European Respiratory Review最新文献

Exposure to air pollution has been associated with up to 9 million premature deaths per year worldwide, with the respiratory system a key site for its effects. Air pollution exposure is a well-established risk factor for the development and exacerbation of airways diseases and lung cancer, however relatively little is known regarding the risks associated with air pollution interacting with areas of gas exchange - the alveoli and pulmonary interstitium. In recent years, evidence has emerged identifying a role in the development and progression of sub-clinical interstitial lung abnormalities as well as progression and risk of exacerbation of fibrotic interstitial lung diseases. This review outlines the epidemiologic evidence that air pollution perturbs alveolar health. It considers the different components of ambient air pollution, how penetration to the alveoli is determined by particle size and whether the response to alveolar exposure may be modulated by personal susceptibility factors. We discuss potential acute and chronic pathogenic mechanisms of injury upon the pulmonary interstitium and how these may contribute to the development and/or progression of interstitial processes. Finally, we explore current knowledge gaps and the potential for air pollution interventions in vulnerable individuals to support alveolar homeostasis and so prevent disease development and/or progression.

Pulmonary fibrosis remains a devastating and often fatal condition due to the lack of effective treatments that halt disease progression. Rodent models of pulmonary fibrosis are crucial to identify candidate targets and novel therapeutic agents. However, the attrition rate of novel drug candidates in clinical trials remains high. This review suggests complementing traditional methods used to evaluate antifibrotic therapies in rodent models, such as histopathological and biochemical markers, and lung function tests, with innovative imaging technologies. These imaging techniques could improve the predictive power and translatability of animal studies in human clinical trials. Notably, previous studies in mice and other rodents have observed compensatory lung enlargement in response to lung injury, questioning whether the conventional view of pulmonary fibrosis as a restrictive disease applies to rodents. By adding longitudinal image-based biomarkers, we aim to better unravel the complexity of lung responses and facilitate more effective drug development for pulmonary fibrosis, ultimately improving patient outcomes.

Background: Limited evidence exists on air pollution's systemic impact on lung function and mediating biomarkers. This study comprehensively evaluated associations between air pollution, COPD and lung function, while exploring biomarker mediation.

Methods: A prospective analysis of 451 566 UK Biobank participants was conducted. Land use regression models estimated exposure to particulate matter (PM) ≤2.5 μm (PM_2.5), PM ≤10 μm (PM₁₀), PM with diameters between 2.5 and 10 μm, reflectance measured on PM_2.5 filters and transformed into absorbance (PM_{2.5 absorbance}), nitrogen dioxide (NO₂) and nitrogen oxides (NOx). Linear and Cox regression assessed pollution effects on forced expiratory volume in 1 s (FEV₁), forced vital capacity (FVC), FEV₁:FVC ratio, peak expiratory flow (PEF) and COPD incidence. A meta-analysis synthesised results with prior cohorts (PROSPERO: CRD42023411304). Mediation analysis evaluated biomarkers.

Results: Elevated PM_2.5, PM_{2.5 absorbance}, NO_x and NO₂ correlated with reduced lung function (measured as FEV₁, FVC, FEV₁:FVC ratio and PEF) and higher COPD risk (hazard ratio: 1.08-1.15). Race-stratified analyses revealed interactions, with White populations showing greater COPD susceptibility. Meta-analysis confirmed air pollution-COPD links. Mediation analyses implicated plasma lipid metabolites, inflammatory cell counts and cytokines as mechanistic intermediaries.

Conclusion: Air pollution associates with lung function decline and elevated COPD risk, with White populations disproportionately affected. Lipid, inflammatory and haematological biomarkers mediate this relationship. Findings underscore the urgency of air pollution control to mitigate respiratory harm and inform targeted preventive and therapeutic strategies.

Introduction: Pulmonary hypertension is a pathophysiological disorder with poor prognosis. Exercise intolerance and lower physical activity levels are common features of pulmonary hypertension and affect patients' quality of life. Exercise training effectively improves clinical outcomes in this population, but access to rehabilitation centres is often limited. A home-based exercise training component could be an accessible and cost-effective alternative, but the efficacy and safety of this approach in pulmonary hypertension remain unclear.

Methods: We conducted a systematic review and meta-analysis of studies retrieved from six international databases. The studies evaluated home-based exercise interventions in patients with pulmonary hypertension, including both stand-alone and hybrid setups, and assessed safety, efficacy (exercise capacity, cardiorespiratory outcomes and functional class) and adherence.

Results: We included 19 studies. Compared with inactive controls, home-based exercise training improved the 6-min walk distance (mean difference (MD) 54.85 m, p<0.01), peak oxygen uptake (standardised MD 0.83 mL·kg^-1·min^-1, p<0.01), ventilatory efficiency (MD -3.93, p<0.01) and quality of life scores. Improvements in clinical outcomes were comparable between home-based and centre-based interventions. No clinical worsening or exercise training-related severe adverse events were reported; however, most studies did not report health-related self-monitoring strategies at home. The level of adherence was generally high, and the drop-out rates were comparable between home-based and centre-based interventions.

Conclusion: Home-based exercise interventions appear to be viable alternatives to centre-based programmes for patients with pulmonary hypertension, showing comparable improvements in clinical outcomes. However, limited reporting on self-monitoring may affect the overall safety assessment. Further research is needed to determine the optimal implementation of these interventions.

Right-sided heart dysfunction (RHD) has emerged as a critical yet often underappreciated aspect of acute respiratory distress syndrome (ARDS). This review describes the role of RHD in ARDS, providing an updated overview of its pathophysiology, diagnosis and potential treatments. Several mechanisms contribute to increased right ventricular (RV) afterload in ARDS, including hypoxic vasoconstriction, hypercapnia, acidosis, in situ thrombosis and an imbalance between pulmonary vasoconstrictors and vasodilators. Mechanical ventilation, a cornerstone in ARDS management, can worsen haemodynamic instability due to impaired lung compliance. Systemic implications of RHD include renal dysfunction due to impaired organ perfusion and venous congestion. Volume overload further exacerbates RV strain, setting off a vicious cycle of deteriorating RV function, interventricular septal bowing, reduced left ventricular preload and ultimately circulatory failure. The diagnosis and management of RHD in ARDS require an integrated approach that combines invasive haemodynamic monitoring, imaging techniques and noninvasive assessments. Specific treatment options targeting RHD in ARDS remain limited. Titration of positive end-expiratory pressure plays a critical role in mitigating RHD. Prone positioning has shown inconsistent effects on RV function which require further investigation. Inhaled pulmonary vasodilators, such as nitric oxide and prostacyclins, are commonly used to modulate pulmonary vascular tone in ARDS. Small studies suggest that levosimendan and commonly used vasoactive drugs such as norepinephrine, epinephrine, vasopressin and milrinone may improve RV function in ARDS. However, no pharmacologic treatment is specifically approved for ARDS-associated RHD. Large-scale clinical trials are necessary to identify the most effective treatment strategies for specific patient populations.

Background: Flexible bronchoscopy is an essential, invasive procedure used in clinical practice for diagnosing and treating bronchial, pulmonary, thoracic and other diseases. Due to concerns about the potential for intense stimulation during flexible bronchoscopy operations, sedation is recommended by most countries and regions for all patients without contraindications. However, the use of sedative and analgesic substances for sedation during flexible bronchoscopy may result in respiratory depression, potentially leading to hypoxaemia and/or hypercapnia. Considering these side-effects and associated risks, some countries and regions do not recommend this approach.

Objective: This review aims to compare and analyse differences between currently published guidelines on sedation during flexible bronchoscopy and expert consensus in five key aspects: the necessity of sedation, qualifications of the person in charge of sedation, selection of sedative or anaesthetic drugs, sedation depth and perioperative monitoring, and oxygen supplementation and remedies.

Conclusions: Undeniably, more attention and clinical evidence are needed to address the controversies and disputes existing among currently published guidelines on sedation during flexible bronchoscopy or expert consensus. Furthermore, international cooperation is necessary to establish standard international training and practice guidelines for sedation during flexible bronchoscopy.

Chronic respiratory diseases impart a huge global disease burden. Many cases of adult chronic respiratory disorders are recognised to originate early in life during critical phases of lung growth and development. We therefore reviewed the longitudinal evolution of common childhood respiratory diseases across the lifespan. We included studies relating childhood respiratory health (preterm birth, asthma, low lung function or bronchiectasis) to respiratory health in adolescents and adults, including COPD.The negative impact of preterm birth (with or without bronchopulmonary dysplasia) on future respiratory health has now been quantified, with many having increasing deviation of lung function from the norm over their life course. While previous studies report children with asthma frequently "outgrow their disease" by adolescence or early adulthood, recent data describe asthma trajectories that include relapse, early-onset adult-remitting, and early-onset persistent childhood asthma. Evidence is emerging in adults of the negative impact of chronic productive cough, breathlessness and lower lung function on future respiratory and cardiovascular health and all-cause mortality. In addition, we found that in general, childhood respiratory health and adverse lung function trajectories are inextricably linked to adult respiratory health and cardiovascular events, as well as cardiovascular and all-cause mortality. Thus, we highlight the importance of pulmonary assessments in high-risk groups during childhood (e.g. preterm birth, parental smokers, early life hospitalisation for acute lower respiratory infections). Our review emphasises the importance of childhood respiratory health and the need for interventions to reduce or manage disease burden, which require a whole-of-society approach across the life course.

Background: Several studies have reported lung function impairment following COVID-19. Less is known about the subsequent recovery.

Research question: What is the recovery in lung function after COVID-19 during the first year after infection?

Methods: We conducted a systematic review and meta-analysis of studies that monitored individuals' lung function from the time of infection to at least 1 year after infection. Primary outcomes were change in percent predicted forced expiratory volumes in 1 s (FEV₁), forced vital capacity (FVC) and diffusing capacity for carbon monoxide (D _LCO). Mean differences (MDs) with 95% confidence intervals were estimated using a random effects model.

Results: We included 23 studies (n=3347 participants). 20 (86.9%) studies had their first follow-up 3 months after infection and 21 (91.3%) had their second follow-up 12 months after infection. The MDs between the second and first follow-up visits of FEV₁, FVC and D _LCO were 3.1% (95% CI 1.8-4.5; p<0.01), 4.4% (95% CI 2.7-6.0; p<0.01) and 6.6% (95% CI 4.4-8.9; p<0.01), respectively. Recovery of FEV₁, FVC and D _LCO was greater in mechanically ventilated patients compared to individuals with less severe disease. Current smoking status, pre-existing chronic lung disease and age did not impact recovery during the first year after infection.

Interpretation: Recovery in lung function was evident during the first year after COVID-19, with the largest improvement in patients with the most severe infection. Further follow-up and large-scale studies are warranted to establish recovery trajectories of COVID-19 and other respiratory infections to identify patient subgroups needing additional follow-up to ascertain modifiable factors influencing pulmonary recovery.