (n=95 interventions) as a means to reduce loop gain. We estimated the loop gain on therapy (LG therapy ), using the baseline loop gain (using hyperpnoea length/cycle length) and its expected reduction (18% per 1% inspired carbon dioxide), and tested the specific hypothesis that LG therapy predicts CSR persistence (LG therapy >1) versus resolution (LG therapy <1).As predicted, when LG therapy >1.0, CSR continued during therapy in 23 out of 25 (92%) trials. A borderline loop gain zone (0.8therapy <1) yielded an unpredictable outcome, while LG therapy <0.8 consistently yielded CSR resolution (37 out of 37 trials). A threshold of LG therapy =0.9 determined outcome in 76 out of 95 (80%) trials.We establish proof-of-concept that control theory provides predictive insight into CSR resolution in heart failure. Thus, we now have a means to calculate the size of interventions needed to ameliorate CSR on a patient-by-patient basis., (Copyright ©ERS 2016.)