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Background: Oronasal masks are used widely for treating OSA with CPAP. However, oronasal CPAP is associated with lower effectiveness and lower adherence than nasal CPAP.

Research question: What is the impact of oral route and lateral position in patients well adapted to oronasal CPAP? Can these patients be switched to nasal CPAP?

Study design and methods: Patients with OSA receiving oronasal CPAP underwent two CPAP polysomnography titrations in random order using an oronasal mask with two independent sealed compartments connected to two separate pneumotachographs. One study was performed with the nasal and oral compartments opened and the other study was performed with only the oral compartment opened. CPAP titration was carried out in the supine and lateral positions. Finally, the patients were offered a nasal mask. A third polysomnography test was performed using nasal CPAP.

Results: Twenty patients with OSA (baseline apnea-hypopnea index [AHI], 52 ± 21 events/h) adapted to oronasal CPAP were studied. Most patients (75%) were oronasal breathers with optimal CPAP. Oral CPAP was less effective to treat OSA than oronasal CPAP, evidenced by a higher residual AHI (median, 2 [interquartile range (IQR), 1-6.0] vs 12.5 [IQR, 1.8-28.3); P = .003), despite a significantly higher CPAP level (median, 10 cm H₂O [IQR, 9-10 cm H₂O] vs 11 cm H₂O [IQR, 10-12 cm H₂O]; P = .003). The residual AHI was significantly lower in the lateral position for both oronasal and oral CPAP. Finally, patients (75%) agreed to change and preferred to continue using a nasal mask, which resulted in lower CPAP and better OSA control.

Interpretation: Our results indicate that the effectiveness of oronasal CPAP to abolish OSA is decreased significantly when patients are required to breathe exclusively through the mouth. Oronasal CPAP efficacy is significantly better in the lateral position. The transition to nasal mask results in higher CPAP effectiveness to treat OSA.

Clinical trial registry: ClinicalTrials.gov; No.: NCT05272761; URL: www.

Clinicaltrials: gov.

Background: Cystic fibrosis (CF) transmembrane conductance regulator (CFTR) modulators are available to the majority of people with CF in the United States; little is known about pregnancy outcomes with modulator use. The aim of this retrospective study was to determine the impact of CFTR modulators on maternal outcomes.

Research question: Does pregnancy differentially affect outcomes in female individuals with CF with and without CFTR modulator exposure?

Study design and methods: Data on pregnancies from 2010 to 2021 were collected from 11 US adult CF centers. Multivariable longitudinal regression analysis was performed to assess whether changes in percent predicted FEV₁ (ppFEV₁), BMI, pulmonary exacerbations (PEx), and Pseudomonas aeruginosa prevalence differed from prior to, during, and following pregnancy according to CFTR modulator use while adjusting for confounders. Infant outcomes are also described based on maternal modulator use.

Results: Among 307 pregnancies, mean age at conception was 28.5 years (range, 17-42 years), before pregnancy ppFEV₁ was 74.2, and BMI was 22.3 kg/m². A total of 114 pregnancies (37.1%) had CFTR modulator exposure during pregnancy (77 with highly effective modulator therapy [HEMT] and 37 with other modulators). The adjusted mean change in ppFEV₁ from before pregnancy to during pregnancy was -2.36 (95% CI, -3.56 to -1.16) in the unexposed group and 2.60 (95% CI, 0.23 to 4.97) in the HEMT group, with no significant change from during pregnancy to 1 year after pregnancy. There was an overall decline in ppFEV₁ from before pregnancy to after pregnancy in the no modulator group (-2.56; 95% CI, -3.62 to -1.49) that was not observed in the HEMT group (1.10; 95% CI, -1.13 to 3.34). PEx decreased from before pregnancy to after pregnancy in the HEMT group, and BMI increased from before pregnancy to during pregnancy in all groups but with no significant change after pregnancy. Missing infant outcomes data precluded firm conclusions.

Interpretation: We observed superior pregnancy and after pregnancy pulmonary outcomes in individuals who used HEMT, including a preservation of ppFEV₁, compared with those unexposed to HEMT.

Background: Exacerbations in COPD can be life-threatening and can lead to irreversible declines in lung function and quality of life. Medications that reduce exacerbation burden are an unmet need, because exacerbations put patients at risk of more exacerbations and decrease quality of life. Ensifentrine is a first-in-class selective dual inhibitor of phosphodiesterase 3 and 4 with demonstrated nonsteroidal antiinflammatory activity and bronchodilatory effects.

Research question: Does ensifentrine reduce the rate or risk of COPD exacerbations?

Study design and methods: A prespecified, pooled analysis of the phase 3 clinical trials Ensifentrine as a Novel Inhaled Nebulized COPD Therapy (ENHANCE)-1 (ClinicalTrials.gov Identifier: NCT04535986) and ENHANCE-2 (ClinicalTrials.gov Identifier: NCT04542057) was conducted to assess the effect of ensifentrine on exacerbation rate and risk (time to first exacerbation). The trials included symptomatic patients aged 40 to 80 years with moderate to severe COPD who received 3 mg twice-daily ensifentrine over 24 weeks or placebo. Subgroup analyses and frequent exacerbator transition risk assessment were conducted post hoc.

Results: In total, 975 patients treated with ensifentrine and 574 patients who received placebo were included in the pooled analysis, including 62% of patients receiving concomitant long-acting muscarinic antagonist or long-acting β₂-agonist therapy and 18% receiving concomitant inhaled corticosteroid therapy. Ensifentrine was associated with significant reductions in the rate (rate ratio, 0.59; 95% CI, 0.43-0.80; P < .001) and risk (hazard ratio, 0.59; 95% CI, 0.44-0.81; P < .001) of moderate to severe exacerbations compared with placebo. Reductions in the rate and risk of exacerbations generally were consistent across patient subgroups, including age, sex, race, background maintenance medication use, chronic bronchitis, eosinophil count, COPD severity, and exacerbation history. Ensifentrine was associated with a numerical delay in transitioning from an infrequent exacerbator (Global Initiative for Chronic Obstructive Lung Disease group B) to a frequent exacerbator (Global Initiative for Chronic Obstructive Lung Disease group E) compared with placebo.

Interpretation: Ensifentrine reduced the rate of exacerbations and increased the time to first exacerbation among patients with COPD across a broad range of clinically relevant subgroups.

Case presentation: A 21-year-old man with a history of glucose-6-phosphate dehydrogenase deficiency experienced an acute onset of atraumatic left upper abdominal and flank pain. An initial contrast-enhanced CT scan of the chest, abdomen, and pelvis revealed a consolidation in the left lower lobe, a small pleural effusion, and enlarged mesenteric lymph nodes. The patient was prescribed nonsteroidal antiinflammatory drugs for a presumed viral syndrome and was discharged. He returned the next day with increased pain, new onset of shortness of breath, and a fever of 38.6 °C. A diagnosis of community-acquired pneumonia was made, and doxycycline was prescribed. Twenty-four hours later, he presented again with severe pain, worsening dyspnea, and hypoxemia. A CT angiogram of the chest showed persistent consolidation in the left lower lobe and a now large left pleural effusion. He was admitted to the internal medicine service for the management of pneumonia and presumed para-pneumonic effusion.

Background: Although it is generally accepted that aerobic exercise training does not change lung structure or function, some work suggests that greater pulmonary vascular structure and function are associated with higher exercise capacity (peak rate of oxygen consumption [V˙o₂peak]).

Research question: Is there a cross-sectional association between the pulmonary vasculature and V˙o₂peak? We hypothesized that those with higher CT blood vessel volumes and pulmonary diffusing capacity for carbon monoxide (Dlco) would have higher V˙o₂peak, independent of airflow limitation.

Study design and methods: Participants from the Canadian Cohort Obstructive Lung Disease (CanCOLD) study were categorized as follows: participants with normal spirometry who had never smoked (n = 263), participants with normal spirometry who had ever smoked (n = 407), and COPD: individuals with spirometric airflow obstruction (n = 334). Total vessel volume (TVV), volume for vessels < 5 mm² in cross-sectional area (BV5), and volume for vessels between 5 and 10 mm² in cross-sectional area (BV5-10) were generated from CT scans and used as indices of pulmonary vascular structure. Dlco was used as an index of pulmonary microvascular function. V˙o₂peak was evaluated via incremental cardiopulmonary exercise testing.

Results: General linear regression models revealed that even after controlling for FEV₁, emphysema severity, and body morphology, Dlco, TVV, BV5, and BV5-10, were independently associated with V˙o₂peak. Interaction effects were observed between COPD and TVV, BV5, and BV5-10, indicating a weaker association between pulmonary vascular volumes and V˙o₂peak in COPD.

Interpretation: Our results suggest that pulmonary vascular structure and Dlco are independently associated with V˙o₂peak, regardless of severity of airflow limitation and emphysema, suggesting that these associations are not limited to COPD.