BackgroundIn 2022, new guidelines for the diagnosis and treatment of pulmonary hypertension (PH) revised the hemodynamic definition, reducing the mean pulmonary artery pressure threshold from ≥ 25 to > 20 mmHg. The optimal threshold of transthoracic echocardiography (TTE) parameters and the predictive capability require further validation. This study aims to investigate the diagnostic value of TTE parameters under the new hemodynamic criteria.MethodsRetrospective analysis of PH patients who underwent right heart catheterization and TTE examination between 2017 and 2022 in a single center. Logistic regression was employed to ascertain the predictive capacity of parameters across various conditions. Receiver operating characteristic curves were used to determine the optimal cutoff values based on the new criteria.ResultsIn a cohort of 213 patients, the optimal cutoff values identified were a tricuspid annular plane systolic excursion (TAPSE) to systolic pulmonary arterial pressure (sPAP) ratio of < 0.50 mm/mmHg, a right ventricular outflow tract acceleration time (RVOT-AT) of < 93 ms, and a right atrial area (RAA) > of 14.5 cm2. Regardless of the inclusion of tricuspid regurgitation velocity (TRV) and related parameters, RVOT-AT < 93 ms manifested as an effective predictive parameter. A combination of RVOT-AT < 93 ms, main pulmonary artery diameter > 25 mm and RAA > 14.5 cm2 exhibited better specificity.ConclusionThe threshold values for TAPSE/sPAP, RVOT-AT, and RAA should be adjusted to improve the predictive capacity of PH based on revised criteria in this single-center dataset. RVOT-AT was a promising indirect parameter, and the utilization of combined indirect indicators may enhance diagnostic accuracy, particularly in instances where satisfactory TRV measurements are unavailable.

Background and Objective: Given the involvement of neuropeptides in the pathophysiology of obstructive sleep apnea syndrome (OSAS), this study investigated the associations between plasma levels of β-endorphin (β-EP) and neuropeptide Y (NPY) and OSAS severity and evaluated their potential as predictive biomarkers.Methods: A total of 48 snoring patients undergoing polysomnography (PSG) were categorized into non-OSAS, mild, moderate, and severe OSAS groups (n = 12 per group) based on the apnea–hypopnea index (AHI). Plasma levels of β-EP and NPY were measured using ELISA. Statistical analyses included one-way ANOVA, Spearman's correlation, and receiver operating characteristic (ROC) curve analysis to assess predictive performance.Results: Plasma β-EP levels exhibited significant elevation in moderate (p=0.003) and severe OSAS groups (p=0.032) compared to the non-OSAS group. Notably, NPY levels demonstrated marked differences across all OSAS severity groups (p < 0.01), with significantly higher concentrations observed in mild, moderate, and severe OSAS patients versus non-OSAS controls (p < 0.01). A progressive increase in NPY levels was observed with advancing OSAS severity, accompanied by statistically significant intergroup differences (p < 0.01). Correlation analyses revealed strong positive associations between NPY levels and both BMI (p < 0.0001) and AHI (p < 0.0001). In contrast, β-EP correlated positively with AHI (p < 0.0001) but not with BMI (p=0.0931). ROC curve analysis identified β-EP (cutoff: 9.405 ng/L) as a moderate predictor of OSAS (AUC = 0.7986, p < 0.01; sensitivity: 72.22%, specificity: 83.33%). Strikingly, NPY (cutoff: 19.29 ng/L) exhibited perfect discriminative capacity (AUC = 1, p < 0.0001; sensitivity: 97.22%, specificity: 100%).Conclusions: Plasma β-EP and NPY levels are associated with OSAS severity and may serve as potential biomarkers. However, further validation in larger cohorts is needed to confirm their clinical utility.

Pulmonary embolism (PE) at high altitude (HA) is a potentially life-threatening but underrecognized condition. Unlike low-altitude PE, high-altitude pulmonary embolism (HA-PE) may result from unique hypoxia-driven mechanisms, including hemoconcentration, endothelial dysfunction, and a hypercoagulable state. In this narrative review, we summarize current evidence on the epidemiology, pathophysiology, diagnosis, management, and prognosis of HA-PE, based on the literature published between 2010 and 2025 retrieved from PubMed and CNKI. This review summarizes the epidemiological profile, clinical features, altitude-related diagnostic challenges, limitations of current therapeutic strategies, and the prognosis of HA-PE. A more comprehensive understanding of HA-PE is crucial for enhancing early detection and developing altitude-adapted management approaches.

Background: Chronic obstructive pulmonary disease (COPD) is an increasing cause of morbidity and mortality worldwide, and acute exacerbations are the major health issues in COPD patients. In this study, we aimed to investigate the role of the delta neutrophil index (DNI) with other hematologic parameters in managing and guiding COPD patients admitted with acute exacerbations.Methods: In this retrospective study, COPD patients treated internally in pulmonology clinic, intensive care unit, and anesthesiology and reanimation unit with acute exacerbation between May 2021 and December 2023 were investigated. Records from daily visits were evaluated retrospectively. Patients were divided into two groups according to the causative organism: bacterial or nonbacterial.Results: Patients with cardiac failure were found to have significantly higher median DNI values (p : 0.026), whereas patients with other comorbidities that were not individually recorded have substantially lower median DNI values (p : 0.026). White blood cell (WBC), neutrophil, immature granulocyte values (both absolute value and percent), thrombocyte, platelet–lymphocyte ratio (PLR), neutrophil–lymphocyte ratio (NLR), C-reactive protein (CRP), procalcitonin, positive blood culture, positive systemic inflammatory response syndrome (SIRS) criteria, and sepsis were significantly higher in patients with bacterial acute exacerbation. Hospitalization duration was also significantly longer in the same group (p : 0.006). No statistically significant correlation was found between median DNI values and early mortality rate (within 28 days), readmission within 30 days and 6 months.Conclusion: In this study, we have shown that the serum procalcitonin level, WBC, NLR, and PLR measurement can be used to distinguish bacterial and nonbacterial COPD exacerbations. The DNI revealed no prognostic predictive value regarding early mortality, mechanic ventilation need, or readmission in 30 days and 6 months.

Background: Nonresolving or slowly resolving pneumonia (NRP) poses a diagnostic challenge because infectious and noninfectious etiologies often mimic community-acquired pneumonia on imaging. Endobronchial ultrasound-guided transbronchial lung biopsy (EBUS-TBLB) improves tissue acquisition for peripheral lesions, whereas metagenomic next-generation sequencing (mNGS) offers culture-independent pathogen detection. Whether their combination enhances etiological clarification of NRP remains uncertain.Methods: A total of 109 consecutive adults with NRP unresponsive to standard antimicrobial therapy were randomized to EBUS-TBLB alone (n = 66) or EBUS-TBLB + mNGS (n = 43). Baseline characteristics, diagnostic yield, and procedure-related complications were recorded. Diagnostic positivity, sensitivity for infectious agents, and safety profiles were compared using χ2 or Fisher's exact tests, with p < 0.05 considered significant.Results: Overall diagnostic yield increased from 50.0% with EBUS-TBLB to 72.1% with the combined approach (χ2 = 4.37, p < 0.05). mNGS significantly improved detection of bacterial/fungal pneumonia (0% vs. 13.9%; p < 0.05) and pulmonary tuberculosis (0% vs. 20.9%; p < 0.05). Malignancy remained the predominant diagnosis (57.8% of all cases); yields for most tumor subtypes were comparable between groups. Complication rates did not differ between the two groups: minor bleeding (19.7% vs. 23.3%), hypoxia (50.0% vs. 48.8%), pneumothorax (4.5% vs. 0%), and delayed recovery (4.5% vs. 7.0%) (p > 0.05). No severe adverse events occurred.Conclusions: EBUS-TBLB + mNGS represents a paradigm shift in the diagnosis of complex respiratory cases, integrating imaging with advanced genomics to enhance precision medicine. In practice, early implementation of the EBUS-TBLB + mNGS diagnostic protocol in patients with NRP can help exclude malignancy or confirm an infectious etiology.

A diffusely thickened or hard pleura is a special type of macroscopic appearance associated with benign or malignant conditions. Medical thoracoscopy (MT) is the gold standard for pleural pathology, but its diagnostic yield is imperfect. Although cryobiopsy may provide greater and deeper tissue, its impact on the diagnostic yield remains uncertain, and safety concerns persist. We evaluated the efficacy and safety of cryoprobe biopsy as a salvage technique following negative or inconclusive flexible forceps biopsy during MT under the guidance of rapid on-site evaluation (ROSE). This prospective study enrolled 280 patients with undiagnosed exudative pleural effusion who underwent MT. After the initial flexible forceps biopsy and ROSE, 37 patients with negative ROSE results underwent cryoprobe biopsy. A total of 37 (21 males and 16 females) patients, aged 56.43 ± 16.09 (range: 22–78) years with negative ROSE results, underwent cryoprobe biopsy. CB established a definitive histopathological diagnosis in 33/37 (89.2%) patients, which was significantly higher than that achieved with FFB, i.e., 21/37 (56.8%; p=0.002). CB resulted in significantly larger pleural specimens (9.86 ± 2.69 mm) in comparison to FFB (2.89 ± 1.15 mm, 95% confidence interval [CI]: 6.01–7.93; p < 0.001). Furthermore, CB was faster than FFB (median durations of 15 and 31 min, respectively; p < 0.001). CB had improved tissue quality for CGP testing in 20 NSCLC patients compared to FFB (18/20 versus 8/15, p=0.036). No significant complications were noted. Cryoprobe biopsy is a safe and effective salvage technique for patients with undiagnosed pleural effusion who show negative results on flexible forceps biopsy during MT. It provides larger, higher-quality specimens with a higher positivity rate, potentially avoiding the need for repeat procedures and facilitating timely diagnosis and treatment.

Chronic obstructive pulmonary disease (COPD) is a lung condition characterized by persistent airway obstruction and is associated with various phenotypes and endotypes. While eosinophilic inflammation is typically seen in asthma, it also occurs in COPD, with known increases in eosinophil counts during exacerbations. However, the impact of cumulative tobacco exposure on eosinophil counts is not well understood. This study aims to investigate this relationship. Data for this prospective study were collected from three centers, involving patients diagnosed with COPD. Patients' demographic data and eosinophil levels were documented. They were categorized according to GOLD Stages A, B, and E, and each group was analyzed relative to the amount of cigarette smoking. The study enrolled 227 COPD patients, predominantly male (92.5%) with an average age of 64.6 years. Of the study population, 39.8% (n: 90) were current smokers, and 86.9% had a smoking history of more than 20 packs/year. The average smoking history of our patients was 52.38 ± 30.69 (mean ± SD) pack/year. Our patients had an average smoking history of 39.49 ± 12.56 years. No statistically significant results were found between the amount of cigarettes smoked and eosinophil counts. However, in the correlation between smoking history and eosinophil counts, higher eosinophil counts were found in those who had former smoking compared to current smokers or never smokers. While the number of pack-years and the duration of smoking increased from Stage A to Stage E, daily cigarette consumption remained constant, and eosinophil counts did not show a significant correlation with the quantity of tobacco. Eosinophil counts in COPD patients did not vary significantly with either the amount of tobacco exposure or the severity of COPD as categorized by GOLD stages. These findings suggest that factors other than tobacco exposure may influence eosinophil levels in COPD patients.

Background: Pulmonary hypertension (PH) in patients undergoing lung transplantation (LT) for pulmonary fibrosis can impair lung function, reduce physical activity, and decrease survival. However, data on outcomes at 1 and 5 years of follow-up remain limited. Methods: In this prospective cohort study, pulmonary function, the 6-min walk test (6MWT), and the St. George's Respiratory Questionnaire (SGRQ) were assessed pretransplant, at hospital discharge, and at 3, 6, and 12 months posttransplant. Additionally, minimal clinically important differences (MCIDs) between patients with and without PH were evaluated. Survival rates were calculated using the Kaplan-Meier method and analyzed using the log-rank test. Results: The study included 39 patients undergoing LT for pulmonary fibrosis. Of these, 82% (32/39) had PH, with a median age of 52.6 years (SD: 10.2). In both the PH and non-PH groups, lung function, 6MWD, and SGRQ total scores showed progressive improvement from pre-LT to 1 year posttransplant. Patients without PH demonstrated MCID in 6MWT and SGRQ total scores from pre-LT through the 6- and 12-month follow-up. The overall 1-year survival rate was 84.6%, with an average survival of 10.51 months (95% CI: 9.29-11.73). The 5-year overall survival rate was 61.5%, with an average survival of 44.89 months (95% CI: 37.62-52.16). No statistically significant differences in survival were found based on sex (p=0.322 and 0.206), mean pulmonary artery pressure (mPAP) (p=0.232 and 0.486), age (p=0.375 and 0.959), or body mass index (BMI) (p=0.884 and 0.594) at 1 and 5 years. Conclusion: Survival at 1 and 5 years was lower in patients with PH. However, no significant differences in survival were observed based on sex, mPAP, age, or BMI. Statistically significant improvements in FVC, FEV1, 6MWT, and SGRQ total scores were observed both before and after LT, continuing through 1 year of follow-up. The 6MWT and SGRQ showed MCID both prior to surgery and during follow-up at 6 and 12 months, in both PH and non-PH patients.

Venous thromboembolism (VTE) is widespread and poses significant risks of illness and death, making it a vital public health issue. Obstructive sleep apnea (OSA), which is the most prevalent sleep disorder, is connected to an increased possibility of cardiovascular diseases and VTE. The length of VTE treatment hinges mainly on the frequency of its recurrence in patients. Our data about VTE and its recurrence in OSA patients are limited. In this review, we aim to investigate the risk of VTE recurrence in OSA patients and evaluate the role of continuous positive airway pressure (CPAP) therapy in mitigating this risk. A literature search gathered information about VTE pathogenesis and its potential recurrence mechanism in OSA. The recurrent episodes of partial or complete obstruction of the upper airway in OSA lead to intermittent lack of oxygen. Hypoxemia acts as a central cornerstone of VTE incidence in OSA patients, leads to activating all the vertices of Virchow's triad, and creates the appropriate condition for the developmental and even recurrence of VTE. Intermittent hypoxia causes an increase in the inflammatory state and coagulation activity, leading to oxidative stress and endothelial dysfunction. Furthermore, it results in heightened viscosity and venous stasis. The results of previous studies on VTE recurrence in OSA patients are conflicting. Even though the use of CPAP leads to diminished proinflammatory cytokines and oxidative stress indicators, there is currently insufficient clinical evidence to support that this therapy can prevent recurrent VTE in patients with OSA. Further investigation is necessary to gain a better comprehension of the probability and frequency of relapse of VTE in OSA patients, as the present research has generated inconclusive outcomes.

Hypoxic pulmonary hypertension (HPH) lacks effective treatments. The research is designed to examine the effectiveness of Notoginsenoside R1 (NGR1) in addressing HPH and to explore its molecular mechanisms. Under hypoxic conditions, we created a rat model of HPH and treated the animals with NGR1. We assessed the therapeutic effects of NGR1 on HPH through hemodynamic measurements and pulmonary artery vascular remodeling. We employed transcriptomic analysis to evaluate gene expression changes in HPH rats. We conducted untargeted metabolomics to examine how NGR1 influences the metabolic profile of HPH rats. NGR1 treatment significantly improved hemodynamic parameters and ameliorated pulmonary artery vascular remodeling in HPH rats. Transcriptomic analysis identified Pck1 as the most significantly altered gene. NGR1 intervention significantly improved the expression of vascular remodeling-related proteins. NGR1 reversed the expression of glycolysis-related genes. NGR1 reduced the levels of glycolysis-related metabolites. Further analysis revealed that NGR1 treatment decreased PFKL, HK2, and LDHA protein expression and lowered lactate levels in lung tissue. Our findings demonstrate that NGR1 effectively alleviates the pathological features of HPH in rats. NGR1 inhibits hypoxia-induced glycolysis-mediated pulmonary artery remodeling, mitigates vascular endothelial damage, and suppresses the abnormal proliferation of smooth muscle cells and fibroblasts.