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Background: According to the most recent pulmonary hypertension (PH) guidelines, a main pulmonary artery (MPA) diameter > 25 mm on transthoracic echocardiography supports the diagnosis of PH. However, the size of the pulmonary artery (PA) may vary according to body size, age, and cardiac phases.

Research question: (1) What are the reference limits for PA size on transthoracic echocardiography, considering differences in body size, sex, and age? (2) What is the diagnostic value of the PA size for classifying PH? (3) How does the selection of different reference groups (healthy volunteers vs patients referred for right heart catheterization [RHC]) influence the diagnostic OR (DOR)?

Study design and methods: The study included a reference cohort of 248 healthy individuals as control patients, 693 patients with PH proven by RHC, and 156 patients without PH proven by RHC. In the PH cohort, 300 had group 1 PH, 207 had group 2 PH, and 186 had group 3 PH. MPA and right PA diameters and areas were measured in the upper sternal short-axis and suprasternal notch views. Reference limits (5th-95th percentile) were based on absolute values and height-indexed measures. Quantile regression analysis was used to derive median and 95th quantile reference equations for the PA measures. DORs and probability diagnostic plots for PH were then determined using healthy control and non-PH cohorts.

Results: The 95th percentile for indexed MPA diameter was 15 mm/m in diastole and 19 mm/m in systole in both sexes. Quantile regression analysis revealed a weak age effect (pseudo-R² of 0.08-0.10 for MPA diameters). Among measures, the MPA size in diastole had the highest DOR (156.2; 95% CI, 68.3-357.5) for detection of group 1 PH. Similarly, the DORs were also high for groups 2 and 3 PH when compared with the control cohort but significantly lower compared with the non-PH cohort.

Interpretation: This study presents novel reference limits for MPA based on height indexing and quantile regression.

Case presentation: A 52-year-old woman with a history of leiomyoma uteri and tobacco-use disorder in remission presented with 2 months of progressive back pain. Her pain was located between her shoulder blades and was described as constant with intermittent sharp, stabbing sensation. It was nonradiating and aggravated by inspiration. She denied fever, cough, shortness of breath, chest pain, or recent changes in weight or appetite. Two days prior, she was evaluated in the ED for similar symptoms and prescribed naproxen and cyclobenzaprine for suspected musculoskeletal pain. However, she received minimal relief, which prompted her visit. She underwent a total hysterectomy 13 years ago for benign uterine fibroid tumors. She had a 15-pack-year history but quit smoking 3 years ago. Family history was notable for colon and pancreatic cancer in her father and breast cancer in her maternal aunt.

Background: Associations between air pollution and the acute exacerbations (AEs) of COPD have been established primarily in time-series studies in which exposure and health data were at the aggregate level, limiting the identification of susceptible populations.

Research question: Are air pollutants associated with the onset of AEs of COPD in China? Who is more susceptible to the effects of air pollutants?

Study design and methods: Data regarding AEs of COPD were obtained from the Acute Exacerbation of Chronic Obstructive Pulmonary Disease Registry (ACURE) study, and air pollution data were assigned to individuals based on their residential address. We adopted a time-stratified case-crossover study design combined with conditional logistic regression models to estimate the associations between six air pollutants and AEs of COPD. Stratified analyses were performed by individual characteristics, disease severity, COPD types, and the season of exacerbations.

Results: A total of 5,746 patients were included. At a 2-day lag, for each interquartile range increase in fine particulate matter and inhalable particulate matter concentrations, ORs for AEs of COPD were 1.054 (95% CI, 1.012-1.097) and 1.050 (95% CI, 1.009-1.092), respectively. The associations were more pronounced in participants who were younger than 65 years, who had experienced at least one severe AE of COPD in the past year, who had received a diagnosis of COPD between 20 and 50 years of age, and who had experienced AEs of COPD in the cool seasons. By contrast, significant associations for nitrogen dioxide, sulfur dioxide, and carbon monoxide lost significance when excluding patients collected before 2020 or with greater distance from the monitoring station, and no significant association was observed for ozone.

Interpretation: This study provides robust evidence that short-term exposure to fine particulate matter and inhalable particulate matter was associated with higher odds of AEs of COPD onset. Individuals who are young, have severe COPD, or whose first diagnosis of COPD was made when they were between 20 and 50 years of age and experience an exacerbation during the cooler seasons may be particularly susceptible.

Trial registry: ClinicalTrials.gov; No.: NCT2657525; URL: www.

Clinicaltrials: gov.

Background: The varied treatment response to inhaled corticosteroids (ICS) in patients with COPD and the associated increased risk of pneumonia necessitate a personalized ICS therapeutic approach. This is informed by blood eosinophil count (BEC), which predicts ICS treatment response. However, BEC appears to change in response to ICS treatment.

Research question: Does (1) BEC measured on ICS treatment (2) BEC measured off ICS treatment, or (3) the change in BEC during ICS treatment best predict treatment response to ICS in COPD?

Study design and methods: The Fluticasone Salmeterol on COPD Exacerbations Trial (FLAME), a 52-week, double-blind randomized controlled trial compared long-acting beta-2 agonists (LABAs)/long-acting muscarinic antagonists (LAMAs) with LABA/ICS. Corticosteroids were prohibited during a 4-week run-in period. We chose patients previously on ICS, thereby allowing BEC before and after the run-in period to represent BEC on and off ICS, respectively. In this post hoc analysis, we revisited outcome data, exploring how the three BEC biomarkers interacted with treatment response to the ICS-containing regimen.

Results: Our study showed that LABA/LAMA combination was superior, or at least noninferior, to LABA/ICS in curbing exacerbations for most FLAME participants. However, higher BEC off ICS, higher BEC on ICS, and significant BEC suppression during ICS treatment corresponded to superior response to LABA/ICS in terms of exacerbation rate, time to first exacerbation, and time to first pneumonia. In a subgroup, including 9% of participants, BEC changed significantly during ICS treatment (≥ 200 cells/μL), and higher BEC on ICS did not predict ICS treatment response. For these patients, BEC off ICS and BEC change proved more predictive. Excess pneumonia risk associated with ICS appeared to be confined to patients who do not benefit from this treatment. BEC was not predictive of treatment effects on lung function and health status.

Interpretation: This exploratory analysis advocates preferentially using BEC off ICS or BEC change during ICS treatment for guiding ICS treatment decisions. BEC measured on ICS is less predictive of treatment response.

Clinical trial registration: ClinicalTrials.gov; No.: NCT01782326; URL: www.

Clinicaltrials: gov.