SHOCK最新文献

{"title":"Ferroptosis as a Novel Pathway in the Pathogenesis of Necrotizing Enterocolitis.","authors":"Jasmine Lee, Sharon Joseph, Krishna Manohar, Jianyun Liu, W Chris Shelley, John Brokaw, Christian Henriquez, Troy A Markel","doi":"10.1097/SHK.0000000000002592","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002592","url":null,"abstract":"<p><strong>Abstract: </strong>Necrotizing enterocolitis (NEC) is a severe gastrointestinal condition that primarily affects premature infants and is characterized by inflammation and necrosis of the intestinal tissue. Despite numerous efforts, it remains the single leading cause of death in neonatal gastrointestinal disease. This review explores the emerging role of ferroptosis-a form of regulated cell death driven by iron-dependent lipid peroxidation-in the pathogenesis of NEC. The purpose of this review is to address the unique vulnerability of neonates to ferroptosis, which is influenced by their developmental stage and the oxidative stress associated with prematurity. We will next examine the implications of ferroptosis in NEC, discussing how its dysregulation may contribute to the inflammatory processes and tissue damage observed in this devastating neonatal condition. Furthermore, we evaluate the potential of targeting ferroptosis as a therapeutic strategy for mitigating NEC. By elucidating the connection between ferroptosis and NEC, this review aims to inspire future studies to explore this understudied relationship and to promote the investigation of novel therapeutic approaches targeting the ferroptotic pathway.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transplantation of viable allogeneic mitochondria protects kidney function in a mouse model of haemorrhagic shock and rhabdomyolysis-induced acute renal injury.","authors":"Yu-Li Pang, Shi-Yuan Fang, Chien-Chi Huang, Ming-Wei Lin, Jun-Neng Roan, Kuen-Jer Tsai, Chen-Fuh Lam","doi":"10.1097/SHK.0000000000002579","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002579","url":null,"abstract":"<p><strong>Methods: </strong>Mice were subjected to acute hemorrhagic shock and rhabdomyolysis through blood withdrawal and intramuscular glycerol injection. Mitochondria (100 μg) were freshly isolated from the soleus muscles of naïve mice. Mitochondria or placebo solution was randomly delivered into arterial catheter 1 hour after the induction of AKI. The mice were euthanised 36 hours later, and blood samples and kidneys were collected for analysis.</p><p><strong>Results: </strong>IVIS imaging confirmed increased expression of fluorescence-labelled allogeneic mitochondrial accumulation in AKI kidneys. Mitochondrial transplantation significantly decreased the elevated serum levels of urea nitrogen, creatinine and potassium. The protein expression of endogenous antioxidant molecules (Nrf-2, heme oxygenase-1 and superoxide dismutases) was significantly increased. The BAX-to-Bcl-2 ratio and expression of cleaved caspace-3 were also reduced in the mitochondrial-transplanted animals, indicating the attenuation of mitochondrial-mediated apoptosis in the kidney tissues of AKI mice. Histopathological examination confirmed that degrees of renal tubular injury were improved following mitochondrial transplantation.</p><p><strong>Conclusions: </strong>Transplantation of freshly isolated mitochondria augments endogenous antioxidant capacity and ameliorates mitochondrial apoptosis in the injured kidney tissues after haemorrhagic shock and rhabdomyolysis-induced AKI. Allogeneic mitochondrial transplantation could be a potential and feasible therapeutic option for prevention and management of AKI secondary to major trauma.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143674655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Detection of hypovolaemia by the Hypotension Prediction Index is associated with gastrointestinal microcirculation dysfunction in a porcine model of haemorrhage.","authors":"Simon Davies, Zhongping Jian, Feras Hatib, Amy Gomes, Monty Mythen","doi":"10.1097/SHK.0000000000002578","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002578","url":null,"abstract":"<p><strong>Background: </strong>Post operative gastrointestinal dysfunction is a common complication following critical illness. The splanchnic circulation is sensitive to changes in volume status and is unduly impacted by volume loss compared to other organ systems. A raised Hypotension Prediction Index (HPI) value has been associated with decreased gastrointestinal microcirculation flow in haemorrhage models at 5% volume loss. The aim of this study was to assess whether HPI can detect a 5% volume deficit and whether this is associated with a decrease in GI microvascular flow.</p><p><strong>Methods: </strong>Ten anaesthetised, mechanically ventilated Yorkshire/Landrace cross breed pigs were studied. Haemorrhage was performed removing 1% aliquots of blood until 10% of blood volume was removed. Once complete the removed blood was reinfused in 2% aliquots. Haemodynamic and intestinal microcirculatory measurements were performed at each stage. A repeated measurement one-way ANOVA was used to compared changes from baseline measurements during haemorrhage, and the final haemorrhage stage during reinfusion.</p><p><strong>Results: </strong>There was a significant change in MAP from baseline values at 3% haemorrhage with a 6.0 mmHg decrease (95% CI 0.2 to 11.8, p < 0.05) from 93(3) mmHg to 87(4) mmHg. HPI showed a significant rise from baseline values from 17(6) to 44(22) with a MD of 26.4 (95% CI 2.1 to 50.7, p < 0.005) at 5% haemorrhage. For classifying if a model was greater than 5% volume deplete the area under the curve for the analysed variables were HPI 0.97 (95% CI 0.90-0.98, p < 0.0001), SVV 0.80 (95% CI 0.73-0.89, p < 0.0001), and MAP 0.90 (95% CI 0.85-0.95, p < 0.0001). There were significant decreases in microcirculation scores comparing baseline with 1% haemorrhage (MD -1.89, 95% CI -2.49 to -1.29, P < 0.0001), 1% haemorrhage with 2% haemorrhage (MD -1.90, 95% CI -2.67 to -1.15, P < 0.0001), up to 4% haemorrhage compared with 5% (MD -1.34, 95% CI -2.31 to -0.37, P < 0.0001).</p><p><strong>Conclusion: </strong>Intestinal microcirculation is disrupted with minimal volume loss and is reduced by almost 75% at a blood loss of 5% volume. The reduction in gastrointestinal MFI is not captured in clinically significant changes in commonly measured parameters, however, is reflected in changes in the hypotension prediction index at 5% volume loss.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USF2 exacerbates sepsis-induced acute kidney injury and ferroptosis through LPCAT3-mediated NRF2/HO-1/GPX4 pathway.","authors":"Ren Huang, Yan Guan, Wenjuan Huang, Yan Shang, Yanhong Xu, Shuqi Li, Rongwen Wan","doi":"10.1097/SHK.0000000000002588","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002588","url":null,"abstract":"<p><strong>Abstract: </strong>Background: Sepsis-acute kidney injury (AKI) is a common complication in critically ill patients with a very high mortality rate. Lysophosphatidylcholine acyltransferase 3 (LPCAT3) is crucial in lipid metabolism; however, its role in the pathogenesis of sepsis-AKI remains unclear.Methods: Human renal tubular epithelial (HK2) cells stimulated with lipopolysaccharide (LPS) were used to establish sepsis-AKI cell models. Various assays, including cell counting kit 8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU) staining, flow cytometry, and enzyme linked immunosorbent assay (ELISA) were employed to analyze the effects of LPS on HK2 cells. The levels of Fe2+, reactive oxygen species (ROS) fluorescence intensity, and glutathione (GSH) were measured to assess the impact of LPS on oxidative stress in HK2 cells. The expression of relevant genes was assessed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot. In terms of mechanism, the PROMO and JASPAR databases, chromatin immunoprecipitation (CHIP) assay, and dual luciferase reporter assay were engaged to predict and validate the transcriptional binding between upstream transcription factor 2 (USF2) and LPCAT3. In vivo experimentsinvolved injecting adenovirus carrying Ad-sh-LPCAT3 via the tail vein to investigate the functional role of LPCAT3 in mice subjected to cecal ligation puncture (CLP)-induced sepsis-AKI. Histological analyses were performed using hematoxylin and eosin (H&E) staining, MASSON staining, and immunohistochemistry (IHC).Results: LPS inhibited the proliferation of HK2 cells while inducing apoptosis, inflammatory responses, and ferroptosis. LPCAT3 expression was up-regulated in sepsis-AKI tissues and cells. Moreover, LPCAT3 knockdown weakened the sepsis-AKI in HK2 cells. Mechanistically, LPCAT3 was transcriptionally regulated by USF2, and LPCAT3 reversed the effects of si-USF2 in sepsis-AKI cell models via the nuclear factor erythroid 2-related factor 2/heme oxygenase-1/glutathione peroxidase 4 (NRF2/HO-1/GPX4) pathway. Mouse experiments demonstrated that LPCAT3 intensified sepsis-AKI through the same molecular mechanism in vivo.Conclusion: USF2 knockdown resulted in the down-regulation of LPCAT3, thereby modulating the NRF2/HO-1/GPX4 pathway and aggravating sepsis-AKI and ferroptosis.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Baicalin inhibits cell apoptosis, inflammation and ferroptosis in ulcerative colitis by influencing SP1-mediated transcription of SLC6A14.","authors":"Huifang Sun, Lijuan Hu, Peipei Hao, Yawei Liu, Ying Tian","doi":"10.1097/SHK.0000000000002587","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002587","url":null,"abstract":"<p><strong>Abstract: </strong>Background: Baicalin is considered to be able to alleviate the progression of ulcerative colitis (UC), but the underlying molecular mechanism needs to be further elucidated.Methods: TNF-α-induced human normal colorectal mucosa cells (FHC) were used to mimic UC models in vitro, and trinitrobenzene sulfonic acid (TNBS)-injected rats were used to construct UC models in vivo. Cell proliferation and apoptosis were determined by CCK8 assay, EdU assay and flow cytometry. Inflammation factors were examined by ELISA, and ferroptosis-related markers were detected by corresponding kit. The mRNA and protein levels of solute carrier family 6 member 14 (SLC6A14) and specific protein 1 (SP1) were analyzed by qRT-PCR and western blot. The interaction between SP1 and SLC6A14 promoter was verified by ChIP assay and dual-luciferase reporter assay.Results: Baicalin enhanced proliferation, while repressed apoptosis, inflammation and ferroptosis in TNF-α-induced FHC cells. SLC6A14 was upregulated in UC patients, and baicalin could decrease SLC6A14 expression. SLC6A14 overexpression reversed the inhibitory effect of baicalin on TNF-α-induced FHC cell injury. SP1 could bind to SLC6A14 promoter region to upregulate its expression, and ectopic expression of SLC6A14 also abolished the suppressive effect of SP1 knockdown on TNF-α-induced FHC cell injury. Baicalin reduced SP1 expression to downregulate SLC6A14. Also, baicalin alleviated UC process in vivo via repressing inflammation and ferroptosis.Conclusion: Baicalin repressed SP1-mediated transcription of SLC6A14 to restrain cell apoptosis, inflammation and ferroptosis, thus alleviating UC progression.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TEAD1 knockdown impedes the inflammation and ferroptosis by mediating MMP3 in cerebral ischemia reperfusion.","authors":"Junjie Lu, Jing Su, Liang Zhu, Meng Xu, Li Zhao","doi":"10.1097/SHK.0000000000002589","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002589","url":null,"abstract":"<p><strong>Background: </strong>Cerebral ischemia-reperfusion (IR) injury is a frequent complication of ischemic stroke with the adverse impact on the clinical prognosis. This study focused on the molecular mechanism associated with TEA domain transcription factor 1 (TEAD1) and matrix metalloproteinase 3 (MMP3) in cerebral IR.</p><p><strong>Methods: </strong>In vitro, IR model was established using oxygen-glucose deprivation/reoxygenation (OGD/R) in human brain microvascular endothelial cells (HBMVECs). TEAD1 and MMP3 mRNA and protein examination were performed by RT-qPCR and western blot. Cell viability and apoptosis were measured using cell counting kit-8 assay and flow cytometry. Enzyme-linked immunosorbent assay was conducted for detection of inflammatory cytokines. Ferroptosis was evaluated via kits. TEAD1 and MMP3 interaction was proved by RNA immunoprecipitation assay. In vivo, IR was induced in rats by Middle Cerebral Artery Occlusion-Reperfusion (MCAO/R) model. Brain injury in rats was assessed by tetrazolium chloride staining, evans blue extravasation, neurological function score, and cerebral water content detection.</p><p><strong>Results: </strong>OGD/R induced the prominent upregulation of MMP3 in HBMVECs. After knockdown of MMP3, apoptosis, inflammation and ferroptosis were all mitigated in OGD/R-treated HBMVECs. TEAD1 could enhance MMP3 expression by targeting the promoter. TEAD1 silence impeded OGD/R-mediated inflammation and ferroptosis via reducing MMP3. In MCAO/R model, TEAD1 inhibition protected brain tissues of rats against cerebral IR injury by affecting MMP3.</p><p><strong>Conclusion: </strong>The above evidence elucidated that TEAD1 facilitated cerebra inflammation and ferroptosis in vitro and in vivo IR models through targeting MMP3, suggesting the involvement of TEAD1/MMP3 axis in cerebral IR injury.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DEVELOPMENT OF ENDOTHELIOPATHY: A SHARED HALLMARK ACROSS CRITICALLY ILL PATIENT POPULATIONS.","authors":"Sara Fernández, Ana Belén Moreno-Castaño, Daniel N Marco, Helena Ventosa-Capell, Maribel Diaz-Ricart, Pedro Castro","doi":"10.1097/SHK.0000000000002571","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002571","url":null,"abstract":"<p><strong>Abstract: </strong>Endotheliopathy has been increasingly recognized as a key feature of critical illness. Different diseases and syndromes manifest endothelial dysfunction in their severe forms. Septic syndrome, SARS-CoV-2 disease spectrum and cell therapy-associated toxicities represent paradigmatic examples of endotheliopathy, in intensive care units (ICU). As common features, and in response to the environment associated with these conditions, endothelial cells develop a pro-inflammatory and pro-thrombotic phenotype, switching its secretion behavior of anticoagulant and pro-fibrinolytic factors towards a hypercoagulative and hypofibrinolytic state. Intravascular microthrombi, release of neutrophil extracellular traps, detached endothelial cells and exposure of a highly reactive extracellular matrix towards platelets, result in turbulent blood flow and agglutination of circulating cells, ultimately leading to tissue hypoperfusion. Levels of endothelial damage biomarkers correlate with disease severity and, therefore, implementation of biomarkers panels could enhance prediction, differential diagnosis, and severity stratification in critical illness conditions. Development of strategies to protect the endothelium could mitigate pro-inflammatory and pro-coagulant responses, offering therapeutic potential for the endotheliopathy-associated conditions of critically ill patients.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143658535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal association between medication use and sepsis: A two-sample Mendelian randomization study.","authors":"Mingfen Sun, Yi Chen, Zhaoquan Jin, Bo Yang, Minghui Zhu","doi":"10.1097/SHK.0000000000002582","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002582","url":null,"abstract":"<p><strong>Abstract: </strong>Objective: This study aimed to explore the causal association between genetically predicted medication use and sepsis.Methods: Utilizing summary data from genome-wide association studies (GWAS) on selected medications use and sepsis, a two-sample Mendelian randomization (MR) design was employed. Analysis was conducted using the Inverse Variance Weighted (IVW), weighted median, weighted mode, and MR-Egger regression methods. Sensitivity analysis included MR-Egger, MR-PRESSO, Cochran's Q, and leave-one-out methods.Results: The IVW method suggested that genetically predicted medication use, including Drugs used in diabetes (OR=1.08, 95%CI: 1.02 - 1.15, p=0.015), Diuretics (OR=1.08, 95%CI: 1.01 - 1.15, p=0.034), Thyroid preparations (OR=1.08, 95%CI: 1.03 - 1.13, p=0.001), and Adrenergics (OR=1.09, 95%CI: 1.01 - 1.18, p=0.037), might be causally associated with a higher risk of sepsis. Datasets for drugs in diabetes, antithrombotic agents, renin-angiotensin system agents, anilides, and glucocorticoids may exhibit heterogeneity. MR-Egger regression results indicated minimal influence of horizontal pleiotropy on all associations except possibly for antithrombotic agents and sepsis. MR-PRESSO test found no outliers. Leave-one-out analysis confirmed associations were not driven by any single factor. After removing confounders, the IVW method suggested that genetically predicted diuretics use (OR=1.17, 95%CI: 1.03 - 1.34, p=0.018) might be causally associated with a higher risk of sepsis, while drugs used in diabetes, thyroid preparations, and inhaled adrenergics were not. No heterogeneity was observed. MR-Egger regression results indicated the minimal influence of horizontal pleiotropy on all associations. MR-PRESSO test found no outliers. Leave-one-out analysis confirmed any single factor did not drive associations.Conclusions: This study found that prior use of diuretics may increase sepsis risk, with inconclusive evidence for other medications.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143658581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NEUTROPHIL PERCENTAGE-TO-ALBUMIN RATIO IS ASSOCIATED WITH 30-DAY ALL-CAUSE MORTALITY IN SEPTIC CHOLANGITIS PATIENTS: A COHORT STUDY.","authors":"Jie Liu, Pengfei Wang, Jiajun Ji","doi":"10.1097/SHK.0000000000002574","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002574","url":null,"abstract":"<p><strong>Background: </strong>Neutrophil percentage-to-albumin ratio (NPAR) has been proven to correlate with the poor prognosis of various diseases. This study aims at investigating the prognostic value of NPAR for septic cholangitis patients from Medical Information Mart Intensive Care IV database (MIMIC-IV).</p><p><strong>Methods: </strong>Overall, 329 adult septic cholangitis patients were retrospectively included, of whom 82 experienced deaths within 30 days. Cox regression, restricted cubic spline, as well as Kaplan-Meier curves were employed to evaluate the association between NPAR and 30-day mortality. Hazard ratio (HR) and 95% confidential interval (95% CI) were calculated. Receiver operating characteristic (ROC) curves and integrated discrimination improvement (IDI) analysis were utilized to assess the predictive efficacy of NPAR.</p><p><strong>Results: </strong>NPAR was significantly associated with 30-day mortality in multivariable Cox analysis (HR = 1.52, 95%CI = 1.16-1.99, P = 0.003). Kaplan-Meier curves indicated NPAR in the second quartile (range from 2.55-2.93) demonstrated the lowest mortality (log-rank test: P < 0.001). RCS curves showed a U-shaped relationship between NPAR and 30-day mortality, and an inflection point of appropriately 2.73 was discovered. HRs and 95%CIs on the left and right sides of the inflection point, were 0.299 (0.114-0.781, P = 0.014) and 1.955 (1.362-2.807, P < 0.001), respectively. NPAR exhibited a moderate AUROC (0.668) for the prediction of 30-day mortality. Importantly, addition of the NPAR into illness score models can significantly improve the predictive ability.</p><p><strong>Conclusions: </strong>A U-shaped nonlinear association was observed between NPAR and 30-day all-cause mortality in septic cholangitis patients. NPAR emerged as a potential marker for the prognosis of critical cholangitis patients.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143731432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Right ventricular dysfunction as a mortality determinant for patients with cardiogenic shock induced by acute myocardial infarction.","authors":"Amin Daoulah, Shaber Seraj, Ahmed Elmahrouk, Nooraldaem Yousif, Prashanth Panduranga, Wael Almahmeed, Abdulrahman Arabi, Mohammed Alshehri, Hatem M Aloui, Amr A Arafat, Mohammed A Qutub, Waleed Alharbi, Rajesh Rajan, Mokhtar Abdirahman Kahin, Abdullah Alenezi, Said Al Maashani, Taher Hassan, Jassim Alswuaidi, Awad Alqahtani, Mubarak Abdulhadi Aldossari, Mohammed Al Jarallah, Ali Alshehri, Abdelmaksoud Elganady, Badr Alzahrani, Abdulrahman M Alqahtani, Faisal Omar M Al Nasser, Haitham Amin, Mohamed N Alama, Alaa Aldossari, Sultan Al Obaikan, Alsayed Ali Almarghany, Omar Kanbr, Ahmed Jamjoom, Youssef Elmahrouk, Ibrahim A M Abdulhabeeb, Mohammed Balghith, Ahmad S Hersi, Abeer Said Mohamed Al Rawahi, Marwa Abd Elghany Albasiouny Alkholy, Adnan Fathey Hussien, Abdulrahman Almoghairi, Mohamed Mohammednabil A Alama, Mohamed Ajaz Ghani, Ayman Uthman Alhussini, Ayman Basardah, Bandar Alshehri, Laura AlObaid, Sara Shawki Sasti, Seraj Abualnaja, Tarique Shahzad Chachar, Hassan Khan, Shahrukh Hashmani, Ahmed A Ghonim, Khalid Almerri, Razan W Alsofayan, Abeer M Shawky, Amir Lotfi","doi":"10.1097/SHK.0000000000002583","DOIUrl":"https://doi.org/10.1097/SHK.0000000000002583","url":null,"abstract":"<p><strong>Background: </strong>Cardiogenic shock (CS) secondary to acute myocardial infarction (AMI) is a major cause of in-hospital mortality. With the addition of right ventricular dysfunction (RVD), it is associated with poorer outcomes. This study examines the impact of RVD on mortality in CS-AMI patients, highlighting the importance of early RVD identification and tailored management.</p><p><strong>Methods: </strong>Data from the Gulf Cardiogenic Shock (Gulf-CS) registry-a multicenter registry of CS-AMI patients from six Gulf countries-were analyzed to compare in-hospital and long-term outcomes for patients with and without RVD. RVD was defined by echocardiographic criteria: TAPSE <17 mm, S' wave <12 cm/s, and TAPSE/PASP ratio < 0.34. Multivariable logistic and Cox regression models were used to identify in-hospital and follow-up mortality predictors.</p><p><strong>Results: </strong>Among 1,513 CS-AMI patients, RVD was independently associated with higher in-hospital mortality (55.87% vs. 42.89%, p < 0.001) and lower survival at 6, 12, 18, and 24 months (58%, 35%, 18%, and 6% vs. 73%, 53%, 38%, and 30%; p < 0.001). Predictors of in-hospital mortality included advanced SCAI shock stage, cardiac arrest, age, NSTEMI, number of vessels affected, and elevated creatinine, while follow-up mortality was associated with advanced SCAI stage, reduced LVEF, elevated BUN, history of CABG and comorbidities including COPD and prior CVA.</p><p><strong>Conclusion: </strong>RVD is a significant independent predictor of both in-hospital and long-term mortality in CS-AMI, highlighting the need for early RVD assessment and specific interventions. This study's findings support the integration of RV-focused management strategies to improve survival outcomes in this high-risk population.</p>","PeriodicalId":21667,"journal":{"name":"SHOCK","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143658536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}