Pulmonary Circulation最新文献_第10页

Reply to the letter to the editor entitled "Bridging the species divide: The limits of rat models in capturing human PVOD mechanisms" by Perros F. et al. 对 Perros F. 等人题为 "弥合物种鸿沟：Perros F. 等人题为 "弥合物种鸿沟：大鼠模型在捕捉人类 PVOD 机制方面的局限性 "的回信。

IF 2.2 4区医学

Pulmonary Circulation Pub Date : 2024-11-13 eCollection Date: 2024-10-01 DOI: 10.1002/pul2.70015

Amit Prabhakar, Rahul Kumar, Meetu Wadhwa, Rubin M Tuder, Nicholas W Morrell, Brian B Graham, Giorgio Lagna, Akiko Hata

引用次数: 0

The metabolic and physiologic impairments underlying long COVID associated exercise intolerance. 长期 COVID 相关运动不耐受的代谢和生理缺陷。

IF 2.2 4区医学

Pulmonary Circulation Pub Date : 2024-11-13 eCollection Date: 2024-10-01 DOI: 10.1002/pul2.70009

Brooks P Leitner, Phillip Joseph, Andres Figueroa Quast, Maria Alejandra Ramirez, Paul M Heerdt, Jose G Villalobos, Inderjit Singh

{"title":"The metabolic and physiologic impairments underlying long COVID associated exercise intolerance.","authors":"Brooks P Leitner, Phillip Joseph, Andres Figueroa Quast, Maria Alejandra Ramirez, Paul M Heerdt, Jose G Villalobos, Inderjit Singh","doi":"10.1002/pul2.70009","DOIUrl":"10.1002/pul2.70009","url":null,"abstract":"Data from invasive CPET (iCPET) revealed long COVID patients have impaired systemic oxygen extraction (EO2), suggesting impaired mitochondrial ATP production. However, it remains uncertain whether the initial severity of SARS-CoV-2 infection has implications on EO2 and exercise capacity (VO2) nor has there been assessment of anerobic ATP generation in long COVID patients. iCPET was performed on 47 long COVID patients (i.e., full cohort; n = 8 with severe SARS-CoV-2 infection). In a subset of patients (i.e., metabolomic cohort; n = 26) metabolomics on venous and arterial blood samples during iCPET was performed. In the full cohort, long COVID patients exhibited reduced peak EO2 with reduced peak VO2 (90 ± 17% predicted) relative to cardiac output (118 ± 23% predicted). Peak VO2 [88% predicted (IQR 81% - 108%) vs. 70% predicted (IQR 64% - 89%); p = 0.02] and EO2 [0.59(IQR 0.53-0.62) vs. 0.53(IQR 0.50-0.48); p = 0.01) were lower in severe versus mild infection. In the metabolomic cohort, 12 metabolites were significantly consumed, and 41 metabolites were significantly released (p-values < 0.05). Quantitative metabolomics demonstrated significant increases in inosine and succinate arteriovenous gradients during exercise. Peak VO2 was significantly correlated with peak venous succinate (r = 0.68; p = 0.0008) and peak venous lactate (r = 0.49; p = 0.0004). Peak EO2 and consequently peak VO2 impact long COVID patients in a severity dependent manner. Exercise intolerance associated with long COVID is defined by impaired aerobic and anaerobic energy production. Peak venous succinate may serve as a potential biomarker in long COVID.","PeriodicalId":20927,"journal":{"name":"Pulmonary Circulation","volume":"14 4","pages":"e70009"},"PeriodicalIF":2.2,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560803/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142627001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bridging the species divide: The limits of rat models in capturing human PVOD mechanisms. 弥合物种鸿沟：大鼠模型在捕捉人类 PVOD 机制方面的局限性。

IF 2.2 4区医学

Pulmonary Circulation Pub Date : 2024-11-13 eCollection Date: 2024-10-01 DOI: 10.1002/pul2.70016

Frédéric Perros, Cédric Chaveroux, David Montani

引用次数: 0

Infection and pulmonary vascular diseases consortium: United against a global health challenge. 感染与肺血管疾病联盟：团结起来，应对全球健康挑战。

IF 2.2 4区医学

Pulmonary Circulation Pub Date : 2024-11-12 eCollection Date: 2024-10-01 DOI: 10.1002/pul2.70003

S D Oliveira, S Almodóvar, G Butrous, V De Jesus Perez, A Fabro, B B Graham, A Mocumbi, P S Nyasulu, O Tura-Ceide, R K F Oliveira, N K Dhillon

{"title":"Infection and pulmonary vascular diseases consortium: United against a global health challenge.","authors":"S D Oliveira, S Almodóvar, G Butrous, V De Jesus Perez, A Fabro, B B Graham, A Mocumbi, P S Nyasulu, O Tura-Ceide, R K F Oliveira, N K Dhillon","doi":"10.1002/pul2.70003","DOIUrl":"https://doi.org/10.1002/pul2.70003","url":null,"abstract":"Leveraging the potential of virtual platforms in the post-COVID-19 era, the Infection and Pulmonary Vascular Diseases Consortium (iPVDc), with the support of the Pulmonary Vascular Research Institute (PVRI), launched a globally accessible educational program to highlight top-notch research on inflammation and infectious diseases affecting the lung vasculature. This innovative virtual series has already successfully brought together distinguished investigators across five continents - Asia, Europe, South and North America, and Africa. Moreover, these open global forums have contributed to a comprehensive understanding of the complex interplay among immunology, inflammation, infection, and cardiopulmonary health, especially concerning pulmonary hypertension and related pulmonary disorders. These enlightening discussions have not only heightened awareness about the impact of various pathogenic microorganisms, including fungi, parasites, and viruses, on the onset and development of pulmonary vascular diseases but have also cast a spotlight on co-infections and neglected illnesses like schistosomiasis - a disease that continues to impose a heavy socioeconomic burden in numerous regions worldwide. Thus, the overall goal of this review article is to present the most recent breakthroughs from infectious PVDs as well as bring to light the scientific and educational insights from the 2023 iPVDc/PVRI virtual symposium series, shaping our understanding of these crucial health issues in this more than ever interconnected world.","PeriodicalId":20927,"journal":{"name":"Pulmonary Circulation","volume":"14 4","pages":"e70003"},"PeriodicalIF":2.2,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142626894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Delta-like ligand 4 inhibitor drug treatment induces pulmonary hypertension in cancer clinical trials. 在癌症临床试验中，Delta 样配体 4 抑制剂药物治疗会诱发肺动脉高压。

IF 2.2 4区医学

Pulmonary Circulation Pub Date : 2024-11-08 eCollection Date: 2024-10-01 DOI: 10.1002/pul2.12450

Casandra E Besse, Nolan M Winicki, Cristian Puerta, Moises Hernandez, Jason X-J Yuan, Patricia A Thistlethwaite

引用次数: 0

Quantitative pulmonary perfusion in acute pulmonary embolism and chronic thromboembolic pulmonary hypertension. 急性肺栓塞和慢性血栓栓塞性肺动脉高压的定量肺灌注。

IF 2.2 4区医学

Pulmonary Circulation Pub Date : 2024-11-08 eCollection Date: 2024-10-01 DOI: 10.1002/pul2.12445

Jacob V Hansen, Mette W Poulsen, Jens E Nielsen-Kudsk, Mannudeep K Kalra, Mads D Lyhne, Asger Andersen

{"title":"Quantitative pulmonary perfusion in acute pulmonary embolism and chronic thromboembolic pulmonary hypertension.","authors":"Jacob V Hansen, Mette W Poulsen, Jens E Nielsen-Kudsk, Mannudeep K Kalra, Mads D Lyhne, Asger Andersen","doi":"10.1002/pul2.12445","DOIUrl":"https://doi.org/10.1002/pul2.12445","url":null,"abstract":"Current methods for quantifying perfusion from computed tomography pulmonary angiography (CTPA) often rely on semi-quantitative scoring systems and requires an experienced evaluator. Few studies report on absolute quantitative variables derived from the images, and the methods are varied with mixed results. Dual-energy CTPA (DE-CTPA) enables automatic quantification of lung and lobar perfusion with minimal user interaction by utilizing machine learning based software. We aimed to evaluate differences in DE-CTPA derived quantitative perfusion variables between patients with acute pulmonary embolism (PE) and chronic thromboembolic pulmonary hypertension (CTEPH). This retrospective, single-center, observational study included 162 adult patients diagnosed with PE (n = 81) or CTEPH (n = 81) and scanned using dual-energy CT between 2020 and 2023. Mann-Whitney U tests and permutational analysis of variance (PERMANOVA) were used for comparative analyses. We found whole lung perfusion blood volume to be lower (p < 0.001) in PE patients (median 3399 mL [2554, 4284]) than in CTEPH patients (median 4094 mL [3397, 4818]). The same was observed at single lung and lobar level. PERMANOVA encompassing all perfusion variables showed a difference between the two groups (F-statistic = 13.3, p = 0.002). Utilizing logistic regression, right and left lower lobe perfusion blood volume showed some ability to differentiate between PE and CTEPH with area under the receiver operation characteristics curve values of 0.71 (95% CI: 0.56; 0.84) and 0.72 (95% CI: 0.56; 0.86). Pulmonary perfusion is lower in patients with PE than patients with CTEPH, highlighted by differences in DECT-derived perfusion blood volume. Quantitative perfusion variables might be useful to differentiate between the two diseases.","PeriodicalId":20927,"journal":{"name":"Pulmonary Circulation","volume":"14 4","pages":"e12445"},"PeriodicalIF":2.2,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11544464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142626981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Comorbidity profiles and pulmonary embolism risk assessment: Leveraging the Charlson Comorbidity Index for improved prognostication in a national data set. 合并症概况和肺栓塞风险评估：利用 Charlson 生病指数改进全国数据集的预后。

IF 2.2 4区医学

Pulmonary Circulation Pub Date : 2024-11-07 eCollection Date: 2024-10-01 DOI: 10.1002/pul2.70010

Truong-An Ho, Ka U Lio, Palakkumar Patel, Yichen Wang, Hammad Arshad, Si Li, Parth Rali

{"title":"Comorbidity profiles and pulmonary embolism risk assessment: Leveraging the Charlson Comorbidity Index for improved prognostication in a national data set.","authors":"Truong-An Ho, Ka U Lio, Palakkumar Patel, Yichen Wang, Hammad Arshad, Si Li, Parth Rali","doi":"10.1002/pul2.70010","DOIUrl":"https://doi.org/10.1002/pul2.70010","url":null,"abstract":"Current risk assessment of pulmonary embolism (PE) stratifies patients based on hemodynamic stability, clinical parameters of severity, right ventricular dysfunction and cardiac injury but fails to integrate a wide variety of comorbid conditions. The Charlson Comorbidity Index (CCI) predicts mortality based on patients' diseases and provides a system to quantify disease burden. The National Inpatient Sample (NIS) database (2016-2018) was used to identify patients with PE and calculate CCI score groups of 0, 1-2, 3-5, and ≥6 and stratify them by outcome. Of 561,625 patients with PE, 176,460 (31.4%) had CCI score of 0, 223,870 (39.8%) had CCI of 1-2, 102,305 (18.2%) had CCI of 3-5, and 58,990 (10.5%) had CCI ≥ 6. Higher CCI scores were associated with increased mortality: CCI 1-2 (adjusted odds ratio [aOR] 2.09), CCI 3-5 (aOR 3.12), CCI ≥ 6 (aOR 5.44) compared to CCI 0, along with stepwise increases in shock and mechanical ventilation with each increase in CCI score group. CCI scores ≥3 had increased length of stay (1.4-1.72 days) and increased total hospital costs ($3651-$4265) compared to CCI0. Patients with CCI ≥ 3 were less likely to receive systemic thrombolysis, catheter directed thrombolysis and mechanical thrombectomy. Acute PE in patients with elevated comorbidity scores is associated with higher morbidity and mortality, increased hospital resource utilization, and decreased usage of advanced therapies in a large cohort reflective of patients across the United States. Integration of comorbidities in risk assessment profiles identifies patients with higher short-term mortality which may guide management strategy.","PeriodicalId":20927,"journal":{"name":"Pulmonary Circulation","volume":"14 4","pages":"e70010"},"PeriodicalIF":2.2,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541855/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142606148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hemodynamic markers independent of pulmonary capillary wedge pressure can discriminate between pre and postcapillary exercise-induced pulmonary hypertension. 独立于肺毛细血管楔压的血流动力学指标可区分毛细血管运动前和运动后诱发的肺动脉高压。

IF 2.2 4区医学

Pulmonary Circulation Pub Date : 2024-11-06 eCollection Date: 2024-10-01 DOI: 10.1002/pul2.70002

Margaret Montovano, Paul J Scheel, Ilton M Cubero Salazar, Paul M Hassoun, Ryan J Tedford, Steven Hsu

引用次数: 0

Extracorporeal membrane oxygenation (ECMO) support for children with pulmonary hypertension: A single-institutional experience of outcomes. 为肺动脉高压患儿提供体外膜肺氧合（ECMO）支持：单一机构的成果经验。

IF 2.2 4区医学

Pulmonary Circulation Pub Date : 2024-10-25 eCollection Date: 2024-10-01 DOI: 10.1002/pul2.12442

Christopher Nemeh, Nicholas Schmoke, William Patten, Eunice Clark, Yeu S Wu, Pengchen Wang, Paul Kurlansky, William Middlesworth, Eva W Cheung, Erika B Rosenzweig

{"title":"Extracorporeal membrane oxygenation (ECMO) support for children with pulmonary hypertension: A single-institutional experience of outcomes.","authors":"Christopher Nemeh, Nicholas Schmoke, William Patten, Eunice Clark, Yeu S Wu, Pengchen Wang, Paul Kurlansky, William Middlesworth, Eva W Cheung, Erika B Rosenzweig","doi":"10.1002/pul2.12442","DOIUrl":"10.1002/pul2.12442","url":null,"abstract":"Pediatric pulmonary arterial hypertension (PAH) can present with a wide spectrum of disease severity. Pulmonary hypertension (PH) crises can lead to acute decompensation requiring extracorporeal membrane oxygenation (ECMO) support, including extracorporeal cardiopulmonary resuscitation (eCPR). We evaluated outcomes for pediatric PH patients requiring ECMO. A single-institution retrospective review of pediatric PAH patients with World Symposium on PH (WSPH) groups 1 and 3 requiring ECMO cannulation from 2010 through 2022 (n = 20) was performed. Primary outcome was survival to hospital discharge. Secondary outcomes were survival to decannulation and 1-year survival. Of 20 ECMO patients, 16 (80%) survived to decannulation and 8 (40%) survived to discharge and 1 year follow up. Of three patients who had two ECMO runs; none survived. There were five patients who had eCPR for the first run; one survived to discharge. The univariate logistic regression model showed that venovenous ECMO was associated with better survival to hospital discharge than venoarterial ECMO, (OR: 0.12, 95% CI: 0.01-0.86, p = 0.046). PH medications (administered before, during, or after ECMO) were not associated with survival to discharge. For children with decompensated PAH requiring ECMO, mortality rate is high, and management is challenging. While VA ECMO is the main configuration for decompensated PH, VV ECMO could be considered if there is adequate ventricular function, presence of a systemic to pulmonary shunt, or an intercurrent treatable illness to improve survival to discharge. A multidisciplinary approach with requisite expertise should be utilized on a case-by-case basis until more reliable data is available to predict outcomes.","PeriodicalId":20927,"journal":{"name":"Pulmonary Circulation","volume":"14 4","pages":"e12442"},"PeriodicalIF":2.2,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11502935/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142506831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transcriptome analyses reveal common immune system dysregulation in PAH patients and Kcnk3-deficient rats. 转录组分析揭示了 PAH 患者和 Kcnk3 基因缺陷大鼠的共同免疫系统失调。

IF 2.2 4区医学

Pulmonary Circulation Pub Date : 2024-10-23 eCollection Date: 2024-10-01 DOI: 10.1002/pul2.12434

Grégoire Ruffenach, Hélène Le Ribeuz, Mary Dutheil, Kristell El Jekmek, Florent Dumont, Anaïs Saint-Martin Willer, Marc Humbert, Véronique Capuano, Lejla Medzikovic, Mansoureh Eghbali, David Montani, Fabrice Antigny

{"title":"Transcriptome analyses reveal common immune system dysregulation in PAH patients and Kcnk3-deficient rats.","authors":"Grégoire Ruffenach, Hélène Le Ribeuz, Mary Dutheil, Kristell El Jekmek, Florent Dumont, Anaïs Saint-Martin Willer, Marc Humbert, Véronique Capuano, Lejla Medzikovic, Mansoureh Eghbali, David Montani, Fabrice Antigny","doi":"10.1002/pul2.12434","DOIUrl":"https://doi.org/10.1002/pul2.12434","url":null,"abstract":"Pulmonary arterial hypertension (PAH) is a severe disease caused by progressive distal pulmonary artery obstruction. One cause of PAH are loss-of-function mutations in the potassium channel subfamily K member 3 (KCNK3). KCNK3 encodes a two-pore domain potassium channel, which is crucial for pulmonary circulation homeostasis. However, our understanding of the pathophysiological mechanisms underlying KCNK3 dysfunction in PAH is still incomplete. Taking advantage of unique Kcnk3-deficient rats, we analyzed the transcriptomic changes in the lungs from homozygous Kcnk3-deficient rats and wild-type (WT) littermates and compared them to PAH patient transcriptomic data. Transcriptome analysis of lung tissue obtained from WT and Kcnk3-deficient rats identified 1915 down- or upregulated genes. In addition, despite limited similarities at the gene level, we found a strong common signature at the pathway level in PAH patients and Kcnk3-deficient rat lungs, especially for immune response. Using the dysregulated genes involved in the immune response, we identified Spleen Associated Tyrosine Kinase (SYK), a significantly downregulated gene in human PAH patients and Kcnk3-deficient rats, as a hub gene. Our data suggests that the altered immune system response observed in PAH patients may be partly explained by KCNK3 dysfunction through the alteration of SYK expression.","PeriodicalId":20927,"journal":{"name":"Pulmonary Circulation","volume":"14 4","pages":"e12434"},"PeriodicalIF":2.2,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11497494/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142516595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0