Myocardial ischemia–reperfusion injury (MIRI) remains a major challenge in reperfusion therapy for acute myocardial infarction. The role of deubiquitinating enzyme ubiquitin-specific protease 43 (USP43) in this process, however, remains largely unexplored. In this study, we found that USP43 expression was significantly upregulated in murine hearts subjected to ischemia/reperfusion and in primary cardiomyocytes following hypoxia/reoxygenation. Genetic knockout of Usp43 conferred substantial protection against ischemia/reperfusion-induced myocardial injury, inflammation, and cardiomyocyte death, whereas cardiac-specific overexpression of USP43 exacerbated these detrimental effects. Consistent with these findings, USP43 knockdown attenuated hypoxia/reoxygenation-induced damage in primary cardiomyocytes, while its overexpression promoted cell death. Mechanistically, integrated transcriptomic and biochemical assays revealed apoptosis signal-regulating kinase 1 (ASK1) as a key USP43 substrate. USP43 directly binds to ASK1 and removes its K48-linked ubiquitin chains, thereby shielding ASK1 from proteasomal degradation. This post-translational modification leads to ASK1 protein stabilization and hyperactivation of the downstream ASK1-JNK/P38 mitogen-activated protein kinase (MAPK) signaling. Importantly, pharmacologically inhibiting ASK1 rescued the detrimental phenotype caused by USP43 overexpression. In summary, we identify USP43 as a novel regulator that exacerbates MIRI by promoting ASK1-mediated cell death. Targeting the USP43-ASK1 signaling axis may therefore warrant further investigation as a research target to elucidate the mechanisms of MIRI.

This study aimed to evaluate in-hospital mortality and to identify predictors of mortality in coronary artery bypass grafting (CABG) patients receiving veno-arterial extracorporeal membrane oxygenation (VA-ECMO) support. We retrospectively analysed data from adult patients who received VA-ECMO for cardiogenic shock after CABG at our centre between 2014 and 2025. Among the 10,256 patients who underwent CABG, 74 received ECMO postoperatively. Among these, 33 patients (44.6

High-risk patients undergoing percutaneous coronary intervention (PCI) are prone to serious complications, such as ischemia-reperfusion injury, hemodynamic collapse, and cardiogenic shock. While mechanical circulatory support (MCS) may mitigate these risks, its prophylactic use is limited by increased healthcare costs and device-related complications. Preemptive insertion of femoral arteriovenous sheaths, a novel strategy designed to facilitate rapid MCS deployment in emergency situations, may address these concerns, but its clinical benefits remain unclear. In this multicenter retrospective study, we analyzed outcomes from 443 high-risk PCI patients to evaluate whether pre-inserting vascular sheaths before PCI improves patient outcomes. After propensity score matching, 110 matched pairs of patients were compared. Pre-insertion of vascular sheaths was associated with lower all-cause in-hospital mortality (4.5% vs. 18.2%; OR, 0.21; 95% CI, 0.08 ~ 0.59; P = 0.003) and a lower rate of poor neurological outcomes (9.1% vs. 19.1%; OR, 0.42; 95% CI, 0.19 ~ 0.96; P = 0.037). No significant differences were observed regarding the incidence of cardiogenic shock, MCS usage, or vascular complications. Our findings indicate that routine pre-insertion of vascular sheaths prior to high-risk PCI was associated with improved survival and better neurological outcomes, without a detectable increase in procedural complications, supporting its broader implementation in clinical practice.

Objective:To externally validate previously published prognostic models developed exclusively from pre-extracorporeal cardiopulmonary resuscitation (ECPR) variables in a contemporary ECPR cohort. Methods:We conducted a bicenter retrospective external validation of four published pre-ECPR prognostic models (Lee, RESCUE-IHCA, CHIU-S1, and CHIU-S2) in adult patients treated with ECPR between January 2015 and December 2024. Model performance was evaluated for in-hospital survival and favorable neurological outcome (FNO; Cerebral Performance Category 1-2) in the overall cohort, in-hospital cardiac arrest (IHCA), and cardiac-origin cardiac arrest (Cardio_CA) subgroups. Discrimination (the area under the receiver operating characteristic curve, AUROC), calibration, overall model fit (Brier score), and decision curve analysis (DCA) were assessed. For point-based CHIU scores, validation focused on observed outcome rates across predefined risk strata. Results:Among 214 patients, 79.0% (169/214) had IHCA; survival to discharge was 45.8% and FNO occurred in 24.8%. Discrimination for survival was modest across models (overall ECPR AUROC 0.608-0.709; IHCA 0.586-0.672; Cardio_CA 0.591-0.689) but was higher for FNO (overall ECPR 0.709-0.764; IHCA 0.696-0.744; Cardio_CA 0.698-0.718). The Lee model showed poor calibration with slopes far below 1, whereas RESCUE-IHCA model underestimated survival but demonstrated better calibration (slopes close to 1), higher overall accuracy (lower Brier scores) and broader clinical utility (wider net-benefit ranges in DCA). CHIU models provided limited risk separation between adjacent strata. Conclusions:In this external validation, pre-ECPR models showed modest performance, with better discrimination for neurological outcome than for survival. RESCUE-IHCA showed the most favorable overall performance. Future studies should develop and validate more robust, transportable tools.

Timely pathogen identification is crucial for guiding antimicrobial therapy in severe pneumonia requiring veno-venous extracorporeal membrane oxygenation (vv-ECMO). Compared with slow and often insensitive conventional culture, metagenomic next-generation sequencing (mNGS) enables more rapid and comprehensive pathogen detection and may improve clinical management. This study aimed to evaluate the clinical impact of mNGS compared with conventional culture in non-immunocompromised patients undergoing vv-ECMO for severe pneumonia. The retrospective study explored non-immunocompromised patients with severe pneumonia who received vv-ECMO support between January 2017 and June 2023. A total of 151 patients were categorized into the mNGS group and the non-mNGS group, based on whether they underwent mNGS testing. Furthermore, they were stratified into the Death group and Survive group according to their survival status at day 30. Demographics, laboratory test results, pathogens, antibiotic treatment, and clinical outcomes data were recorded and analyzed. The positivity rate identified through the mNGS method (73.3

Myocarditis is inflammatory injury of the myocardium and causes approximately 30,000 deaths globally each year. Fulminant myocarditis is an extremely severe form of myocarditis. Currently, the clinical evaluation of myocarditis and fulminant myocarditis is primarily based on symptoms, ECG findings, and biochemical markers. Cardiac magnetic resonance and endomyocardial biopsy can provide further support for the diagnosis, but both have limitations in routine practice. Recent studies have shown that cell-free DNA (cfDNA) has distinct methylation patterns depending on the organ of origin, suggesting new possibilities for tracking specific types of organ damage. The core mechanism of fulminant myocarditis is a cytokine storm, leading to multiorgan damage, differing from clinically suspected myocarditis. We performed Genome-wide cfDNA methylation detection on plasma from 20 healthy donors and 22 patients (fulminant myocarditis: clinically suspected myocarditis = 9:13, COVID-19 positive: COVID-19 negative = 14:8) and found that cfDNA can be used to specifically identify early multiorgan damage caused by fulminant myocarditis, and its AUC is superior to traditional biochemical indicators such as troponin, high-sensitivity troponin, and lactate dehydrogenase. This is critically important for the timely clinical recognition and treatment of this condition. Furthermore, our study findings suggest that SARS-CoV-2 infection may exacerbate the severity of myocarditis and multiorgan damage. In summary, cfDNA shows great potential as a noninvasive, early, and sensitive biomarker for reflecting disease severity and systemic injury in fulminant myocarditis, which may help guide earlier risk stratification and intervention.

Background This study aimed to evaluate the clinical applicability of metagenomic next-generation sequencing (mNGS) in non-immunocompromised patients undergoing veno-venous extracorporeal membrane oxygenation (vv-ECMO) for severe pneumonia. Methods The retrospective study explored non-immunocompromised patients with severe pneumonia who received vv-ECMO support between January 2017 and June 2023. A total of 151 patients were categorized into the mNGS group and the non-mNGS group, based on whether they underwent mNGS testing. Furthermore, they were stratified into the Death group and Survive group according to their survival status at day 30. Demographics, laboratory test results, pathogens, antibiotic treatment, and clinical outcomes data were recorded and analyzed. Results The positivity rate identified through the mNGS method (73.3%) was notably higher than that obtained through conventional culture (43.1%, P < 0.001). mNGS exhibited superior capabilities in identifying co-infections compared to conventional culture (70.9% vs. 30.1%, P < 0.001). Furthermore, the 30-day mortality rate within the mNGS group demonstrated a significant decrease compared to the no-mNGS group (P = 0.045). Additionally, Kaplan-Meier survival analysis yielded comparable outcomes in both groups (P = 0.035). Factors protecting against adverse outcomes encompassed prolonged hospital stay time, extended ECMO duration, lower Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, successful ECMO weaning, and the application of mNGS. Antibiotic adjustments were implemented in 29 patients (58%) in the mNGS group and 39 patients (38.6%) in the no-mNGS group, with a markedly higher adjustment ratio in the former, demonstrating statistical significance (P = 0.024). Following adjustment of the treatment plan, the mNGS group demonstrated reduced APACHE II scores compared to the no-mNGS group after 5 days of treatment (P = 0.006). Conclusions The mNGS technique, with its superior pathogen detection rate, emerges as a promising tool for microbiological diagnosis and antibiotic management, ultimately contributing to enhanced patient outcomes.

This study investigated the role of long-chain acyl-CoA dehydrogenase (ACADL) in lung adenocarcinoma (LUAD). ACADL was significantly downregulated in human LUAD tissues compared to normal lung tissues. In vitro, ectopic expression of ACADL in murine LLC cells decreased cell viability, migration, and invasion, while ACADL knockdown exhibited the opposite effect. In vivo, ACADL overexpression impeded tumor growth and metastasis. Mechanistically, ACADL hindered tumor progression by inducing cell cycle arrest, promoting apoptosis, and suppressing the epithelial-mesenchymal transition (EMT) process. These findings suggest ACADL acts as a tumor suppressor in LUAD progression.

BackgroundCongenital tracheal stenosis (CTS) is a rare but life-threatening malformation of the trachea. Surgical reconstruction is the treatment of choice in symptomatic cases which is highly risky and is rarely performed in extremely premature infants. With this, reporting a case of CTS managed by tracheal reconstructive surgery under ECMO in a baby weighing 1.47 kg at 32 + 1 WOG was the first ever case in China.Case presentationA premature newborn with a very low birth weight (VLBW) was admitted to our institute for breathing difficulties, requiring mechanical ventilation, and experienced two unsuccessful attempts of extubation. The team performed tracheal reconstructive surgery supported by ECMO after identifying lower tracheal stenosis through a bronchoscopy examination. One month after the surgery, oxygen support was able to discontinue. The patient's entire hospitalization was incredibly challenging, marked by hemodynamic instability with persistent anemia, and disseminated intravascular coagulation (DIC), which were managed with great care. Despite the difficult stay, a follow-up bronchoscopy revealed no obstruction or tracheal stenosis, leading to a successful discharge.ConclusionAdvancements in diagnostic techniques and innovative management methods have made diagnosing and treating CTS easier, even in premature infants. Our case is the first in China to successfully undergo tracheal reconstructive surgery supported by ECMO, inspiring future achievements in the medical field.

BackgroundThe incidence of cardiac arrest (CA) during percutaneous coronary intervention (PCI) is relatively rare. However, when it does occur, the mortality rate is extremely high. Extracorporeal cardiopulmonary resuscitation (ECPR) has shown promising survival rates for in-hospital cardiac arrests (IHCA), with low-flow time being an independent prognostic factor for CA. However, there is no definitive answer on how to reduce low-flow time.MethodsThis retrospective study, conducted at a single center, included 39 patients who underwent ECPR during PCI between January 2016 and December 2022. The patients were divided into two cohorts based on whether standby extracorporeal membrane oxygenation (ECMO) was utilized during PCI: standby ECPR (SBE) (n = 13) and extemporaneous ECPR (EE) (n = 26). We compared the 30-day mortality rates between these two cohorts and investigated factors associated with survival.ResultsCompared to the EE cohort, the SBE cohort showed significantly lower low-flow time (P < 0.01), ECMO operation time (P < 0.01), and a lower incidence of acute kidney injury (AKI) (P = 0.017), as well as peak lactate (P < 0.01). Stand-by ECMO was associated with improved 30-day survival (p = 0.036), while prolonged low-flow time (p = 0.004) and a higher SYNTAX II score (p = 0.062) predicted death at 30 days.ConclusionsStandby ECMO can provide significant benefits for patients who undergo ECPR for CA during PCI. It is a viable option for high-risk PCI cases and may enhance the overall prognosis. The low-flow time remains a critical determinant of survival.

ObjectivesMetagenomic next-generation sequencing (mNGS) is emerging as a novel diagnostic technology for various infectious diseases; however, limited studies have investigated its application in etiological diagnosis of early onset pneumonia (EOP) among patients undergoing extracorporeal cardiopulmonary resuscitation (ECPR) following in-hospital cardiac arrest (IHCA), The clinical significance of early mNGS in predicting short-term prognosis of IHCA patients after ECPR remains unclear.MethodsThis retrospective study included 76 patients with IHCA who underwent ECPR at the First Affiliated Hospital of Zhengzhou University from January 2018 to December 2022. Baseline characteristics and etiological data of all patients during their hospitalization were collected and statistically analyzed. The primary outcome of this study was the diagnosis of EOP, while the secondary outcomes included successful extracorporeal membrane oxygenation (ECMO) weaning and survival at discharge. Additionally, the characteristics of bronchoalveolar lavage fluid (BALF) flora in these patients were compared by analyzing both mNGS results and culture results.ResultsMultivariate logistic regression were employed to analyze the predictors of ECMO weaning failure, mortality at discharge, and the incidence of EOP. Ultimately, patients with lower SOFA scores on admission [OR (95%CI): 1.447 (1.107-1.890), p=0.007] and those who underwent early mNGS testing within 48 hours after ECPR [OR (95%CI): 0.273 (0.086-0.865), p=0.027] demonstrated a higher probability of successful weaning from ECMO. Patients with higher SOFA scores on admission [OR (95%CI): 2.404 (1.422-4.064), p=0.001], and elevated lactate levels [OR (95%CI): 1.176 (1.017-1.361), p=0.029] exhibited an increased likelihood of mortality at discharge. Furthermore, early mNGS detection [OR (95%CI): 0.186 (0.035-0.979), p=0.047], and lower CRP levels (48h-7d after ECMO) [OR (95%CI):1.011 (1.003-1.019), p=0.006] were associated with a reduced incidence of EOP. In addition, the pathogens detected by mNGS within 48 hours after ECPR were mainly oral colonizing bacteria and viruses, and viruses were in the majority, while all BALF cultures were negative. In contrast, between 48 hours and 7 days after ECPR, BALF cultures were positive in all EOP patients.ConclusionsEarly mNGS testing to identify microbial flora facilitates timely adjustment of antibiotic regimens, thereby reducing the incidence of EOP and improving short-term prognosis in patients undergoing ECPR following IHCA.

Abstract Objective The aim of this study was to elucidate the mechanism of beraprost sodium (BPS) in the intervention of myocardial fibrosis after myocardial infarction (MI) through glycogen synthase kinase‐3β (GSK‐3β) and to provide new ideas for intervention in myocardial fibrosis. Materials and Methods MI model rats given BPS and cardiac fibroblasts (CFs) treated with BPS and TGF‐β. HE staining and Masson staining were used to detect the pathological changes of myocardial tissue. Fibrotic markers were detected by immunohistochemical staining. The expressions of GSK‐3β, cAMP response element binding protein (CREB), and p‐CREB were analyzed by qPCR and western blot analysis. EDU staining was used to detect the proliferation of CFs. The promoter activity of GSK‐3β was detected by luciferase assay. Chromatin immunoprecipitation assay was used to detect the binding levels of GSK‐3β promoter and Y‐box binding protein 1 (YBX1). The levels of intracellular cyclic adenosine monophosphate (cAMP) were analyzed by enzyme‐linked immunosorbent assay (ELISA). Results After operation, BPS improved myocardial fibrosis and upregulated GSK‐3β protein expression in male SD rats. BPS can down‐regulate α‐smooth muscle actin (α‐SMA) level and up‐regulate GSK‐3β protein expression in CFs after TGF‐β stimulation. Furthermore, GSK‐3β knockdown can reverse the effect of BPS on TGF‐β‐activated CFs, enhance α‐SMA expression, and promote the proliferation of CFs. BPS could regulate GSK‐3β expression by promoting the binding of GSK‐3β promoter to YBX1. BPS induced upregulation of p‐CREB and cAMP, resulting in reduced fibrosis, which was reversed by the knockdown of GSK‐3β or prostaglandin receptor (IPR) antagonists. Conclusion BPS treatment increased the binding of YBX1 to the GSK‐3β promoter, and GSK‐3β protein expression was upregulated, which further caused the upregulation of p‐CREB and cAMP, and finally inhibited myocardial fibrosis.

Objectives:This study aims to explore the pathogen-detected effect of mNGS technology and its clinical application in non-immunocompromised patients with severe pneumonia supported by vv-ECMO.Methods:A retrospective analysis was conducted on a cohort of 50 non-immunocompromised patients who received vv-ECMO support for severe pneumonia between January 2016 and December 2022. These patients were divided into two groups based on their discharge outcomes: the deterioration group (Group D), which included 31 cases, and the improvement group (Group I), consisting of 19 cases. Baseline characteristics and clinical data were collected and analyzed.Results:Among the 50 patients enrolled, Group D exhibited a higher prevalence of male patients (80.6% vs. 52.6%, p < 0.05), more smokers (54.8% vs. 21.1%, p < 0.05), and were older than those in Group I (55.16 ± 16.34 years vs. 42.32 ± 19.65 years, p < 0.05). Out of the 64 samples subjected to mNGS detection, 55 (85.9%) yielded positive results, with a positivity rate of 83.7% (36/43) in Group D and 90.5% (19/21) in Group I. By contrast, the positive rate through traditional culture stood at 64.9% (74/114). Among the 54 samples that underwent both culture and mNGS testing, 23 (42.6%) displayed consistent pathogen identification, 13 (24.1%) exhibited partial consistency, and 18 (33.3%) showed complete inconsistency. Among the last cases with complete inconsistency, 14 (77.8%) were culture-negative, while two (11.1%) were mNGS-negative, and the remaining two (11.1%) presented mismatches. Remarkably, mNGS surpassed traditional culture in pathogen identification (65 strains vs. 23 strains). Within these 65 strains, 56 were found in Group D, 26 in Group I, and 17 were overlapping strains. Interestingly, a diverse array of G+ bacteria, fungi, viruses, and special pathogens were exclusive to Group D. Furthermore, Acinetobacter baumannii, Pseudomonas aeruginosa, and Klebsiella pneumoniae were more prevalent in Group D compared to Group I. Importantly, mNGS prompted antibiotic treatment adjustments in 26 patients (52.0%).Conclusions:Compared with the conventional culture, mNGS demonstrated a higher positive rate, and emerges as a promising method for identifying mixed pathogens in non-immunodeficient patients with severe pneumonia supported by vv-ECMO. However, it is crucial to combine the interpretation of mNGS data with clinical information and traditional culture results for a comprehensive assessment.

目的 探讨血液灌流技术在冠脉动脉旁路移植术(CABG)联合心脏瓣膜置换体外循环(CPB)过程中是否能够有效吸附炎性细胞因子,从而降低体外循环相关急性肾损伤(CPB-AKI)发生率,改善预后.方法 将2022年2月至2023年2月在郑州大学第一附属医院心血管外科行CABG联合心脏瓣膜置换的60例患者采用数字表法随机分为实验组和对照组,每组30例.使用血液灌流技术的患者为血液灌流(HP)组,不使用HA380的患者为对照组,根据纳入和排除标准确定56例患者(HP组30,对照组26).分析术前、术中及术后白细胞、中性粒细胞、淋巴细胞、血肌酐、肾小球滤过率、白细胞介素(IL)-6、IL-8、IL-10和肿瘤坏死因子-α(TNF-α)结果,比较两组AKI发生率、重症监护室(ICU)住院时间、机械通气(MV)时间、术后住院时间和30天生存结局.应用SPSS 22.0统计软件分析,应用Graphpad prism 6.0软件进行作图.结果 HP组TNF-α在术后0、6、24 h均低于对照组[(1.98±0.96)pg/ml 比(3.10±1.52)pg/ml,t=-3.261,P＜0.05;(1.02±0.18)pg/ml比(2.68±0.81)pg/ml,t=-10.290,P＜0.05;(1.07±0.67)pg/ml 比(1.74±1.01)pg/ml,t=-2.893,P＜0.05].HP组术中 IL-6[(4.40±0.94)pg/ml 比(6.30±1.88)pg/ml,t=-4.668,P＜0.05],术后 IL-6(0h)[(111.00±54.55)pg/ml 比(228.18±93.01)pg/ml;t=-5.638,P＜0.05],术后 IL-8(0、6、24 h)[(44.60±11.15)pg/ml 比(82.85±23.14)pg/ml,t=-7.690,P＜0.05;(19.45±7.96)pg/ml 比(25.49±12.39)pg/ml,t=-2.200,P＜0.05;(13.85±5.53)pg/ml 比(18.34±9.77)pg/ml,t=-2.073,P＜0.05],术后 IL-10(0、6、24 h)[(42.61±13.06)pg/ml 比(84.95±23.17)pg/ml,t=-8.250,P＜0.05;(5.91±3.91)pg/ml 比(12.77±7.99)pg/ml,t=-3.989,P＜0.05;(4.34±2.57)pg/ml 比(7.06±4.61)pg/ml,t=-2.672,P＜0.05]均低于对照组.HP组术后C反应蛋白(C-reactive protein,CRP)、中性粒细胞计数高于对照组[(83.73±50.47)ng/ml比(132.37±75.62)ng/ml,t=-2.785,P＜0.05;(10.92±4.42)×109/L 比(13.52±3.40)×109/L,t=-2.443,P＜0.05],而术后淋巴细胞低于对照组[(0.61±0.35)×109/L 比(0.40±0.19)×109/L,t=2.841,P＜0.05].56例患者有18例(32.14％)术后发生AKI,其中HP组6例(20.00％),对照组12例(46.15％),两组间AKI的发生率差异有统计学意义(20.00％比46.15％,x2=4.455,P＜0.05).对照组 MV 时间较 HP组长[17.8(13.6,30.8)h 比 25.0(15.5,49.5)h,Z=2.285,P＜0.05].HP 组30 d内无死亡,而对照组有2例患者死亡,1例因脑出血,1例因心跳骤停,两组间存活率差异无统计学意义(100.0％比92.3％,P＞0.05).结论 血液灌流技术可降低炎性细胞因子水平,降低术后AKI的发生率,缩短MV时间,改善CABG联合心脏瓣膜置换患者预后.

Objective. To clarify the protective effect of simvastatin on myocardial ischemia reperfusion injury (MIRI) and the underlying mechanism. Materials and Methods. The MIRI model in rats was firstly constructed. Twenty-four male rats were randomly assigned into the sham group, ischemia-reperfusion (I/R) group, and simvastatin group, with 8 rats in each group. Contents of superoxide dismutase (SOD) and malondialdehyde (MDA), as well as serum levels of CK and inflammatory factors, in rats were determined by the enzyme-linked immunosorbent assay (ELISA). Lactate dehydrogenase (LDH) activity in the three groups was examined. Through flow cytometry and Cell Counting Kit-8 (CCK-8) assay, apoptosis and viability in each group were detected, respectively. Relative levels of HMGB1, Kruppel-like factor 2 (KLF2), eNOS, and thrombomodulin (TM) were finally determined. Results. Simvastatin treatment markedly enhanced SOD activity and reduced contents of MDA, LDH, and creatine kinase (CK) in MIRI rats. The increased apoptosis and decreased viability following MIRI were partially reversed by simvastatin treatment. Besides, MIRI resulted in the upregulation of inflammatory factors and chemokines. Their elevations were abolished by simvastatin. In MIRI rats, simvastatin upregulated KLF2 and p-eNOS. Conclusions. Simvastatin protects inflammatory response at post-MIRI through upregulating KLF2, thus improving cardiac function.

Objectives Extracorporeal membrane oxygenation (ECMO) patients with or without transport both have high hospital mortality rate and there are few data on adult VA-ECMO transport patients. Hence, this study was designed to analyze factors that affect the outcomes of patients with ECMO transport. Methods This study retrospectively enrolled 126 ECMO patients transferred from regional hospital to the First Affiliated Hospital of Zhengzhou University by our ECMO team during June 2012 to Sept 2020. Data were calculated and analyzed. Results The median distance of transportation was 141 (76–228) km, the median transport time consuming was 3 (1.3–4) h, the percentage of complications during transport was 40.5% (except for bleeding on cannula site, and no one death during transport), and the survival rate in hospital was 38.9%. Compared with survivors, the non-survivors were older and showed higher SOFA score, longer time with ECMO assisted, longer time in ICU and in hospital. However, after divided into VA-ECMO and VV-ECMO groups, the older age showed no significant difference between survivors and non-survivors groups of VA-ECMO patients. Moreover, the Cox regression survival analysis showed that higher SOFA score and lactate level indicated higher ICU mortality of VA-ECMO patients while higher SOFA score, higher lactate level, older age and lower MAP after transportation (<70mmHg) indicated higher ICU mortality of VV-ECMO patients. However, there was no significant difference of comorbidities and complications in survivors and non-survivors groups of ECMO patients. Conclusions The transportation for ECMO patients can be feasible performed although life-threatening complications might occur. The SOFA score and the lactate level could be used to evaluate the risk of ICU mortality of transportation ECMO patients. Besides, lower MAP after transportation (<70mmHg) had potential predictive value for short-term outcome of VV-ECMO patients.

Abstract Background The anti-coagulation protocol of patients with hemorrhage risk primary disease who need extracorporeal membrane oxygenation (ECMO) supported is controversial. This study evaluated the feasibility of a new anti-coagulation strategy, that is heparin-free after 3000 IU heparin loaded in veno-venous ECMO (VV ECMO) supported acute respiratory failure patients with hemorrhage risk. Methods A retrospective study was performed in a series of hemorrhage risk patients supported with VV ECMO at the First Affiliated Hospital of Zhengzhou University, between June 2012 to Sept 2020. A total of 70 patients received a low heparin bolus of 3000 units for cannulation but without subsequent, ongoing heparin administration. Patients were divided into survival (n = 25) and non-survival group (n = 45). Data of coagulation, hemolysis and membrane lung function were calculated and analyzed. The complications of patients were recorded. Finally, the binary Logistic regression was conducted. Results The longest heparin-free time was 216 h, and the mean heparin-free time was 102 h. Compared with survivors, the non-survivors were showed higher baseline SOFA score and lower platelet counts in 0.5 h, 24 h, 48 h and 96 h after ECMO applied. However, there was no significant differences between survivors and non-survivors in ACT, APTT, INR, D-dimer, fibrinogen, LDH, blood flow rate, Δp and Ppost-MLO2 (all p < 0.05) of all different time point. Moreover, only the baseline SOFA score was significantly associated with mortality (p < 0.001, OR(95%CI): 2.754 (1.486–5.103)) while the baseline levels of ACT, APTT, INR, platelet, D-dimer, fibrinogen and LDH have no association with mortality. The percentage of thrombosis complications was 54.3% (38/70) including 3 oxygenator changed but there was no significant difference of complications in survival and non-survival groups (p > 0.05). Conclusions The anticoagulation protocol that no heparin after a 3000 units heparin bolus in VV ECMO supported acute respiratory failure patients with hemorrhage risk is feasible.

Background: The anti-coagulation protocol of patients with hemorrhage risk primary disease who need extracorporeal membrane oxygenation (ECMO) supported is controversial. This study evaluated the safety of heparin-free after 3000IU heparin loaded in veno-venous ECMO (VV ECMO ) supported acute respiratory failure patients with hemorrhage risk. Methods: A retrospective study was performed in a series of hemorrhage risk patients supported with VV ECMO at the First Affiliated Hospital of Zhengzhou University, between June 2012 to Sept 2020. A total of 70 patients received a low heparin bolus of 3000 units for cannulation but without subsequent, ongoing heparin administration. Patients were divided into survival (n=25) and non-survival group (n=45). Data of coagulation, hemolysis and membrane lung function were calculated and analyzed. The complications of patients were recorded. Finally, the binary Logistic regression was conducted. Results: The longest heparin-free time was 216 hours, and the mean heparin-free time was 102 hours. The percentage of thrombosis complications was 54.3% (38/70) including 3 oxygenator changed but there was no significant difference of complications in survival and non-survival groups (p>0.05). Compared with survivors, the non-survivors were showed higher baseline SOFA score and lower platelet counts in 0.5 hour, 24 hours, 48 hours and 96 hours after ECMO applied. However, there was no significant differences between survivors and non-survivors in ACT, APTT, INR, D-dimer, fibrinogen, LDH, blood flow rate, Δp and P post-ML O 2 (all p<0.05) of all different time point. Moreover, only the baseline SOFA score was significantly associated with mortality (p<0.001, OR(95%CI): 2.754 (1.486-5.103)) while the baseline levels of ACT, APTT, INR, platelet, D-dimer, fibrinogen and LDH have no association with mortality. Conclusions: The anticoagulation protocol that no heparin after a 3000 units heparin bolus in VV ECMO supported acute respiratory failure patients with hemorrhage risk is safe.

Objectives There are few studies of metagenomic next-generation sequencing (mNGS) in immunocompromised patients assisted by veno-venous extracorporeal membrane oxygenation (vv-ECMO). The present study is aimed to investigate the pathogen-detected effect and clinical therapy value of mNGS technologies in immunocompromised patients assisted by vv-ECMO. Methods Our study retrospectively enrolled 46 immunocompromised patients supported by vv-ECMO from Jan 2017 to June 2021 at the First Affiliated Hospital of Zhengzhou University, respectively. Patients were divided into the deterioration group (Group D) (n = 31) and improvement group (Group I) (n = 15) according to their outcomes. Baseline characteristics and etiological data of patients during hospitalization of 2 groups were compared. The pathogens detected by mNGS and antibiotic regimens guided by mNGS in immunocompromised patients assisted by vv-ECMO were analyzed. Results Compared with Group I, the deterioration patients showed a higher percentage of chronic obstructive pulmonary disease (COPD) (32.3% vs. 6.7%, p < 0.01) and were significantly older (47.77 ± 16.72 years vs. 32 ± 15.05 years, p < 0.01). Within 48 h of being ECMO assisted, the consistency of the samples detected by traditional culture and mNGS at the same time was good (traditional culture vs. mNGS detection, the positive rate of bronchoalveolar lavage fluid (BALF) culture: 26.1% vs. 30.4%; the positive rate of blood sample culture: 12.2% vs. 12.2%, p > 0.05). However, mNGS detected far more pathogen species and strains than conventional culture (30 strains vs. 78 strains, p < 0.01); the most popular pathogen was Klebsiella pneumoniae. Parts of patients had their antibiotic treatment adjustments, and the improvement patients showed less usage of broad-spectrum antibiotics. Conclusions mNGS may play a relatively important role in detecting mixed pathogens and personalized antibiotic treatment in immunocompromised patients assisted by vv-ECMO.

Acute respiratory distress syndrome (ARDS) is an acute lung injury associated with high morbidity and mortality. This study aimed to establish an accurate prediction model for mortality risk in ARDS. 70% of patients from the Medical Information Mart for Intensive Care Database (MIMIC-III) were selected as the training group, and the remaining 30% as the testing group. Patients from a Chinese hospital were used for external validation. Univariate and multivariate regressions were used to screen the independent predictors. The receiver operating characteristic curve (ROC) analysis, the Hosmer–Lemeshow test, and the calibration curve were used for evaluating the performance of the model. Age, hemoglobin, heart failure, renal failure, Simplified Acute Physiology Score II (SAPS II), immune function impairment, total bilirubin (TBIL), and PaO 2 /FiO 2 were identified as independent predictors. The algorithm of the prediction model was: ln (Pr/(1 + Pr)) = −3.147 + 0.037 ∗ age − 0.068 ∗ hemoglobin + 0.522 ∗ heart failure (yes) + 0.487 ∗ renal failure (yes) + 0.029 ∗ SAPS II + 0.697 ∗ immune function impairment (yes) + 0.280 ∗ TBIL (abnormal) − 0.006 ∗ PaO 2 /FiO 2 (Pr represents the probability of death occurring). The AUC of the model was 0.791 (0.766–0.816), and the internal and the external validations both confirmed the good performance of the model. A nomogram for predicting the risk of death in ARDS patients was developed and validated. It may help clinicians early identify ARDS patients with high risk of death and thereby help reduce the mortality and improve the survival of ARDS.