Pub Date : 2024-11-30Epub Date: 2024-11-18DOI: 10.21037/jtd-24-497
Jan van Egmond, Leo H D J Booij
Mechanical ventilation, essential for critically ill patients, contrasts with natural respiration, primarily due to differences in pleural pressure (Ppleural ). Natural inspiration decreases Ppleural , pulling the lungs away from the thoracic wall, whereas positive pressure inspiration increases Ppleural , pushing the lungs against the thoracic wall. This shift has several consequences. First, elevated Ppleural during positive pressure ventilation can lead to cyclic airway closure, particularly in the dependent lung regions. This increases the risk of atelectasis, that impairs oxygenation and may lead to further complications such as pneumonia. Second, the increase in Ppleural disrupts the balance maintained by negative Ppleural and capillary forces. This disruption reduces the lubricating pleural fluid between the pleurae, increasing friction and shear stress on the lung tissues, which may lead to damage and conditions such as ventilator-induced lung injury and pneumothorax. Furthermore, airway closure can worsen lung compliance, making mechanical ventilation more challenging and increasing the risk of lung overstretching. This necessitates careful management of ventilation settings, particularly the use of positive end-expiratory pressure (PEEP) and recruitment maneuvers to minimize these adverse effects. Protective strategies, such as synchronizing mechanical ventilation with the patient's breathing efforts, prone positioning, and careful application of PEEP, are crucial in reducing Ppleural and its associated risks. Since negative pressure ventilation (NPV) inherently lowers Ppleural , it may help avoid many of the adverse side effects previously discussed. Therefore, reconsidering and reintroducing NPV in a modern context should be seriously explored.
{"title":"The role of pleural pressure in inducing pneumothorax and other adverse effects of positive pressure ventilation.","authors":"Jan van Egmond, Leo H D J Booij","doi":"10.21037/jtd-24-497","DOIUrl":"10.21037/jtd-24-497","url":null,"abstract":"<p><p>Mechanical ventilation, essential for critically ill patients, contrasts with natural respiration, primarily due to differences in pleural pressure (<i>P<sub>pleural</sub></i> ). Natural inspiration decreases <i>P<sub>pleural</sub></i> , pulling the lungs away from the thoracic wall, whereas positive pressure inspiration increases <i>P<sub>pleural</sub></i> , pushing the lungs against the thoracic wall. This shift has several consequences. First, elevated <i>P<sub>pleural</sub></i> during positive pressure ventilation can lead to cyclic airway closure, particularly in the dependent lung regions. This increases the risk of atelectasis, that impairs oxygenation and may lead to further complications such as pneumonia. Second, the increase in <i>P<sub>pleural</sub></i> disrupts the balance maintained by negative <i>P<sub>pleural</sub></i> and capillary forces. This disruption reduces the lubricating pleural fluid between the pleurae, increasing friction and shear stress on the lung tissues, which may lead to damage and conditions such as ventilator-induced lung injury and pneumothorax. Furthermore, airway closure can worsen lung compliance, making mechanical ventilation more challenging and increasing the risk of lung overstretching. This necessitates careful management of ventilation settings, particularly the use of positive end-expiratory pressure (PEEP) and recruitment maneuvers to minimize these adverse effects. Protective strategies, such as synchronizing mechanical ventilation with the patient's breathing efforts, prone positioning, and careful application of PEEP, are crucial in reducing <i>P<sub>pleural</sub></i> and its associated risks. Since negative pressure ventilation (NPV) inherently lowers <i>P<sub>pleural</sub></i> , it may help avoid many of the adverse side effects previously discussed. Therefore, reconsidering and reintroducing NPV in a modern context should be seriously explored.</p>","PeriodicalId":17542,"journal":{"name":"Journal of thoracic disease","volume":"16 11","pages":"8103-8109"},"PeriodicalIF":2.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-30Epub Date: 2024-11-18DOI: 10.21037/jtd-24-1166
Xiaoxia Ping, Qian Meng, Nan Jiang, Su Hu
Background: The mutation status of epidermal growth factor receptor (EGFR) in lung adenocarcinoma is significantly associated with postoperative progression-free survival. Computed tomography (CT)-based radiomics analysis may have potential value in predicting EGFR mutation status. This study aims to explore the predictive capacity of radiomics analysis for EGFR mutation status in lung adenocarcinomas presenting as ground-glass nodules (GGNs).
Methods: We included 199 GGNs confirmed by histopathology from 2016 to 2020. The clinical factors and radiographic characteristics were counted and evaluated. All GGNs were manually delineated and the radiomics features were extracted, using the least absolute shrinkage and selection operator for feature selection. Then the radiographic, radiomics, and combined nomogram model were constructed respectively, and compared with each other. Decision curve analysis (DCA) was used to assess the clinical usefulness of the models, while receiver operating characteristic curves and calibration curves were used to evaluate their predictive performance.
Results: Univariate analysis revealed five variables that were significantly different between the EGFR mutant and wild-type groups. Fifteen radiomics features were significantly associated with EGFR mutations. Among the three models, both the radiomics [area under the curve (AUC) =0.818] and the nomogram (AUC =0.820) had good discriminatory ability in predicting EGFR mutation status and performed consistently in the validation cohort (AUC =0.805, and 0.833, respectively), with higher predictive performance than the radiographic model. The DCA showed that when it comes to EGFR mutation status prediction, the nomogram and the radiomics model showed better overall net benefit than the radiographic model.
Conclusions: For preoperatively predicting the status of EGFR mutation in lung adenocarcinomas manifesting as GGNs, the CT-based radiomics analysis will be valuable.
{"title":"A predictive nomogram for <i>EGFR</i> mutation status in lung adenocarcinoma manifesting as ground-glass nodules.","authors":"Xiaoxia Ping, Qian Meng, Nan Jiang, Su Hu","doi":"10.21037/jtd-24-1166","DOIUrl":"10.21037/jtd-24-1166","url":null,"abstract":"<p><strong>Background: </strong>The mutation status of epidermal growth factor receptor (<i>EGFR</i>) in lung adenocarcinoma is significantly associated with postoperative progression-free survival. Computed tomography (CT)-based radiomics analysis may have potential value in predicting <i>EGFR</i> mutation status. This study aims to explore the predictive capacity of radiomics analysis for <i>EGFR</i> mutation status in lung adenocarcinomas presenting as ground-glass nodules (GGNs).</p><p><strong>Methods: </strong>We included 199 GGNs confirmed by histopathology from 2016 to 2020. The clinical factors and radiographic characteristics were counted and evaluated. All GGNs were manually delineated and the radiomics features were extracted, using the least absolute shrinkage and selection operator for feature selection. Then the radiographic, radiomics, and combined nomogram model were constructed respectively, and compared with each other. Decision curve analysis (DCA) was used to assess the clinical usefulness of the models, while receiver operating characteristic curves and calibration curves were used to evaluate their predictive performance.</p><p><strong>Results: </strong>Univariate analysis revealed five variables that were significantly different between the <i>EGFR</i> mutant and wild-type groups. Fifteen radiomics features were significantly associated with <i>EGFR</i> mutations. Among the three models, both the radiomics [area under the curve (AUC) =0.818] and the nomogram (AUC =0.820) had good discriminatory ability in predicting <i>EGFR</i> mutation status and performed consistently in the validation cohort (AUC =0.805, and 0.833, respectively), with higher predictive performance than the radiographic model. The DCA showed that when it comes to <i>EGFR</i> mutation status prediction, the nomogram and the radiomics model showed better overall net benefit than the radiographic model.</p><p><strong>Conclusions: </strong>For preoperatively predicting the status of <i>EGFR</i> mutation in lung adenocarcinomas manifesting as GGNs, the CT-based radiomics analysis will be valuable.</p>","PeriodicalId":17542,"journal":{"name":"Journal of thoracic disease","volume":"16 11","pages":"7477-7489"},"PeriodicalIF":2.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-30Epub Date: 2024-11-29DOI: 10.21037/jtd-24-1148
Wei Chen, Zhao Cai, Shuangqing Liu, Giovanni Sotgiu, Ignacio Martin-Loeches, Yang Cao
Background: Klebsiellapneumoniae (K.pneumoniae) is an opportunistic pathogen that can cause multiple life-threatening infections. Recently, there has been an upward trend in carbapenem-resistant K.pneumoniae infections in China. This epidemiological trend needs to be examined to enable better disease control. We sought to analyze the genomic characteristics, including the prevalent sequence type (ST), resistance, virulence, and evolutionary relationship, of K.pneumoniae strains isolated from patients with different types of infections in northern China to provide theoretical support for the effective prevention and control of the evolution and transmission of K.pneumoniae.
Methods: The STs were analyzed using multi-locus sequence typing (MLST). Drug susceptibility tests were used to examine the resistance of these STs to various antibiotics. A phylogenetic tree of these isolates was constructed using the National Center for Biotechnology Information genome as the reference. Antibiotic resistance genes were identified by comparing the genomic sequences against those in the Comprehensive Antibiotic Resistance Database. Virulence genes were identified using the Virulence Factor database, while the pathogenicity of the isolates was predicted using PathogenFinder.
Results: In total, 38 clinical isolates of K.pneumoniae were identified and sequenced by high-throughput sequencing. Multidrug-resistant ST11 and hypervirulent ST23 were found to be the prevalent K.pneumoniae strains. The distribution of the ST11 strains was strongly correlated with stays in the neurosurgery department (chi square test, P=0.02), while the ST23 strains were more frequently isolated from patients with liver abscesses and gallbladder infections. The ST23 strains were significantly more pathogenic than the other STs (Wilcox test, P<0.001). The resistance analysis showed that the rmtB genes were significantly correlated with amikacin resistance (P<2.2e-16, R2=1). The ST11 strains were also found to co-harbor the KPC-2, rmtB, and TEM-1 genes. To the best of our knowledge, this is the first study to report on the dissemination of such multidrug-resistant K.pneumoniae ST11 strains in Tianjin.
Conclusions: The carbapenem-resistant K.pneumoniae (CRKP) ST11 may become highly virulent K.pneumoniae (CR-hvKP) due to the acquisition of virulence plasmids. Attention should be paid to the evolutionary pressure of a caused by the overuse of antibiotics, which may trigger the further development of multidrug-resistant K.pneumoniae infections.
{"title":"A single-center retrospective study of the molecular epidemiological characteristics of different <i>Klebsiella pneumoniae</i> infections in northern China.","authors":"Wei Chen, Zhao Cai, Shuangqing Liu, Giovanni Sotgiu, Ignacio Martin-Loeches, Yang Cao","doi":"10.21037/jtd-24-1148","DOIUrl":"10.21037/jtd-24-1148","url":null,"abstract":"<p><strong>Background: </strong><i>Klebsiella</i> <i>pneumoniae</i> (<i>K.</i> <i>pneumoniae</i>) is an opportunistic pathogen that can cause multiple life-threatening infections. Recently, there has been an upward trend in carbapenem-resistant <i>K.</i> <i>pneumoniae</i> infections in China. This epidemiological trend needs to be examined to enable better disease control. We sought to analyze the genomic characteristics, including the prevalent sequence type (ST), resistance, virulence, and evolutionary relationship, of <i>K.</i> <i>pneumoniae</i> strains isolated from patients with different types of infections in northern China to provide theoretical support for the effective prevention and control of the evolution and transmission of <i>K.</i> <i>pneumoniae</i>.</p><p><strong>Methods: </strong>The STs were analyzed using multi-locus sequence typing (MLST). Drug susceptibility tests were used to examine the resistance of these STs to various antibiotics. A phylogenetic tree of these isolates was constructed using the National Center for Biotechnology Information genome as the reference. Antibiotic resistance genes were identified by comparing the genomic sequences against those in the Comprehensive Antibiotic Resistance Database. Virulence genes were identified using the Virulence Factor database, while the pathogenicity of the isolates was predicted using PathogenFinder.</p><p><strong>Results: </strong>In total, 38 clinical isolates of <i>K.</i> <i>pneumoniae</i> were identified and sequenced by high-throughput sequencing. Multidrug-resistant ST11 and hypervirulent ST23 were found to be the prevalent <i>K.</i> <i>pneumoniae</i> strains. The distribution of the ST11 strains was strongly correlated with stays in the neurosurgery department (chi square test, P=0.02), while the ST23 strains were more frequently isolated from patients with liver abscesses and gallbladder infections. The ST23 strains were significantly more pathogenic than the other STs (Wilcox test, P<0.001). The resistance analysis showed that the <i>rmtB</i> genes were significantly correlated with amikacin resistance (P<2.2e-16, R<sup>2</sup>=1). The ST11 strains were also found to co-harbor the KPC-2, <i>rmtB</i>, and TEM-1 genes. To the best of our knowledge, this is the first study to report on the dissemination of such multidrug-resistant <i>K.</i> <i>pneumoniae</i> ST11 strains in Tianjin.</p><p><strong>Conclusions: </strong>The carbapenem-resistant <i>K.</i> <i>pneumoniae</i> (CRKP) ST11 may become highly virulent <i>K.</i> <i>pneumoniae</i> (CR-hvKP) due to the acquisition of virulence plasmids. Attention should be paid to the evolutionary pressure of a caused by the overuse of antibiotics, which may trigger the further development of multidrug-resistant <i>K.</i> <i>pneumoniae</i> infections.</p>","PeriodicalId":17542,"journal":{"name":"Journal of thoracic disease","volume":"16 11","pages":"7739-7750"},"PeriodicalIF":2.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635258/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-30Epub Date: 2024-11-29DOI: 10.21037/jtd-24-1050
Hayley Barnes, David Pilcher, Julia Coull, Jesselyn Sin, Eli Dabscheck, Miranda Siemienowicz, Janu Pirakalathanan, Jun Khoo, Duncan Sweeney, Catriona McLean, Piraveen Pirakalathanan, Nina Eikelis, Christina Begka, Glen Westall, Ryan Hoy
Background: The incidence of silicosis has increased due to occupational silica exposure from artificial stone, with no treatments proven to halt or reverse the disease. Whole lung lavage (WLL) involves the instillation of fluid into the lungs to wash out silica particles and disease-causing inflammatory cells. This study aimed to determine the feasibility, safety, and possible benefit of WLL in patients with artificial stone silicosis.
Methods: In this prospective observational study, people with progressive silicosis with ground glass predominant radiological changes underwent WLL. High resolution computed tomography (HRCT) chest, X-ray velocimetry (XV), lung function tests, forced oscillation technique (FOT), and cardiopulmonary exercise tests (CPET) were performed before and six months after the procedure.
Results: Eight patients underwent WLL between June 2021 and November 2022. Five participants had an improvement in the International Classification of High Resolution Computed Tomography for Occupational and Environmental Respiratory Diseases (ICOERD) CT scores and reduction in XV regional ventilation distribution pre- and six months post-WLL. There was no difference in lung function [annualized rate of change in forced vital capacity (FVC) % predicted mean difference (MD) 1.81; 95% CI: -1.53 to 5.15, P=0.27; forced expiratory volume in 1 second (FEV1) % predicted MD -1.13, 95% CI: -5.08 to 2.83, P=0.55; diffusing capacity for carbon monoxide (DLCO) % predicted MD -2.62, 95% CI: -10.04 to 4.80, P=0.46]. There was no significant difference in CPET or FOT measurements. Following WLL, all patients experienced transient throat discomfort, one had fever and two required oral antibiotics. There were no serious adverse events.
Conclusions: WLL for artificial stone silicosis is safe in an expert centre who has experience in performing WLL in this population, and there may be limited benefit in selected patients. Further research is required to select those who will derive the most benefit.
{"title":"Efficacy and safety of a whole lung lavage program for artificial stone silicosis.","authors":"Hayley Barnes, David Pilcher, Julia Coull, Jesselyn Sin, Eli Dabscheck, Miranda Siemienowicz, Janu Pirakalathanan, Jun Khoo, Duncan Sweeney, Catriona McLean, Piraveen Pirakalathanan, Nina Eikelis, Christina Begka, Glen Westall, Ryan Hoy","doi":"10.21037/jtd-24-1050","DOIUrl":"10.21037/jtd-24-1050","url":null,"abstract":"<p><strong>Background: </strong>The incidence of silicosis has increased due to occupational silica exposure from artificial stone, with no treatments proven to halt or reverse the disease. Whole lung lavage (WLL) involves the instillation of fluid into the lungs to wash out silica particles and disease-causing inflammatory cells. This study aimed to determine the feasibility, safety, and possible benefit of WLL in patients with artificial stone silicosis.</p><p><strong>Methods: </strong>In this prospective observational study, people with progressive silicosis with ground glass predominant radiological changes underwent WLL. High resolution computed tomography (HRCT) chest, X-ray velocimetry (XV), lung function tests, forced oscillation technique (FOT), and cardiopulmonary exercise tests (CPET) were performed before and six months after the procedure.</p><p><strong>Results: </strong>Eight patients underwent WLL between June 2021 and November 2022. Five participants had an improvement in the International Classification of High Resolution Computed Tomography for Occupational and Environmental Respiratory Diseases (ICOERD) CT scores and reduction in XV regional ventilation distribution pre- and six months post-WLL. There was no difference in lung function [annualized rate of change in forced vital capacity (FVC) % predicted mean difference (MD) 1.81; 95% CI: -1.53 to 5.15, P=0.27; forced expiratory volume in 1 second (FEV1) % predicted MD -1.13, 95% CI: -5.08 to 2.83, P=0.55; diffusing capacity for carbon monoxide (DLCO) % predicted MD -2.62, 95% CI: -10.04 to 4.80, P=0.46]. There was no significant difference in CPET or FOT measurements. Following WLL, all patients experienced transient throat discomfort, one had fever and two required oral antibiotics. There were no serious adverse events.</p><p><strong>Conclusions: </strong>WLL for artificial stone silicosis is safe in an expert centre who has experience in performing WLL in this population, and there may be limited benefit in selected patients. Further research is required to select those who will derive the most benefit.</p>","PeriodicalId":17542,"journal":{"name":"Journal of thoracic disease","volume":"16 11","pages":"7630-7639"},"PeriodicalIF":2.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Seawater drowning (SWD) has been an escalating hazard in recent years. It can not only cause immediate death but can also inflict severe complications, such as acute lung injury (ALI), which greatly increases the mortality rate. Thus, investigating the mechanism of SWD induced lung injury and discovering effective treatments is of great importance. The aim of this study was to minimize the lethality and disability of SWD-ALI.
Methods: Using male C57BL/6 mice, we established a SWD induced ALI (SWD-ALI) model via the oral laryngoscopy endotracheal injection (LEI) of artificial seawater. We then administered mesenchymal stem cells (MSCs) via laryngoscopy endotracheal nebulized inhalation. We tested our hypotheses using pulmonary function tests, micro-computed tomography (Micro-CT), hematoxylin and eosin (HE) staining, Masson staining, immunofluorescence, immunoblotting, flow cytometry, transcriptome sequencing, quantitative real-time polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay (ELISA).
Results: We successfully established the SWD-ALI model via LEI method of seawater. The results indicated that SWD induced severe ALI by activating the Snail-mediated epithelial-mesenchymal transition (EMT) pathway through the tumor necrosis factor alpha (TNFα) inflammatory response. Further, we administered transoral laryngoscopy endotracheal nebulization to the SWD mice treated with inhaled MSCs. Non-invasive pulmonary function tests revealed that the respiratory symptoms and respiratory function of the mice were significantly alleviated. Additionally, the histological injury and air-blood barrier, and inflammatory response were significantly mitigated, and TNFα-mediated Snail expression was significantly down-regulated. Importantly, we used Masson staining to examine mouse lung tissue after 28 days of drowning and found that the SWD mice suffered from significant long-term pulmonary fibrosis injury, and MSCs treatment significantly attenuated the degree of fibrosis.
Conclusions: Our research revealed that SWD triggered severe ALI, followed by long-term pulmonary fibrosis. However, treatment with nebulized MSCs significantly mitigated the ALI and slowed the progression of fibrosis.
{"title":"Mesenchymal stem cell treatment alleviates seawater drowning induced lung injury by inhibiting the TNFα/Snail/EMT pathway.","authors":"Jinxia Liu, Lingping Zhao, Chunsun Li, Yali Jia, Zhen Yang, Zhixin Liang, Haiyang Wang, Xiuqing Ma, Chengcheng Su, Jiabo Ren, Zhenfei Mo, Wenli Liu, Peixin Wu, Yue Yin, Shangshu Liu, Wen Yue, Jiafei Xi, Liangan Chen","doi":"10.21037/jtd-24-1471","DOIUrl":"10.21037/jtd-24-1471","url":null,"abstract":"<p><strong>Background: </strong>Seawater drowning (SWD) has been an escalating hazard in recent years. It can not only cause immediate death but can also inflict severe complications, such as acute lung injury (ALI), which greatly increases the mortality rate. Thus, investigating the mechanism of SWD induced lung injury and discovering effective treatments is of great importance. The aim of this study was to minimize the lethality and disability of SWD-ALI.</p><p><strong>Methods: </strong>Using male C57BL/6 mice, we established a SWD induced ALI (SWD-ALI) model via the oral laryngoscopy endotracheal injection (LEI) of artificial seawater. We then administered mesenchymal stem cells (MSCs) via laryngoscopy endotracheal nebulized inhalation. We tested our hypotheses using pulmonary function tests, micro-computed tomography (Micro-CT), hematoxylin and eosin (HE) staining, Masson staining, immunofluorescence, immunoblotting, flow cytometry, transcriptome sequencing, quantitative real-time polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay (ELISA).</p><p><strong>Results: </strong>We successfully established the SWD-ALI model via LEI method of seawater. The results indicated that SWD induced severe ALI by activating the Snail-mediated epithelial-mesenchymal transition (EMT) pathway through the tumor necrosis factor alpha (TNFα) inflammatory response. Further, we administered transoral laryngoscopy endotracheal nebulization to the SWD mice treated with inhaled MSCs. Non-invasive pulmonary function tests revealed that the respiratory symptoms and respiratory function of the mice were significantly alleviated. Additionally, the histological injury and air-blood barrier, and inflammatory response were significantly mitigated, and TNFα-mediated Snail expression was significantly down-regulated. Importantly, we used Masson staining to examine mouse lung tissue after 28 days of drowning and found that the SWD mice suffered from significant long-term pulmonary fibrosis injury, and MSCs treatment significantly attenuated the degree of fibrosis.</p><p><strong>Conclusions: </strong>Our research revealed that SWD triggered severe ALI, followed by long-term pulmonary fibrosis. However, treatment with nebulized MSCs significantly mitigated the ALI and slowed the progression of fibrosis.</p>","PeriodicalId":17542,"journal":{"name":"Journal of thoracic disease","volume":"16 11","pages":"7836-7852"},"PeriodicalIF":2.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p><strong>Background: </strong>The prognosis for patients diagnosed with idiopathic pulmonary fibrosis (IPF) is exceedingly grim, and there are currently no pharmacological interventions available that effectively reduce mortality rates. Emerging evidence underscores the intimate connection between mitochondrial dysfunction and the onset and advancement of IPF. However, there remains a scarcity of prognostic models for assessing the risk associated with mitochondrial-related genes in IPF. This study aims to develop a comprehensive prognostic model for IPF that incorporates mitochondrial-related genes to enhance risk assessment and guide clinical decision-making.</p><p><strong>Methods: </strong>Two IPF-related microarray expression profiling datasets (GSE28042 and GSE70866) accompanied with survival data were acquired from the Gene Expression Omnibus (GEO) database. The "limma" R package was used to identify differentially expressed mitochondrial-related genes between normal samples and IPF samples. The prognostic model was constructed using univariate Cox regression, the least absolute shrinkage and selection operator (LASSO) Cox regression analyses, and multivariate Cox regression analysis. Multivariate independent prognostic analysis was conducted to ascertain whether the risk score could serve as an independent prognostic factor for predicting clinicopathological outcomes. A nomogram was employed to forecast the survival probability of IPF patients, providing valuable support for clinical decision-making processes. The CIBERSORT algorithm was utilized to examine discrepancies in immune cell infiltration within the model. The expression of genes screened from the prognostic model was validated in external data sets and western blot assays.</p><p><strong>Results: </strong>We developed a prognostic model for mitochondrial-related risks, incorporating <i>ARMCX2</i> and <i>ACOT11</i>, and subsequently validated its predictive efficacy in the validation set. The IPF samples were stratified into high-risk and low-risk groups based on the median of the risk score. According to Kaplan-Meier curve analysis, the high-risk group exhibited inferior outcomes compared to the low-risk group. The time-dependent receiver operating characteristic (ROC) analysis demonstrated the accurate prognostic capability of the risk model for IPF. A nomogram, accompanied by calibration curves, was presented to predict 1-, 2-, and 3-year survival in IPF patients. The risk model we employed not only unveiled significant disparities in functional enrichment between the high-risk and low-risk groups, but also demonstrated a robust correlation with the infiltration of specific immune cells.</p><p><strong>Conclusions: </strong>In this study, the mitochondrial-related prognostic model incorporating <i>ARMCX2</i> and <i>ACOT11</i> demonstrates potential clinical utility for informing decision-making in IPF patients and offers valuable insights for future therapeutic interventions.<
{"title":"Establishment and validation of a prognostic model for idiopathic pulmonary fibrosis based on mitochondrial-related genes.","authors":"Xuewen Wang, Luqin Yang, Yuxuan Wang, Xinran Dou, Yonghao Li, Ke Wang, Huilan Zhang","doi":"10.21037/jtd-24-760","DOIUrl":"10.21037/jtd-24-760","url":null,"abstract":"<p><strong>Background: </strong>The prognosis for patients diagnosed with idiopathic pulmonary fibrosis (IPF) is exceedingly grim, and there are currently no pharmacological interventions available that effectively reduce mortality rates. Emerging evidence underscores the intimate connection between mitochondrial dysfunction and the onset and advancement of IPF. However, there remains a scarcity of prognostic models for assessing the risk associated with mitochondrial-related genes in IPF. This study aims to develop a comprehensive prognostic model for IPF that incorporates mitochondrial-related genes to enhance risk assessment and guide clinical decision-making.</p><p><strong>Methods: </strong>Two IPF-related microarray expression profiling datasets (GSE28042 and GSE70866) accompanied with survival data were acquired from the Gene Expression Omnibus (GEO) database. The \"limma\" R package was used to identify differentially expressed mitochondrial-related genes between normal samples and IPF samples. The prognostic model was constructed using univariate Cox regression, the least absolute shrinkage and selection operator (LASSO) Cox regression analyses, and multivariate Cox regression analysis. Multivariate independent prognostic analysis was conducted to ascertain whether the risk score could serve as an independent prognostic factor for predicting clinicopathological outcomes. A nomogram was employed to forecast the survival probability of IPF patients, providing valuable support for clinical decision-making processes. The CIBERSORT algorithm was utilized to examine discrepancies in immune cell infiltration within the model. The expression of genes screened from the prognostic model was validated in external data sets and western blot assays.</p><p><strong>Results: </strong>We developed a prognostic model for mitochondrial-related risks, incorporating <i>ARMCX2</i> and <i>ACOT11</i>, and subsequently validated its predictive efficacy in the validation set. The IPF samples were stratified into high-risk and low-risk groups based on the median of the risk score. According to Kaplan-Meier curve analysis, the high-risk group exhibited inferior outcomes compared to the low-risk group. The time-dependent receiver operating characteristic (ROC) analysis demonstrated the accurate prognostic capability of the risk model for IPF. A nomogram, accompanied by calibration curves, was presented to predict 1-, 2-, and 3-year survival in IPF patients. The risk model we employed not only unveiled significant disparities in functional enrichment between the high-risk and low-risk groups, but also demonstrated a robust correlation with the infiltration of specific immune cells.</p><p><strong>Conclusions: </strong>In this study, the mitochondrial-related prognostic model incorporating <i>ARMCX2</i> and <i>ACOT11</i> demonstrates potential clinical utility for informing decision-making in IPF patients and offers valuable insights for future therapeutic interventions.<","PeriodicalId":17542,"journal":{"name":"Journal of thoracic disease","volume":"16 11","pages":"7427-7445"},"PeriodicalIF":2.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Artificial intelligence (AI) technology was introduced in medical data area and applied disease prediction models. This study aimed to establish an AI model for predicting lymph node metastasis based on simple medical examinations in patients with non-small cell lung cancer (NSCLC).
Methods: We retrospectively analyzed 988 patients with NSCLC who underwent radical pulmonary resection with mediastinal lymph node dissection between January 2011 and October 2022. We collected clinical characteristics including age, sex, smoking history, tumor marker levels, tumor side, segment location, total tumor size, solid tumor size and consolidation-to-tumor ratio, obtainable from medical interview, blood tests and plain computed tomography (CT) of the chest. All patients were randomly classified into a training set (n=790) and a validation set (n=198). Six algorithms including Support Vector Classification (SVC), k-nearest neighbor algorithm (k-NN), logistic regression (LR), random forest (RF), gradient boosting (GB) and multilayer perceptron (MLP) were created to decide the lymph node metastasis.
Results: The GB model showed the best diagnostic performance, with 80.0% accuracy, 95.6% specificity and an area under the curve (AUC) of 0.75.
Conclusions: An AI model showed high specificity and accuracy for predicting lymph node metastasis. These models have potential to categorize suitable surgical procedures for NSCLC patients without needing contrast-enhanced CT or positron emission tomography.
{"title":"Diagnostic artificial intelligence model predicts lymph node status in non-small cell lung cancer using simplified examination.","authors":"Ryuichi Yoshimura, Yoshitaka Endo, Takuya Akashi, Hiroyuki Deguchi, Makoto Tomoyasu, Wataru Shigeeda, Yuka Kaneko, Hajime Saito","doi":"10.21037/jtd-24-1067","DOIUrl":"10.21037/jtd-24-1067","url":null,"abstract":"<p><strong>Background: </strong>Artificial intelligence (AI) technology was introduced in medical data area and applied disease prediction models. This study aimed to establish an AI model for predicting lymph node metastasis based on simple medical examinations in patients with non-small cell lung cancer (NSCLC).</p><p><strong>Methods: </strong>We retrospectively analyzed 988 patients with NSCLC who underwent radical pulmonary resection with mediastinal lymph node dissection between January 2011 and October 2022. We collected clinical characteristics including age, sex, smoking history, tumor marker levels, tumor side, segment location, total tumor size, solid tumor size and consolidation-to-tumor ratio, obtainable from medical interview, blood tests and plain computed tomography (CT) of the chest. All patients were randomly classified into a training set (n=790) and a validation set (n=198). Six algorithms including Support Vector Classification (SVC), k-nearest neighbor algorithm (k-NN), logistic regression (LR), random forest (RF), gradient boosting (GB) and multilayer perceptron (MLP) were created to decide the lymph node metastasis.</p><p><strong>Results: </strong>The GB model showed the best diagnostic performance, with 80.0% accuracy, 95.6% specificity and an area under the curve (AUC) of 0.75.</p><p><strong>Conclusions: </strong>An AI model showed high specificity and accuracy for predicting lymph node metastasis. These models have potential to categorize suitable surgical procedures for NSCLC patients without needing contrast-enhanced CT or positron emission tomography.</p>","PeriodicalId":17542,"journal":{"name":"Journal of thoracic disease","volume":"16 11","pages":"7320-7328"},"PeriodicalIF":2.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p><strong>Background: </strong>Acute respiratory distress syndrome (ARDS) is a complicated pathological cascade process of excessive pulmonary inflammation and alveolar epithelial cell apoptosis that results in respiratory dysfunction and failure. Some cases of ARDS can result in a more severe state of pulmonary fibrosis, referred to as postinjury lung fibrosis. The mortality and incidence rate of ARDS are high, particularly when it leads to continuing alveolar and interstitial fibrosis, which requires urgent treatment and appropriate management. The lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model has been widely implemented for studying ARDS in humans. In our study, we found alterations in the alveolar macrophage (AM) profile in such a mouse model. Specifically, activin-A produced by dominantly recruited AMs (recAMs) was noted to be implicated in the process of post-injury lung fibrosis.</p><p><strong>Methods: </strong>The ALI animal model in C57BL/6 mice was established via 3.5 mg/kg of LPS intratracheal administration. Single-cell RNA (scRNA) sequencing was used for detailed classification and functional characterization of lung macrophages. Through <i>in vivo</i> experiments, we evaluated the role that activin-A plays in post-injury lung fibrosis in an ALI mouse model using enzyme-linked immunosorbent assay (ELISA), histological staining methods, and immunofluorescence. Through <i>in vitro</i> experiments, we analyzed the effect of activin-A on murine lung epithelial 12 (MLE-12) cells and bone marrow-derived macrophages (BMDMs) using Western blotting (WB), quantitative real-time polymerase chain reaction, RNA sequencing, and immunofluorescence.</p><p><strong>Results: </strong>Our findings revealed that recAMs replaced tissue-resident alveolar macrophages (TRAMs) as the dominant macrophage population in the setting of ALI. The results of Gene Ontology (GO) analysis suggested that activin-A was associated with wound healing and suppressor of mothers against decapentaplegic (SMAD) protein signaling pathways. Immunofluorescence results revealed that the receptor of activin-A mainly localized to alveolar epithelial cells and macrophages. Subsequently, activin-A was specifically found to drive MLE-12 cells to mesenchymal cell transformation via the transforming growth factor-β (TGF-β)/SMAD signaling. Moreover, the results of transcriptome analysis and WB confirmed that activin-A could enhance the concerted activity of Hippo and TGF-β/SMAD pathways in BMDMs, leading to an increased expression of profibrotic mediator. Moreover, yes-associated protein (YAP) and transcriptional coactivated with PDZ-binding motif (TAZ) proteins were found to drive BMDM activin-A expression, which could generate a positive feedback mechanism that perpetuates fibrosis.</p><p><strong>Conclusions: </strong>Our findings revealed that activin-A is involved in the pathological mechanisms in post-injury lung fibrosis by promoting epithelial-mesenchymal tra
{"title":"Exacerbation of pulmonary fibrosis following acute lung injury via activin-A production by recruited alveolar macrophages.","authors":"Ting Pan, Yinzhou Feng, Yufan Li, Yanping Yang, Jian Zhou, Yuanlin Song","doi":"10.21037/jtd-24-680","DOIUrl":"https://doi.org/10.21037/jtd-24-680","url":null,"abstract":"<p><strong>Background: </strong>Acute respiratory distress syndrome (ARDS) is a complicated pathological cascade process of excessive pulmonary inflammation and alveolar epithelial cell apoptosis that results in respiratory dysfunction and failure. Some cases of ARDS can result in a more severe state of pulmonary fibrosis, referred to as postinjury lung fibrosis. The mortality and incidence rate of ARDS are high, particularly when it leads to continuing alveolar and interstitial fibrosis, which requires urgent treatment and appropriate management. The lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model has been widely implemented for studying ARDS in humans. In our study, we found alterations in the alveolar macrophage (AM) profile in such a mouse model. Specifically, activin-A produced by dominantly recruited AMs (recAMs) was noted to be implicated in the process of post-injury lung fibrosis.</p><p><strong>Methods: </strong>The ALI animal model in C57BL/6 mice was established via 3.5 mg/kg of LPS intratracheal administration. Single-cell RNA (scRNA) sequencing was used for detailed classification and functional characterization of lung macrophages. Through <i>in vivo</i> experiments, we evaluated the role that activin-A plays in post-injury lung fibrosis in an ALI mouse model using enzyme-linked immunosorbent assay (ELISA), histological staining methods, and immunofluorescence. Through <i>in vitro</i> experiments, we analyzed the effect of activin-A on murine lung epithelial 12 (MLE-12) cells and bone marrow-derived macrophages (BMDMs) using Western blotting (WB), quantitative real-time polymerase chain reaction, RNA sequencing, and immunofluorescence.</p><p><strong>Results: </strong>Our findings revealed that recAMs replaced tissue-resident alveolar macrophages (TRAMs) as the dominant macrophage population in the setting of ALI. The results of Gene Ontology (GO) analysis suggested that activin-A was associated with wound healing and suppressor of mothers against decapentaplegic (SMAD) protein signaling pathways. Immunofluorescence results revealed that the receptor of activin-A mainly localized to alveolar epithelial cells and macrophages. Subsequently, activin-A was specifically found to drive MLE-12 cells to mesenchymal cell transformation via the transforming growth factor-β (TGF-β)/SMAD signaling. Moreover, the results of transcriptome analysis and WB confirmed that activin-A could enhance the concerted activity of Hippo and TGF-β/SMAD pathways in BMDMs, leading to an increased expression of profibrotic mediator. Moreover, yes-associated protein (YAP) and transcriptional coactivated with PDZ-binding motif (TAZ) proteins were found to drive BMDM activin-A expression, which could generate a positive feedback mechanism that perpetuates fibrosis.</p><p><strong>Conclusions: </strong>Our findings revealed that activin-A is involved in the pathological mechanisms in post-injury lung fibrosis by promoting epithelial-mesenchymal tra","PeriodicalId":17542,"journal":{"name":"Journal of thoracic disease","volume":"16 11","pages":"7709-7728"},"PeriodicalIF":2.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background and objective: Pulmonary nodules (PNs) are small (≤3 cm) radiographic opacities within lung parenchyma. The use of low-dose computed tomography (LDCT) has led to a significant increase in the identification of solitary nodules. Malignant lung nodules comprise only 5% of all nodules, with management differing greatly from benign cases. Despite diagnostic advancements, there is heterogeneity in prognosis, which can result in undertreatment of high-risk patients and inappropriate treatment for low-risk patients. Therefore, accurately distinguishing benign from malignant nodules and effectively stratifying the risk of malignant nodules is a pressing clinical challenge requiring urgent resolution. The main objectives of this review were to explore the research progress in the clinical management of malignant PNs, including early detection, individualized treatment, and prognosis prediction, in order to shed light on precision medicine for patients with PNs.
Methods: The review examined various approaches for the identification and prognosis prediction of early lung cancer characterized by lung nodules, including the use of classical clinicopathological features, liquid biopsy, and artificial intelligence.
Key content and findings: The detection rate of early lung cancer characterized by lung nodules is increasing annually, and accurate identification and prognosis prediction are critical for appropriate therapeutic strategies and precise postoperative management. Classical clinicopathological features, such as demographic and radiological features, play an important role in the diagnosis and prognosis assessment of early lung cancer, but liquid biopsy and artificial intelligence are also promising due to their obvious convenience and accuracy.
Conclusions: The review highlights the importance of precision medicine in the clinical management of malignant lung nodules. The use of classical clinicopathological features, liquid biopsy, and artificial intelligence can contribute to the early detection, individualized treatment, and accurate prognosis prediction for patients with lung nodules, ultimately improving their clinical outcomes.
{"title":"Precise diagnosis and prognosis assessment of malignant lung nodules: a narrative review.","authors":"Miaomiao Wen, Qian Zheng, Xiaohong Ji, Shaowei Xin, Yinxi Zhou, Yahui Tian, Zitong Wan, Jiao Zhang, Jie Yang, Yongfu Ma, Yanlu Xiong","doi":"10.21037/jtd-24-1058","DOIUrl":"10.21037/jtd-24-1058","url":null,"abstract":"<p><strong>Background and objective: </strong>Pulmonary nodules (PNs) are small (≤3 cm) radiographic opacities within lung parenchyma. The use of low-dose computed tomography (LDCT) has led to a significant increase in the identification of solitary nodules. Malignant lung nodules comprise only 5% of all nodules, with management differing greatly from benign cases. Despite diagnostic advancements, there is heterogeneity in prognosis, which can result in undertreatment of high-risk patients and inappropriate treatment for low-risk patients. Therefore, accurately distinguishing benign from malignant nodules and effectively stratifying the risk of malignant nodules is a pressing clinical challenge requiring urgent resolution. The main objectives of this review were to explore the research progress in the clinical management of malignant PNs, including early detection, individualized treatment, and prognosis prediction, in order to shed light on precision medicine for patients with PNs.</p><p><strong>Methods: </strong>The review examined various approaches for the identification and prognosis prediction of early lung cancer characterized by lung nodules, including the use of classical clinicopathological features, liquid biopsy, and artificial intelligence.</p><p><strong>Key content and findings: </strong>The detection rate of early lung cancer characterized by lung nodules is increasing annually, and accurate identification and prognosis prediction are critical for appropriate therapeutic strategies and precise postoperative management. Classical clinicopathological features, such as demographic and radiological features, play an important role in the diagnosis and prognosis assessment of early lung cancer, but liquid biopsy and artificial intelligence are also promising due to their obvious convenience and accuracy.</p><p><strong>Conclusions: </strong>The review highlights the importance of precision medicine in the clinical management of malignant lung nodules. The use of classical clinicopathological features, liquid biopsy, and artificial intelligence can contribute to the early detection, individualized treatment, and accurate prognosis prediction for patients with lung nodules, ultimately improving their clinical outcomes.</p>","PeriodicalId":17542,"journal":{"name":"Journal of thoracic disease","volume":"16 11","pages":"7999-8013"},"PeriodicalIF":2.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Patients presenting with Stanford type A aortic dissection complicated by acute occlusion of the superior mesenteric artery (SMA) exhibit an exceedingly high mortality rate, even if emergency surgery for ascending aorta repair is performed. consequently, appropriate management of acute SMA occlusion arising from acute Stanford type A aortic dissection is crucial. This study aimed to evaluate the safety and efficacy of endovascular treatment of acute mesenteric occlusion first in stable patients with acute type A aortic dissection.
Methods: The study was a single-center case series. Data collected from 11 consecutive patients over 12 years, from March 2010 to November 2022, were retrospectively analyzed. All were expeditiously escorted to the interventional suite via the prioritized green channel of the chest pain center and received the endovascular treatment of acute mesenteric occlusion first. Post-procedure, patients were promptly transferred to the Intensive Care Unit for close monitoring and got standardized medication. After hospital discharge, patients underwent follow-up aortic computed tomography angiography (CTA) at 1 month, 6 months, and annually thereafter to ensure continuous monitoring of the patient's condition and timely identification of any potential complications.
Results: All patients were male, with a mean age of 49.5 years. Time from abdominal distension and pain onset to admission to the catheterization laboratory was 4-13 (mean 6.9) hours. Endovascular repair of the SMA was successfully completed with uneventful hospital courses in all patients. Bowel sounds weakened in 6 cases and disappeared in 5, while bloody stools occurred in 3 without intestinal necrosis. At 2-32 months follow-up, the patients had no abdominal pain, distension nor other signs of mesenteric artery ischemia.
Conclusions: For patients with acute SMA occlusion caused by acute Stanford type A aortic dissection, endovascular treatment first to restore blood supply to the SMA appears feasible, safe and efficacious.
{"title":"Preliminary experience of endovascular treatment of acute mesenteric occlusion in stable patients with acute type A aortic dissection.","authors":"Huiyong Wang, Caiyun He, Yipeng Du, Jian Shi, Xiaolu Hu, Zheng Huang","doi":"10.21037/jtd-24-881","DOIUrl":"10.21037/jtd-24-881","url":null,"abstract":"<p><strong>Background: </strong>Patients presenting with Stanford type A aortic dissection complicated by acute occlusion of the superior mesenteric artery (SMA) exhibit an exceedingly high mortality rate, even if emergency surgery for ascending aorta repair is performed. consequently, appropriate management of acute SMA occlusion arising from acute Stanford type A aortic dissection is crucial. This study aimed to evaluate the safety and efficacy of endovascular treatment of acute mesenteric occlusion first in stable patients with acute type A aortic dissection.</p><p><strong>Methods: </strong>The study was a single-center case series. Data collected from 11 consecutive patients over 12 years, from March 2010 to November 2022, were retrospectively analyzed. All were expeditiously escorted to the interventional suite via the prioritized green channel of the chest pain center and received the endovascular treatment of acute mesenteric occlusion first. Post-procedure, patients were promptly transferred to the Intensive Care Unit for close monitoring and got standardized medication. After hospital discharge, patients underwent follow-up aortic computed tomography angiography (CTA) at 1 month, 6 months, and annually thereafter to ensure continuous monitoring of the patient's condition and timely identification of any potential complications.</p><p><strong>Results: </strong>All patients were male, with a mean age of 49.5 years. Time from abdominal distension and pain onset to admission to the catheterization laboratory was 4-13 (mean 6.9) hours. Endovascular repair of the SMA was successfully completed with uneventful hospital courses in all patients. Bowel sounds weakened in 6 cases and disappeared in 5, while bloody stools occurred in 3 without intestinal necrosis. At 2-32 months follow-up, the patients had no abdominal pain, distension nor other signs of mesenteric artery ischemia.</p><p><strong>Conclusions: </strong>For patients with acute SMA occlusion caused by acute Stanford type A aortic dissection, endovascular treatment first to restore blood supply to the SMA appears feasible, safe and efficacious.</p>","PeriodicalId":17542,"journal":{"name":"Journal of thoracic disease","volume":"16 11","pages":"7342-7349"},"PeriodicalIF":2.1,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}