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Background: The prognosis of patients with coronary artery disease is adversely affected by elevated fasting plasma glucose (FPG) levels. However, the relationship between FPG levels and in-hospital cardiac arrest (IHCA) remains unclear., Objectives: The objective of this study was to investigate the association between FPG levels and IHCA in patients diagnosed with acute coronary syndrome (ACS)., Methods: Data from a total of 31,726 ACS patients fitted with inclusion and exclusion criteria across 241 hospitals in the Improving Care for Cardiovascular Disease in China-ACS project from November 2014 to July 2019 were collected. Different logistic regression models were utilized to examine the associations of FPG levels with IHCA. Sensitivity analyses were then conducted to assess the robustness of the findings. Marginal effect analyses were also employed to evaluate the impact of different therapies., Results: A total of 335 cases of IHCA and 293 in-hospital mortality were recorded throughout the study. A non-linear relationship between FPG levels and IHCA was identified after adjusting for the covariates. Specifically, a significant association was found between elevated FPG levels (≥6.1 mmol/L) and an increased risk of IHCA. These findings remained consistent across different subgroup analyses including both the diabetic and non-diabetic patients. Additionally, the marginal effect analyses revealed that percutaneous coronary intervention could lower the high FPG-related risk., Conclusions: The study findings showed a positive correlation between FPG levels and a higher incidence of IHCA, irrespective of the presence of diabetes.

Purpose: To determine the predictive value of brain natriuretic peptide (BNP) levels for 30-day mortality after return of spontaneous circulation (ROSC) in patients with cardiac arrest (CA) of presumed cardiac etiology., Methods: This retrospective study included 260 patients with CA of presumed cardiac etiology who regained ROSC and was conducted between November 2013 and June 2022 at two tertiary comprehensive hospitals. Cox regression and nomogram models were used to demonstrate the value of BNP level in predicting 30-day mortality rates. Net reclassification improvement (NRI) and integrated discrimination improvement (IDI) were used to compare the ability of the two models to predict 30-day mortality risk., Results: BNP level was a predictive factor for 30-day mortality (hazard ratio [HR] = 1.441; 95 % confidence interval [CI] = 1.198-1.734). The area under curves (AUCs) of BNP level alone and model 2 (male sex, age, non-shockable rhythm, epinephrine, and time to ROSC >30 min) for predicting 30-day mortality were similar(0.813 versus 0.834). Model 1 that included the variables in model 2 and BNP level showed good predictive value (area under curve = 0.887; 95 % CI = 0.836-0.939). Compared to Model 2, Model 1 showed improved comprehensive differentiation and net weight classification of mortality prediction, further demonstrating the predictive value of BNP for 30-day mortality (NRI = 0.451, 95 % CI = 0.267-0.577; IDI = 0.109, 95 % CI = 0.035-0.191)., Conclusion: BNP level was a predictive factor for 30-day mortality after ROSC in patients with CA of presumed cardiac etiology who regained ROSC. The nomogram model included BNP may provide a reference for predicting 30-day mortality., Competing Interests: Declaration of competing interest The authors have no conflicts of interest to declare., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Cardiac arrest (CA) is a serious health concern that often results in mortality or severe neurological dysfunction in the case of survival. Our aim was to explore the neurological prognostic factors in patients with CA. This retrospective observational study included adult patients with CA. We investigated serum neuron-specific enolase (NSE), S100 calcium-binding protein β (S100β), and indices and parameters at 1, 3, 5, 7 and intensive care unit (ICU) discharge days after CA. The primary study endpoint was the Cerebral Performance Category (CPC) scale score at ICU discharge, which was dichotomized as good neurological outcome (CPC 1-2: full recovery or moderate disability) and poor neurological outcome (CPC 3-5: severe disability, vegetative state, or death). Of the 191 adult patients with CA, 42 (22%) had good neurological outcomes, and 149 (78%) had poor neurological outcomes. NSE at 1,3,5,7 and ICU discharge days showed excellent predictive accuracy for neurological outcomes (area under the curve [AUC]: 0.666, 0.716, 0.870, 0.739, and 0.901, respectively). However, S100β exhibited general predictive power (AUC: 0.666, 0.573, 0.607, 0.594, 0.727). Finally, the early warning model, which combined day 1 NSE, day 1 S100β, cardiac arrest time, SOFA scores, APACHE II scores, and age, was used to screen CA patients with poor neurological prognosis at early stages and had an AUC of 0.792. Serum concentrations of NSE and S100β were significantly elevated in CA patients and could be prognostic biomarkers to predict neurological outcomes. Day 1 NSE and S100β combined with multiple indicators could be a decent early warning model for poor neurological prognosis in patients with CA., (© 2024. The Author(s).)

Objectives: Serum lactate and creatinine levels upon admission in cardiac arrest (CA) patients significantly correlate with acute kidney injury (AKI) post-restoration of autonomic circulation. However, the association between serum lactate/creatinine ratio (LCR) and AKI in this population remains unclear. This study aimed to explore the relationship between LCR at admission and cardiac arrest-associated acute kidney injury (CA-AKI)., Design and Methods: We conducted a secondary analysis of previously published data on CA patient resuscitation, categorizing them into tertiles based on LCR levels. Univariate and multivariate logistic regression models and subgroup analyses were employed to investigate the association between LCR and CA-AKI. Non-linear correlations were explored using restricted cubic splines, and a two-piece wise logistic proportional hazards model for both sides of the inflection point was constructed., Results: A total of 374 patients (72.19 % male) were included, with intensive care unit mortality, in-hospital mortality, and neurologic dysfunction rates of 51.87 %, 56.95 %, and 39.57 %, respectively. The overall CA-AKI incidence was 59.09 %. Multivariate logistic proportional hazards analysis revealed a negative association between LCR and CA-AKI incidence (adjusted odds ratio [OR] 0.85, 95 % confidence intervals [CI] = 0.78-0.93, P=0.001). Triple spline restriction analysis depicted an L-shaped correlation between baseline LCR and CA-AKI incidence. Particularly, a baseline LCR<0.051 was negatively associated with CA-AKI incidence (OR 0.494, 95 % CI=0.319-0.764, P=0.002). Beyond the LCR turning point, estimated dose-response curves remained consistent with a horizontal line., Conclusions: Baseline LCR in CA patients exhibits an L-shaped correlation with AKI incidence following restoration of autonomic circulation. The threshold for CA-AKI is 0.051. This finding suggests that LCR may aid in identifying CA patients at high risk of AKI., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

Background: Acute liver failure (ALF) following cardiac arrest (CA) poses a significant healthcare challenge, characterized by high morbidity and mortality rates. This study aims to assess the correlation between serum alkaline phosphatase (ALP) levels and poor outcomes in patients with ALF following CA., Methods: A retrospective analysis was conducted utilizing data from the Dryad digital repository. The primary outcomes examined were intensive care unit (ICU) mortality, hospital mortality, and unfavorable neurological outcome. Multivariable logistic regression analysis was employed to assess the relationship between serum ALP levels and clinical prognosis. The predictive value was evaluated using receiver operator characteristic (ROC) curve analysis. Two prediction models were developed, and model comparison was performed using the likelihood ratio test (LRT) and the Akaike Information Criterion (AIC)., Results: A total of 194 patients were included in the analysis (72.2% male). Multivariate logistic regression analysis revealed that a one-standard deviation increase of ln-transformed ALP were independently associated with poorer prognosis: ICU mortality (odds ratios (OR) = 2.49, 95% confidence interval (CI) 1.31-4.74, P = 0.005), hospital mortality (OR = 2.21, 95% CI 1.18-4.16, P = 0.014), and unfavorable neurological outcome (OR = 2.40, 95% CI 1.25-4.60, P = 0.009). The area under the ROC curve for clinical prognosis was 0.644, 0.642, and 0.639, respectively. Additionally, LRT analyses indicated that the ALP-combined model exhibited better predictive efficacy than the model without ALP., Conclusions: Elevated serum ALP levels upon admission were significantly associated with poorer prognosis of ALF following CA, suggesting its potential as a valuable marker for predicting prognosis in this patient population., (© 2024. The Author(s).)

Objective: The aim of this study was to investigate whether there is a difference in serum nitric oxide levels between patients who return spontaneously after cardiopulmonary resuscitation and those who do not. We also examined the potential of using serum nitric oxide levels as a marker to make an accurate decision about patient survival., Methods: We included 100 consecutive patients who were brought to the emergency clinic due to cardiac arrest. Blood samples were taken from these patients at admission, 30 min after admission, and when resuscitation was terminated., Results: We found that there was a significant difference in NO1 and NO3 values between the group of patients who did not return after cardiopulmonary resuscitation and the group in which spontaneous circulation returned. The NO1 value was significant in the receiver operating characteristic (ROC) analysis, while the NO3 value was not. A higher NO1 value provided a higher rate of survival., Conclusion: Our findings suggest that nitric oxide may be a useful parameter to support the decision about patient survival. A higher NO1 value is associated with a better prognosis and survival rate. Therefore, serum nitric oxide levels may be a suitable indicator to support the decision-making process regarding patient survival.

Background: Ticagrelor, used in acute coronary syndrome (ACS), can be administered via nasogastric tube when oral intake is impossible. We investigated platelet inhibition and pharmacokinetics in resuscitated ACS patients and those undergoing semi-urgent coronary artery bypass graft (CABG) surgery. Our study aimed to assess platelet inhibition with use of the Platelet Function Analyser (PFA) and measured plasma concentrations of ticagrelor and its active metabolite in these ACS patients., Methods: We included resuscitated cardiac arrest patients (STEMI/NSTEMI) and semi-urgent CABG patients. Crushed ticagrelor tablets were administered using a nasogastric tube. PFA closure time (CT) was determined with CT longer than 113 s as reference range. Plasma concentrations of ticagrelor and its active metabolite were measured after protein precipitation, by using liquid chromatography with mass spectrometry detection., Results: In 20 resuscitated patients, 89% showed platelet inhibition at 24 h and 92% at day 4. For semi-urgent CABG patients, 85% exhibited platelet inhibition at 24 h and 84% at day 4. For ticagrelor in resuscitated patients, the median time to peak plasma concentration (Tmax) was 100 h [8; 100] for a median maximal concentration (Cmax) of 615.5 ng/mL [217.5; 1385.0]. For AR-C124910XX median Tmax was 100 h [8; 100] for a Cmax of 131.0 ng/mL [52.1; 177.7]. Among 20 patients undergoing semi-urgent CABG, Tmax for ticagrelor was 100 h [100; 100] for a median Cmax of 857.0 ng/ml [496.8; 1157.5]. For AR-C124910XX, median Tmax was 100 h [43; 100] for a Cmax of 251.0 ng/ml [173.0; 396.5]., Conclusion: Crushed ticagrelor via nasogastric tube achieved targeted platelet inhibition. Pharmacokinetics aligned with previous studies.EudraCT number: 2013-004191-35; Study protocol code: AGO/2013/011; EC/2014/1061; ClinicalTrial.gov identifier: NCT02341729.

Background: Whether blood laboratory analyses differ in patients who later suffer in-hospital cardiac arrest (IHCA) compared to other hospitalised patients remains unknown. The aim of this study was to describe pre-arrest sampling frequencies, results, and trends in blood laboratory analyses in patients with IHCA compared to controls., Methods: This study was a matched case-control study using national registries in Denmark. Cases were defined as patients with IHCA from 2017 to 2021. Controls were defined as hospitalised patients and were matched on age, sex, and date and length of admission. Data on a total of 51 different blood laboratory analyses were obtained. The laboratory analyses of primary interest were lactate, sodium, potassium, and haemoglobin. The index time for cases was defined as the time of cardiac arrest, and a corresponding index time was defined for controls based on the time to cardiac arrest for their corresponding case. Blood sampling frequencies were reported for blood laboratory analyses obtained either within the last 24 h before the index time or between the time of hospital admission and the index time. Blood sampling results were reported for blood laboratory analyses obtained within the last 24 h before the index time., Results: A total of 9268 cases and 92,395 controls were included in this study. Cases underwent more frequent sampling of all blood laboratory analyses compared to controls. This higher sampling frequency was more pronounced for lactate compared to sodium, potassium, or haemoglobin. The last measured lactate was higher in cases (median [IQR]: 2.3 [1.3, 4.9]) compared to controls (median [IQR]: 1.3 [0.9, 2.0]). Differences in sodium, potassium, and haemoglobin were negligible. The proportion of abnormally elevated levels of lactate and potassium increased as time to cardiac arrest decreased; no such effect was seen in controls. No temporal trend was evident for sodium or haemoglobin., Conclusions: Patients with IHCA undergo more frequent blood sampling prior to IHCA and have higher levels of lactate compared to matched controls., (© 2024 The Author(s). Acta Anaesthesiologica Scandinavica published by John Wiley & Sons Ltd on behalf of Acta Anaesthesiologica Scandinavica Foundation.)

Abstract: Objective : To explore the association of serum transactive response DNA binding protein 43 (TDP-43) with 28-day poor neurologic outcome in patients with return of spontaneous circulation (ROSC) after cardiac arrest. Methods : We performed a study between January and December 2023. Eligible patients with ROSC following cardiac arrest were enrolled. Their baseline characteristics were collected, and serum levels of TDP-43, tumor necrosis factor-α, interleukin-6 and 10, C-reactive protein, and neuron-specific enolase (NSE) at 24 h after ROSC were measured. The neurologic function was assessed by the cerebral performance category scores on day 28 after ROSC. Results : A total of 92 patients were included, with 51 and 41 patients in the good and poor neurologic outcome groups, respectively. Serum TDP-43 was significantly higher in the poor than the good neurologic outcome group ( P < 0.05). Univariate and multivariate logistic regression analyses showed that TDP-43, Witnessed CA, IL-6, and NSE were associated with poor 28-day neurologic outcome (all P < 0.05). Restricted cubic spline analysis revealed that TDP-43 at the serum level of 11.64 pg/mL might be an ideal cutoff value for distinguishing between good and poor neurologic outcomes. Area under curve of serum TDP-43 (AUC = 0.78) was close to that of serum NSE (AUC = 0.82). A dynamic nomogram prediction model that combined TDP-43, Witnessed CA, IL-6, and NSE was constructed and validated. Conclusion : Elevated serum TDP-43 level was associated with and could be used together with Witnessed CA, IL-6, and NSE to predict poor 28-day neurologic outcome in patients after ROSC following cardiac arrest., Competing Interests: The authors report no conflicts of interest., (Copyright © 2024 by the Shock Society.)

Background: Evaluate the association between serum urea at admission and during hospital stay with return of spontaneous circulation (ROSC) and in-hospital mortality in patients with in-hospital cardiac arrest (IHCA)., Methods: This retrospective study included patients over 18 years with IHCA attended from May 2018 to December 2022. The exclusion criteria were the absence of exams to calculate delta urea and the express order of "do-not-resuscitate". Data were collected from the electronic medical records. Serum admission urea and urea 24 hours before IHCA were also collected and used to calculate delta urea., Results: A total of 504 patients were evaluated; 125 patients were excluded due to the absence of variables to calculate delta urea and 5 due to "do-not-resuscitate" order. Thus, we included 374 patients in the analysis. The mean age was 65.0 ± 14.5 years, 48.9% were male, 45.5% had ROSC, and in-hospital mortality was 91.7%. In logistic regression models, ROSC was associated with lower urea levels 24 hours before IHCA (OR: 0.996; CI95%: 0.992-1.000; p: 0.032). In addition, increased levels of urea 24 hours before IHCA (OR: 1.020; CI95%: 1.008-1.033; p: 0.002) and of delta urea (OR: 1.001; CI95%: 1.001-1.019; p: 0.023) were associated with in-hospital mortality. ROC curve analysis showed that the area under the ROC curve for mortality prediction was higher for urea 24 hours before IHCA (Cutoff > 120.1 mg/dL) than for delta urea (Cutoff > 34.83 mg/dL)., Conclusions: In conclusion, increased serum urea levels during hospital stay were associated with worse prognosis in IHCA., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Importance: Ventilator-associated pneumonia (VAP) frequently occurs in patients with cardiac arrest. Diagnosis of VAP after cardiac arrest remains challenging, while the use of current biomarkers such as C-reactive protein (CRP) or procalcitonin (PCT) is debated., Objectives: To evaluate biomarkers' impact in helping VAP diagnosis after cardiac arrest., Design Setting and Participants: This is a prospective ancillary study of the randomized, multicenter, double-blind placebo-controlled ANtibiotherapy during Therapeutic HypothermiA to pRevenT Infectious Complications (ANTHARTIC) trial evaluating the impact of antibiotic prophylaxis to prevent VAP in out-of-hospital patients with cardiac arrest secondary to shockable rhythm and treated with therapeutic hypothermia. An adjudication committee blindly evaluated VAP according to predefined clinical, radiologic, and microbiological criteria. All patients with available biomarker(s), sample(s), and consent approval were included., Main Outcomes and Measures: The main endpoint was to evaluate the ability of biomarkers to correctly diagnose and predict VAP within 48 hours after sampling. The secondary endpoint was to study the combination of two biomarkers in discriminating VAP. Blood samples were collected at baseline on day 3. Routine and exploratory panel of inflammatory biomarkers measurements were blindly performed. Analyses were adjusted on the randomization group., Results: Among 161 patients of the ANTHARTIC trial with available biological sample(s), patients with VAP ( n = 33) had higher body mass index and Acute Physiology and Chronic Health Evaluation II score, more unwitnessed cardiac arrest, more catecholamines, and experienced more prolonged therapeutic hypothermia duration than patients without VAP ( n = 121). In univariate analyses, biomarkers significantly associated with VAP and showing an area under the curve (AUC) greater than 0.70 were CRP (AUC = 0.76), interleukin (IL) 17A and 17C (IL17C) (0.74), macrophage colony-stimulating factor 1 (0.73), PCT (0.72), and vascular endothelial growth factor A (VEGF-A) (0.71). Multivariate analysis combining novel biomarkers revealed several pairs with p value of less than 0.001 and odds ratio greater than 1: VEGF-A + IL12 subunit beta (IL12B), Fms-related tyrosine kinase 3 ligands (Flt3L) + C-C chemokine 20 (CCL20), Flt3L + IL17A, Flt3L + IL6, STAM-binding protein (STAMBP) + CCL20, STAMBP + IL6, CCL20 + 4EBP1, CCL20 + caspase-8 (CASP8), IL6 + 4EBP1, and IL6 + CASP8. Best AUCs were observed for CRP + IL6 (0.79), CRP + CCL20 (0.78), CRP + IL17A, and CRP + IL17C., Conclusions and Relevance: Our exploratory study shows that specific biomarkers, especially CRP combined with IL6, could help to better diagnose or predict early VAP occurrence in cardiac arrest patients., Competing Interests: The authors have disclosed that they do not have any potential conflicts of interest., (Copyright © 2024 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of the Society of Critical Care Medicine.)

Introduction: Public training in cardiopulmonary resuscitation and treatment in emergency and intensive care unit have made tremendous progress. However, cardiac arrest remains a major health burden worldwide, with brain damage being a significant contributor to disability and mortality. Lipocalin-type prostaglandin D synthase (L-PGDS), which is mainly localised in the central nervous system, has been previously shown to inhibit postischemia neuronal apoptosis. Therefore, we aim to observe whether serum L-PGDS can serve as a potential biomarker and explore its role in determining the severity and prognosis of patients who have achieved restoration of spontaneous circulation (ROSC)., Methods and Analysis: This is a prospective observational study. The participants (n = 60) who achieve ROSC will be distributed into two groups (non-survivor and survivor) based on 28-day survival. Healthy volunteers (n = 30) will be enrolled as controls. Each individual's relevant information will be extracted from Electronic Medical Record System in Xinhua Hospital, including demographic characteristics, clinical data, laboratory findings and so on. On days 1, 3 and 7 after ROSC, blood samples will be drawn and batch tested on the level of serum neuron-specific enolase, soluble protein 100β, L-PGDS, procalcitonin, tumour necrosis factor-alpha and interleukin-6. The cerebral performance category score was assessed on the 28th day after ROSC., Ethics and Dissemination: This study was performed with the approval of the Clinical Ethical Committee of Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine (Approval No. XHEC-C-2023-130-1). The results will be published in a peer-reviewed journal., Trial Registration Number: Chinese Clinical Trial Registry (ChiCTR2300078564)., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: In-hospital cardiac arrest (IHCA) continues to be associated with high morbidity and mortality. The objective of this study was to study the association of arterial carbon dioxide tension (PaCO2) on survival to discharge and favorable neurologic outcomes in adults with IHCA., Methods: The study population included 353 adults who underwent resuscitation from 2011 to 2019 for IHCA at an academic tertiary care medical center with arterial blood gas testing done within 24 hours of arrest. Outcomes of interest included survival to discharge and favorable neurologic outcome, defined as Glasgow outcome score of 4-5., Results: Of the 353 patients studied, PaCO2 classification included: hypocapnia (PaCO2 <35 mm Hg, n = 89), normocapnia (PaCO2 35-45 mm Hg, n = 151), and hypercapnia (PaCO2 >45 mm Hg, n = 113). Hypercapnic patients were further divided into mild (45 mm Hg < PaCO2 ≤55 mm Hg, n = 62) and moderate/severe hypercapnia (PaCO2 > 55 mm Hg, n = 51). Patients with normocapnia had the highest rates of survival to hospital discharge (52.3% vs. 32.6% vs. 30.1%, P < 0.001) and favorable neurologic outcome (35.8% vs. 25.8% vs. 17.9%, P = 0.005) compared those with hypocapnia and hypercapnia respectively. In multivariable analysis, compared to normocapnia, hypocapnia [odds ratio (OR), 2.06; 95% confidence interval (CI), 1.15-3.70] and hypercapnia (OR, 2.67; 95% CI, 1.53-4.66) were both found to be independently associated with higher rates of in-hospital mortality. Compared to normocapnia, while mild hypercapnia (OR, 2.53; 95% CI, 1.29-4.97) and moderate/severe hypercapnia (OR, 2.86; 95% CI, 1.35-6.06) were both independently associated with higher in-hospital mortality compared to normocapnia, moderate/severe hypercapnia was also independently associated with lower rates of favorable neurologic outcome (OR, 0.28; 95% CI, 0.11-0.73), while mild hypercapnia was not., Conclusions: In this prospective registry of adults with IHCA, hypercapnia noted within 24 hours after arrest was independently associated with lower rates of survival to discharge and favorable neurologic outcome., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Fibroblast Growth Factor 21 (FGF21) is a neuroprotective hormone induced by cold exposure that targets the β-klotho co-receptor. β-klotho is abundant in the newborn brain but decreases rapidly with age. RNA-Binding Motif 3 (RBM3) is a potent neuroprotectant upregulated by FGF21 in hypothermic conditions. We characterized serum FGF21 and RBM3 levels in patients enrolled in a prospective multi-center study of pediatric cardiac arrest (CA) via a secondary analysis of samples collected to evaluate brain injury biomarkers. Patients ( n  = 111) with remnant serum samples available from at least two of three available timepoints (0-24, 24-48 or 48-72 hours post-resuscitation) were included. Serum samples from 20 healthy controls were used for comparison. FGF21 was measured by Luminex and internally validated enzyme-linked immunoassay (ELISA). RBM3 was measured by internally validated ELISA. Of postarrest patients, 98 were managed with normothermia, while 13 were treated with therapeutic hypothermia (TH). FGF21 increased >20-fold in the first 24 hours postarrest versus controls (681 pg/mL [200-1864] vs. 29 pg/mL [15-51], n  = 99 vs. 19, respectively, p  < 0.0001, median [interquartile range]) with no difference in RBM3. FGF21 did not differ by sex, while RBM3 was increased in females versus males at 48-72 hours postarrest (1866 pg/mL [873-5176] vs. 1045 pg/mL [535-2728], n  = 40 vs. 54, respectively, p  < 0.05). Patients requiring extracorporeal membrane oxygenation (ECMO) postresuscitation had increased FGF21 versus those who did not at 48-72 hours (6550 pg/mL [1455-66,781] vs. 1213 pg/mL [480-3117], n  = 7 vs 74, respectively, p  < 0.05). FGF21 and RBM3 did not correlate (Spearman's rho = 0.004, p  = 0.97). We conclude that in a multi-center study of pediatric CA patients where normothermic targeted temperature management was largely used, FGF21 was markedly increased postarrest versus control and highest in patients requiring ECMO postresuscitation. RBM3 was sex-dependent. We provide a framework for future studies examining the effect of TH on FGF21 or use of FGF21 therapy after pediatric CA.

Background:  Post-cardiac arrest syndrome (PCAS) is a frequent complication following successful cardiopulmonary resuscitation and correlates with poor outcome. PCAS is characterized by an excessive inflammatory response to whole-body ischemia and reperfusion. Cytokine adsorption was suggested as an adjunctive treatment option for the removal of cytokines from the patients' blood to restore the physiological equilibrium of pro- and anti-inflammatory activity and thus mitigate hemodynamic instability and end-organ complications., Material and Methods:  To better understand the cellular effects of cytokine adsorption in patients receiving extracorporeal cardiopulmonary resuscitation (ECPR) after in- and out-of-hospital cardiac arrest, we compared the activation status of neutrophils, monocytes, and platelets as well as the formation of platelet-leukocyte complexes in intravenous whole blood samples from an exploratory subgroup ( n  = 24) from the randomized CYTER study., Result:  At 48 hours after initiation of ECPR, flow cytometry analyses did neither reveal significant differences in neutrophil (CD11b, CD66b, L-selectin, and PSGL-1) and monocyte (CD11b, L-selectin, and PSGL-1) surface molecule expression nor in circulating platelet-monocyte complexes between patients receiving cytokine adsorption and those without., Conclusion:  Data did not show a relevant effect of cytokine adsorption on neutrophil and monocyte activation during the first 48 hours after initiation of ECPR., Competing Interests: A.S. reports research grants and lecture fees and travel support from CytoSorbents and lecture fees from Novartis, both outside the submitted work. D.D. reports research grants, lecture fees, and travel support from CytoSorbents, all outside the submitted work., (Thieme. All rights reserved.)

Background: Stress hyperglycemia ratio (SHR) has shown a predominant correlation with transient adverse events in critically ill patients. However, there remains a gap in comprehensive research regarding the association between SHR and mortality among patients experiencing cardiac arrest and admitted to the intensive care unit (ICU)., Methods: A total of 535 patients with their initial ICU admission suffered cardiac arrest, according to the American Medical Information Mart for Intensive Care (MIMIC)-IV database. Patients were stratified into four categories based on quantiles of SHR. Multivariable Cox regression models were used to evaluate the association SHR and mortality. The association between SHR and mortality was assessed using multivariable Cox regression models. Subgroup analyses were conducted to determine whether SHR influenced ICU, 1-year, and long-term all-cause mortality in subgroups stratified according to diabetes status., Results: Patients with higher SHR, when compared to the reference quartile 1 group, exhibited a greater risk of ICU mortality (adjusted hazard ratio [aHR] = 3.029; 95% CI: 1.802-5.090), 1-year mortality (aHR = 3.057; 95% CI: 1.885-4.958), and long-term mortality (aHR = 3.183; 95% CI: 2.020-5.015). This association was particularly noteworthy among patients without diabetes, as indicated by subgroup analysis., Conclusion: Elevated SHR was notably associated with heightened risks of ICU, 1-year, and long-term all-cause mortality among cardiac arrest patients. These findings underscore the importance of considering SHR as a potential prognostic factor in the critical care management of cardiac arrest patients, warranting further investigation and clinical attention., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Lian, Xue, Lu and Zheng.)

Objective: Although the TyG index is a reliable predictor of insulin resistance (IR) and cardiovascular disease, its effectiveness in predicting major adverse cardiac events in hospitalized acute coronary syndrome (ACS) patients has not been validated in large-scale studies. In this study, we aimed to explore the association between the TyG index and the occurrence of MACEs during hospitalization., Methods: We recruited ACS patients from the CCC-ACS (Improving Cardiovascular Care in China-ACS) database and calculated the TyG index using the formula ln(fasting triglyceride [mg/dL] × fasting glucose [mg/dL]/2). These patients were classified into four groups based on quartiles of the TyG index. The primary endpoint was the occurrence of MACEs during hospitalization, encompassing all-cause mortality, cardiac arrest, myocardial infarction (MI), and stroke. We performed Cox proportional hazards regression analysis to clarify the correlation between the TyG index and the risk of in-hospital MACEs among patients diagnosed with ACS. Additionally, we explored this relationship across various subgroups., Results: A total of 101,113 patients were ultimately included, and 2759 in-hospital MACEs were recorded, with 1554 (49.1%) cases of all-cause mortality, 601 (21.8%) cases of cardiac arrest, 251 (9.1%) cases of MI, and 353 (12.8%) cases of stroke. After adjusting for confounders, patients in TyG index quartile groups 3 and 4 showed increased risks of in-hospital MACEs compared to those in quartile group 1 [HR = 1.253, 95% CI 1.121-1.400 and HR = 1.604, 95% CI 1.437-1.791, respectively; p value for trend < 0.001], especially in patients with STEMI or renal insufficiency. Moreover, we found interactions between the TyG index and age, sex, diabetes status, renal insufficiency status, and previous PCI (all p values for interactions < 0.05)., Conclusions: In patients with ACS, the TyG index was an independent predictor of in-hospital MACEs. Special vigilance should be exercised in females, elderly individuals, and patients with renal insufficiency., (© 2024. The Author(s).)

Aim: Extracorporeal cardiopulmonary resuscitation (ECPR) can be considered in selected patients with refractory cardiac arrest. Given the risk of patient futility and high resource utilisation, identifying ECPR candidates, who would benefit from this therapy, is crucial. Previous ECPR studies investigating lactate as a potential prognostic marker have been small and inconclusive. In this study, it was hypothesised that the lactate level (immediately prior to initiation of ECPR) and lactate clearance (within 24 hours after ECPR initiation) are predictors of one-year survival in a large, multicentre study cohort of ECPR patients., Methods: Adult patients with refractory cardiac arrest at three German and four Danish tertiary cardiac care centres between 2011 and 2021 were included. Pre-ECPR lactate and 24-hour lactate clearance were divided into three equally sized tertiles. Multivariable logistic regression analyses and Kaplan-Meier analyses were used to analyse survival outcomes., Results: 297 adult patients with refractory cardiac arrest were included in this study, of which 65 (22%) survived within one year. The pre-ECPR lactate level and 24-hour lactate clearance were level-dependently associated with one-year survival: OR 5.40 [95% CI 2.30-13.60] for lowest versus highest pre-ECPR lactate level and OR 0.25 [95% CI 0.09-0.68] for lowest versus highest 24-hour lactate clearance. Results were confirmed in Kaplan-Meier analyses (each p log rank < 0.001) and subgroup analyses., Conclusion: Pre-ECPR lactate levels and 24 hour-lactate clearance after ECPR initiation in patients with refractory cardiac arrest were level-dependently associated with one-year survival. Lactate is an easily accessible and quickly available point-of-care measurement which might be considered as an early prognostic marker when considering initiation or continuation of ECPR treatment., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)

Objective: Mortality and morbidity rates are very high in patients admitted to the Intensive Care Unit (ICU) after cardiac arrest. In this study, we aimed to determine the mortality rates, risk factors, and predictive factors for mortality in post-cardiac arrest patients admitted to the ICU., Patients and Methods: Following approval from the Ethics Committee, we conducted a retrospective review of patient files for individuals over the age of 18 who received treatment for cardiac arrest in the ICU from January 2017 to June 2020. Demographic data of the patients, comorbidities, arrest location, etiology of arrest, duration of hospitalization, CPR duration, APACHE 2 scores, pH and HCO3 measurements in initial blood gases, lactate levels (1st, 6th, 12th, 24th hour), change in lactate levels (24-1), rate of lactate change, procalcitonin (PRC) levels (1st and 24th hour), change in PRC levels (24-1), rate of PRC change, and blood glucose levels were recorded. The patients were divided into two groups (survivors and non-survivors groups)., Results: 151 patients were included in the study. pH and HCO3 levels were lower in the non-survivors group than in the survivors group. Initial PRC levels were similar in both groups, but the 24th-hour PRC levels were higher, and the changes in PRC levels in the first 24 hours were greater in the non-survivors group. The lactate changes in the first 24 hours were higher in the non-survivors group. The receiver operating characteristic (ROC) curve showed that the HCO3 levels, 1st-, 6th-, 12th-, and 24th-hour lactate levels, and changes in lactate levels had predictability for mortality. In logistic regression analysis, we found that high 24th-hour lactate levels and changes in lactate levels were independent risk factors for mortality., Conclusions: Considering PRC and lactate levels, along with clinical examination and laboratory findings, may improve the accuracy of determining the prognosis of patients experiencing cardiac arrest.

Objectives: Cardiac arrest and subsequent resuscitation have been shown to deplete plasma phospholipids. This depletion of phospholipids in circulating plasma may contribute to organ damage postresuscitation. Our aim was to identify the diminishment of essential phospholipids in postresuscitation plasma and develop a novel therapeutic approach of supplementing these depleted phospholipids that are required to prevent organ dysfunction postcardiac arrest, which may lead to improved survival., Design: Clinical case control study followed by translational laboratory study., Setting: Research institution., Patients/subjects: Adult cardiac arrest patients and male Sprague-Dawley rats., Interventions: Resuscitated rats after 10-minute asphyxial cardiac arrest were randomized to be treated with lysophosphatidylcholine specie or vehicle., Measurements and Main Results: We first performed a phospholipid survey on human cardiac arrest and control plasma. Using mass spectrometry analysis followed by multivariable regression analyses, we found that plasma lysophosphatidylcholine levels were an independent discriminator of cardiac arrest. We also found that decreased plasma lysophosphatidylcholine was associated with poor patient outcomes. A similar association was observed in our rat model, with significantly greater depletion of plasma lysophosphatidylcholine with increased cardiac arrest time, suggesting an association of lysophosphatidylcholine levels with injury severity. Using a 10-minute cardiac arrest rat model, we tested supplementation of depleted lysophosphatidylcholine species, lysophosphatidylcholine(18:1), and lysophosphatidylcholine(22:6), which resulted in significantly increased survival compared with control. Furthermore, the survived rats treated with these lysophosphatidylcholine species exhibited significantly improved brain function. However, supplementing lysophosphatidylcholine(18:0), which did not decrease in the plasma after 10-minute cardiac arrest, had no beneficial effect., Conclusions: Our data suggest that decreased plasma lysophosphatidylcholine is a major contributor to mortality and brain damage postcardiac arrest, and its supplementation may be a novel therapeutic approach., Competing Interests: Dr. Kim’s institution received funding from the Zoll Foundation. Dr. Becker’s institution received funding from Philips, United Therapeutics, and Nihon Kohden; he received funding from ZOLL Medical, the National Institutes of Health, PCORI, and BrainCool. The remaining authors have disclosed that they do not have any potential conflicts of interest., (Copyright © 2021 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.)

Abstract: Previous studies found that high red cell distribution width (RDW) value is associated with poor outcomes among out-of-hospital cardiac arrest survivors. The aim of this study was to investigate whether post-ROSC RDW value was associated with survival and neurological outcomes of in-hospital cardiac arrest (IHCA) patients achieving return of spontaneous circulation (ROSC) but remaining critically ill.This retrospective single-center observational study included IHCA adults with sustained ROSC between January 1, 2017 and January 1, 2021 at an academic medical center in China. PostROSC RDW values were measured within 1 hour after sustained ROSC. The primary outcome was survival to hospital discharge and the secondary outcome was favorable neurological outcome at hospital discharge. The associations between postROSC RDW value and outcomes among IHCA patients with ROSC were evaluated by using multivariate logistic regression.A total of 730 patients with sustained ROSC following IHCA were ultimately included in this study. Of whom 194 (26.6%) survived to hospital discharge and 116 (15.9%) had a favorable neurological outcome at hospital discharge. In multivariable logistic regression analysis, lower postROSC RDW value was independently associated with survival to hospital discharge (odds ratio 0.19, 95% confidence interval 0.15-0.63, P = .017, cut-off value: 15.5%) and favorable neurological outcome at hospital discharge (odds ratio 0.23, 95% confidence interval 0.07-0.87, P < .001, cut-off value: 14.6%). Other independent factors including younger age, initial shockable rhythm, shorter total cardiopulmonary resuscitation duration and post-ROSC percutaneous coronary intervention were also associated with survival to hospital discharge. Regarding favorable neurological outcome at hospital discharge, significant variables other than the aforementioned factors included postROSC targeted temperature management and absence of pre-existing neurological insufficiency.Low postROSC RDW value was associated with survival to hospital discharge and favorable neurological outcome at hospital discharge., Competing Interests: The authors have no conflicts of interests to disclose., (Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.)

Background: Patients with cardiogenic shock or cardiac arrest undergoing venoarterial extracorporeal membrane oxygenation (V-A ECMO) frequently present with blood glucose levels out of normal range. The clinical relevance of such findings in the context of V-A ECMO is unknown. We therefore investigated the prognostic relevance of blood glucose at time of cannulation for V-A ECMO., Methods: We conducted a single-center retrospective registry study. All patients receiving V-A ECMO from October 2010 to January 2020 were included if blood glucose level at time of cannulation were documented. Patients were divided in five groups according to the initial blood glucose level ranging from hypoglycemic (< 80 mg/dl), normoglycemic (80-140 mg/dl), to mild (141-240 mg/dl), moderate (241-400 mg/dl), and severe (> 400 mg/dl) hyperglycemia, respectively. Clinical presentation, arterial blood gas analysis, and survival were compared between the groups., Results: 392 patients met inclusion criteria. Median age was 62 years (51.5-70.0), SAPS II at admission was 54 (43.5-63.0), and 108/392 (27.6%) were female. 131/392 were discharged alive (hospital survival 33.4%). At time of cannulation, survivors had higher pH, hemoglobin, calcium, bicarbonate but lower potassium and lactate levels compared to non-survivors (all p < 0.01). Outcome of patients diagnosed with particularly high (> 400 mg/dl) and low (< 80 mg/dl) blood glucose at time of V-A ECMO cannulation, respectively, was worse compared to patients with normoglycemic, mildly or moderately elevated values (p = 0.02). Glucose was independently associated with poor outcome after adjustment for other predictors of survival and persisted in all investigated subgroups., Conclusion: Arterial blood glucose at time of V-A ECMO cannulation predicts in-hospital survival of patients with cardiac shock or after ECPR. Whether dysglycemia represents a potential therapeutic target requires further evaluation in prospective studies., (© 2021. The Author(s).)

Background: Extracellular cold-inducible RNA-binding protein (eCIRP) acting as a novel damage-associated molecular pattern molecule promotes systemic inflammatory responses, including neuroinflammation in cerebral ischemia. We aimed to observe the changes of serum eCIRP and evaluate whether the increased serum eCIRP was associated with the severity and prognosis in patients with restoration of spontaneous circulation (ROSC)., Methods: A total of 73 patients after ROSC were divided into non-survivor (n = 48) and survivor (n = 25) groups based on 28-day survival. Healthy volunteers (n = 25) were enrolled as controls. Serum eCIRP, procalcitonin (PCT), the pro-inflammatory mediators tumor necrosis factor (TNF)-α, interleukin-6 (IL)-6 and high mobility group protein (HMGB1), the neurological damage biomarkers neuron-specific enolase (NSE), and soluble protein 100β (S100β) were measured on days 1, 3, and 7 after ROSC. Clinical data and laboratory findings were collected, and the Sequential Organ Failure Assessment (SOFA) score and Acute Physiology and Chronic Health Evaluation (APACHE II) were calculated concurrently. Cerebral performance category scores on day 28 after ROSC were recorded., Results: Serum eCIRP, IL-6, TNF-α, PCT, and HMGB1, NSE and S100β were significantly increased within the first week after ROSC. The increased levels of eCIRP were positively correlated with IL-6, TNF-α, lactate, NSE, S100β, CPR time, SOFA score, APACHE II score, and HMGB1 after ROSC. Serum eCIRP on days 1, 3, and 7 after ROSC could predict 28-day mortality and neurological prognosis. Serum eCIRP on day 3 after ROSC had a biggest AUC [0.862 (95% CI: 0.741-0.941)] for 28-day mortality and a biggest AUC [0.807 (95% CI: 0.630-0.981)] for neurological prognosis., Conclusions: Systemic inflammatory response with increased serum eCIRP occurred in patients after ROSC. Increased eCIRP level was positively correlated with the aggravation of systemic inflammatory response and the severity after ROSC. Serum eCIRP serves as a potential predictor for 28-day mortality and poor neurological prognosis after ROSC., Competing Interests: The authors report no conflicts of interest., (Copyright © 2020 by the Shock Society.)

Primary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p < 0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96 h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (score 0.3 ± 0.5 vs. 1.3 ± 0.5, p < 0.05) and hippocampal microglial activation (6 ± 3 vs. 22 ± 4%, p < 0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (2[1-3] vs. 21[16-52] ng/mL, p < 0.01). In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection.

We investigated whether combining the pre-arrest serum albumin level could improve the performance of the Good Outcome Following Attempted Resuscitation (GO-FAR) score for predicting neurologic outcomes in in-hospital cardiac arrest patients. Adult patients who were admitted to a tertiary care hospital between 2013 and 2017 were assessed. Their pre-arrest serum albumin levels were measured within 24 h before the cardiac arrest. According to albumin levels, the patients were divided into quartiles and were assigned 1, 0, 0, and, - 2 points. Patients were allocated to the derivation (n = 419) and validation (n = 444) cohorts. The proportion of favorable outcome increased in a stepwise manner across increasing quartiles (p for trend < 0.018). Area under receiver operating characteristic curve (AUROC) of the albumin-added model was significantly higher than that of the original GO-FAR model (0.848 vs. 0.839; p = 0.033). The results were consistent in the validation cohort (AUROC 0.799 vs. 0.791; p = 0.034). Net reclassification indices of the albumin-added model were 0.059 (95% confidence interval [CI] - 0.037 to 0.094) and 0.072 (95% CI 0.013-0.132) in the derivation and validation cohorts, respectively. An improvement in predictive performance was found by adding the ordinal scale of pre-arrest albumin levels to the original GO-FAR score.

Background: Lactate is a prognostic marker in critically ill patients, although currently available illness severity scores do not include lactate as a predictive parameter. We sought to describe the association between lactate and hospital mortality in patients admitted to the cardiac intensive care unit (CICU) with cardiac arrest (CA) and shock., Methods: Retrospective observational analysis of Mayo Clinic CICU patients admitted from 2007 to 2018 with measured lactate on admission, including patients with and without CA or shock. We examined hospital mortality as a function of admission lactate in patients. Multivariable logistic regression was used to determine predictors of hospital mortality., Results: We included 3,042 patients with a median age of 70 years (IQR 60-80), including 41% females, 26% with CA, and 39% with shock. The median APACHE-IV predicted mortality was 24% (IQR 11-51%), and the median admission lactate was 1.8 mmol/L (IQR 1.1-3.0). Hospital mortality occurred in 23% of patients and rose progressively with higher admission lactate, including in patients with and without CA or shock. After multivariable adjustment for clinical characteristics, therapies, and illness severity, a higher lactate remained associated with increased hospital mortality (adjusted OR 1.13 per mmol/L, 95% CI 1.06-1.20, P < 0.001)., Conclusions: Admission lactate levels are strongly associated with increased hospital mortality among CICU patients, including those with and without CA or shock. The prognostic value of lactate levels is independent of established ICU prognostic scores and dependent on admission diagnosis, which may help inform clinicians caring for CICU patients., Competing Interests: The authors report no conflicts of interest., (Copyright © 2020 by the Shock Society.)

Coagulation abnormalities after successful resuscitation from cardiac arrest may be associated with unfavorable neurologic outcome. We investigated a potential association of activated partial thromboplastin time (aPTT) with neurologic outcome in adult cardiac arrest survivors. Therefore, we included all adults ≥18 years of age who suffered a nontraumatic cardiac arrest and had achieved return of spontaneous circulation between January 2013 and December 2018. Patients receiving anticoagulants or thrombolytic therapy and those subjected to extracorporeal membrane oxygenation support were excluded. Routine blood sampling was performed on admission as soon as a vascular access was available. The primary outcome was 30-day neurologic function, assessed by the Cerebral Performance Category scale (3-5 = unfavorable neurologic function). Multivariable regression was used to assess associations between normal (≤41 seconds) and prolonged (>41 seconds) aPTT on admission (exposure) and the primary outcome. Results are given as odds ratio (OR) with 95% confidence intervals (95% CIs). Out of 1,591 cardiac arrest patients treated between 2013 and 2018, 360 patients (32% female; median age: 60 years [interquartile range: 48-70]) were eligible for analysis. A total of 263 patients (73%) had unfavorable neurologic function at day 30. aPTT prolongation >41 seconds was associated with a 190% increase in crude OR of unfavorable neurologic function (crude OR: 2.89; 95% CI: 1.78-4.68, p  < 0.001) and with more than double the odds after adjustment for traditional risk factors (adjusted OR: 2.01; 95% CI: 1.13-3.60, p  = 0.018). In conclusion, aPTT prolongation on admission is associated with unfavorable neurologic outcome after successful resuscitation from cardiac arrest., Competing Interests: None declared., (Thieme. All rights reserved.)

Background: Critically ill patients with cardiogenic shock could benefit from ventricular assist device support using the Impella microaxial blood pump. However, recent studies suggested Impella not to improve outcomes. We, therefore, evaluated outcomes and predictors in a real-world scenario., Methods: In this retrospective single-center trial, 125 patients suffering from cardiac arrest/cardiogenic shock between 2008 and 2018 were analyzed. 93 Patients had a prior successful cardiopulmonary resuscitation. The primary endpoint was hospital mortality. Associations of covariates with the primary endpoint were assessed by univariable and multivariable logistic regression. Adjusted odds ratios (aOR) and optimal cut-offs (using Youden index) were obtained., Results: Hospital mortality was high (81%). Baseline lactate was 4.7mmol/L [IQR = 7.1mmol/L]. In multivariable logistic regression, only age (aOR 1.13 95%CI 1.06-1.20; p<0.001) and lactate (aOR 1.23 95%CI 1.004-1.516; p = 0.046) were associated with hospital mortality, and the respective optimal cut-offs were >3.3mmol/L and age >66 years. Patients were retrospectively stratified into three risk groups: Patients aged ≤66 years and lactate ≤3.3mmol (low-risk; n = 22); patients aged >66 years or lactate >3.3mmol/L (medium-risk; n = 52); and patients both aged >66 years and lactate >3.3mmol/L (high-risk, n = 51). Risk of death increased from 41% in the low-risk group, to 79% in the medium risk group and 100% in the high-risk group. The predictive abilities of this model were high (AUC 0.84; 95% 0.77-0.92)., Conclusion: Mortality was high in this real-world collective of severely ill cardiogenic shock patients. Better patient selection is warranted to avoid unethical use of Impella. Age and lactate might help to improve patient selection., Competing Interests: The authors have declared that no competing interests exist.

Objectives: Neuron-specific enolase (NSE) is frequently used to predict neurological outcomes in patients with hypoxic brain injury. Hanging can cause hypoxic brain damage, and survivors can suffer from neurological deficits that may impair daily activities. Here, we investigated the utility of the initial serum NSE level as a predictor of neurological outcomes in near-hanging patients with decreased consciousness., Methods: This retrospective multicenter study was conducted in patients who visited the emergency department due to near-hanging injury from October 2013 to February 2019 at three university hospitals in Korea. They were divided into two groups according to the presence of out-of-hospital cardiac arrest. The neurological outcome was determined using the Cerebral Performance Category (CPC) measured at the time of discharge. Multivariate analysis was performed to determine whether initial serum NSE is an independent predictor of neurological outcome., Results: Of the 70 patients included in the study, 44 showed a poor neurological outcome (CPC score = 3-5). Among the 52 patients with cardiac arrest, only 10 (19.2%) were discharged with good neurological outcome (CPC score = 1-2). In the whole cohort, a high serum NSE level was a significant predictor of poor neurological outcome (odds ratio [OR], 1.343; 95% confidence interval [CI], 1.003-1.800, p = 0.048). Among the patients with cardiac arrest, a high serum NSE level was a significant predictor of poor neurological outcome (OR, 1.138; 95% CI, 1.009-1.284, p = 0.036)., Conclusions: In near-hanging patients, a high initial serum NSE level is an independent predictor of poor neurological outcome., Competing Interests: The authors have declared that no competing interests exist.

Background: Current post-resuscitation guidelines recommend oxygen titration in adults with the return of spontaneous circulation after cardiac arrest. However, the optimal peripheral oxygen saturation (SpO 2 ) is still unclear for post-cardiac arrest care., Methods: We conducted a retrospective observational study of prospectively collected data of all cardiac arrest patients admitted to the intensive care units between 2014 and 2015. The main exposure was SpO 2 , which were interfaced from bedside vital signs monitors as 1-min averages, and archived as 5-min median values. The proportion of time spent in different SpO 2 categories was included in separate multivariable regression models along with covariates. The primary outcome measure was hospital mortality and the proportion of discharged home as the secondary outcome was reported., Results: 2836 post-cardiac arrest patients in ICUs of 156 hospitals were included. 1235 (44%) patients died during hospitalization and 818 (29%) patients discharged home. With multivariate regression analysis, the proportion of time spent in SpO 2 of ≤89%, 90%, 91%, and 92% were associated with higher hospital mortality. The proportion of time spent in SpO 2 of 95%, 96%, and 97% were associated with a higher proportion of discharged home outcome, but not associated with hospital mortality., Conclusions: In this retrospective observational study, the optimal SpO 2 for patients admitted to the intensive care unit after cardiac arrest may be 95-97%. Further investigation is warranted to determine if targeting SpO 2 of 95-97% would improve patient-centered outcomes after cardiac arrest., Competing Interests: Declaration of competing interest None of the authors has declared a conflict of interest., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Background: A recent study found serum neurofilament light chain (NfL) levels to be strongly associated with poor neurological outcome in patients after cardiac arrest. Our aim was to confirm these findings in an independent validation study and to investigate whether NfL improves the prognostic value of two cardiac arrest-specific risk scores., Methods: This prospective, single-center study included 164 consecutive adult after out-of-hospital cardiac arrest (OHCA) patients upon intensive care unit admission. We calculated two clinical risk scores (OHCA, CAHP) and measured NfL on admission within the first 24 h using the single molecule array NF-light ® assay. The primary endpoint was neurological outcome at hospital discharge assessed with the cerebral performance category (CPC) score., Results: Poor neurological outcome (CPC > 3) was found in 60% (98/164) of patients, with 55% (91/164) dying within 30 days of hospitalization. Compared to patients with favorable outcome, NfL was 14-times higher in patients with poor neurological outcome (685 ± 1787 vs. 49 ± 111 pg/mL), with an adjusted odds ratio of 3.4 (95% CI 2.1 to 5.6, p < 0.001) and an area under the curve (AUC) of 0.82. Adding NfL to the clinical risk scores significantly improved discrimination of both the OHCA score (from AUC 0.82 to 0.89, p < 0.001) and CAHP score (from AUC 0.89 to 0.92, p < 0.05). Adding NfL to both scores also resulted in significant improvement in reclassification statistics with a Net Reclassification Index (NRI) of 0.58 (p < 0.001) for OHCA and 0.83 (p < 0.001) for CAHP., Conclusions: Admission NfL was a strong outcome predictor and significantly improved two clinical risk scores regarding prognostication of neurological outcome in patients after cardiac arrest. When confirmed in future outcome studies, admission NfL should be considered as a standard laboratory measures in the evaluation of OHCA patients.

Accumulating evidence demonstrated that administration of ω-3 polyunsaturated fatty acid (ω-3 PUFA) or ascorbic acid (AA) following cardiac arrest (CA) improves survival. Therefore, we investigate the effects of ω-3 PUFA combined with AA on myocardial function after CA and cardiopulmonary resuscitation (CPR) in a rat model. Thirty male rats were randomized into 5 groups: (1) sham; (2) control; (3) ω-3 PUFA; (4) AA; (5) ω-3 PUFA + AA. Ventricular fibrillation (VF) was induced and untreated for 6 min followed by defibrillation after 8 min of CPR. Infusion of drug or vehicle occurred at the start of CPR. Myocardial function and sublingual microcirculation were measured at baseline and after return of spontaneous circulation (ROSC). Heart tissues and blood were collected 6 h after ROSC. Myocardial function and sublingual microcirculation improvements were seen with ω-3 PUFA or AA compared to control after ROSC (p < 0.05). ω-3 PUFA + AA shows a better myocardial function than ω-3 PUFA or AA (p < 0.05). ω-3 PUFA or AA decreases pro-inflammatory cytokines, cTnI, myocardium malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) modified proteins compared to control (p < 0.05). ω-3 PUFA and AA combined have lower MDA and 4-HNE modified proteins than alone (p < 0.05). ω-3 PUFA or AA treatment reduces the severity of post-resuscitation myocardial dysfunction, improves sublingual microcirculation, decreases lipid peroxidation and systemic inflammation in the early phase of recovery following CA and resuscitation. A combination of ω-3 PUFA and AA treatment confers an additive effect in suppressing lipid peroxidation and improving myocardial function., (Copyright © 2020 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Early prognostication of neurological outcome in comatose patients after cardiac arrest (CA) is vital for clinicians when assessing the survival time of sufferers and formulating appropriate treatment strategies to avoid the withdrawal of life-sustaining treatment (WLST) from patients. However, there is still a lack of sensitive and specific serum biomarkers for early and accurate identification of these patients. Using an isobaric tag for relative and absolute quantitation (iTRAQ)-based proteomic approach, we discovered 55 differentially expressed proteins, with 39 up-regulated secreted serum proteins and 16 down-regulated secreted serum proteins between three comatose CA survivors with good versus poor neurological recovery. Then, four proteins were selected and were validated via an enzyme-linked immunosorbent assay (ELISA) approach in a larger-scale sample containing 32 good neurological outcome patients and 46 poor neurological outcome patients, and it was confirmed that serum angiotensinogen (AGT) and alpha-1-antitrypsin (SERPINA1) were associated with neurological function and prognosis in CA survivors. A prognostic risk score was developed and calculated using a linear and logistic regression model based on a combination of AGT, SERPINA1 and neuron-specific enolase (NSE) with an area under the curve of 0.865 (P < .001), and the prognostic risk score was positively correlated with the CPC value (R = 0.708, P < .001). We propose that the results of the risk score assessment not only reveal changes in biomarkers during neurological recovery but also assist in enhancing current therapeutic strategies for comatose CA survivors., (© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Takotsubo cardiomyopathy (TTC) is a rare but life-threatening condition that is still not completely understood. Characterised by rapidly reversible ventricular dysfunction without any prior coronary artery disease, it can imitate a myocardial infarction and lead to death if not managed appropriately. This report examines a case of intraoperative cardiac arrest in a patient with no previous cardiac disease, and discusses the factors that may have precipitated this event, as well as the ways of distinguishing the cause of the arrest based on clinical course and investigations, eventually leading to a diagnosis of TTC., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Cardiac arrest (CA) is a leading cause of mortality worldwide. Most of post-resuscitation related deaths are due to post-cardiac arrest syndrome (PCAS). After cardiopulmonary resuscitation (CPR), return of spontaneous circulation (ROSC) leads to renal ischemia-reperfusion injury, also known as PCAS. Many studies have focused on brain and heart injuries after ROSC, but renal failure has largely been ignored. Therefore, we investigated the protective effects of therapeutic hypothermia (TH) on asphyxial CA-induced renal injury in rats. Thirty rats were randomly divided into five groups: 1) the control group (sham); 2) the normothermic CA (nor.); 3) a normothermic CA group that received TH immediately within 2 h after CPR (Hypo. 2 hrs); 4) a normothermic CA group that received TH within 4 h after CPR (Hypo. 4 hrs); and 5) a normothermia CA group that received TH within 6 h after CPR (Hypo. 6 h). One day after CPR, all rats were sacrificed. Compared with the normothermic CA group, the TH groups demonstrated significantly increased survival rate (P < 0.05); decreased serum blood urea nitrogen, creatinine, and lactate dehydrogenase levels; and lower histological damage degree and malondialdehyde concentration in their renal tissue. Terminal deoxynucleotidyl transferase dUTP nick end labeling stain revealed that the number of apoptotic cells significantly decreased after 4 h and 6 h of TH compared to the results seen in the normothermic CA group. Moreover, TH downregulated the expression of cyclooxygenase-2 in the renal cortex compared to the normothermic CA group one day after CPR. These results suggest that TH exerts anti-apoptotic, anti-inflammatory, and anti-oxidative effects immediately after ROSC that protect against renal injury., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Background Total liquid ventilation (TLV) has been shown to prevent neurological damage though ultrafast cooling in animal models of cardiac arrest. We investigated whether its neuroprotective effect could be explained by mitigation of early inflammatory events. Methods and Results Rabbits were submitted to 10 minutes of ventricular fibrillation. After resuscitation, they underwent normothermic follow-up (control) or ultrafast cooling by TLV and hypothermia maintenance for 3 hours (TLV). Immune response, survival, and neurological dysfunction were assessed for 3 days. TLV improved neurological recovery and reduced cerebral lesions and leukocyte infiltration as compared with control (eg, neurological dysfunction score=34±6 versus 66±6% at day 1, respectively). TLV also significantly reduced interleukin-6 blood levels during the hypothermic episode (298±303 versus 991±471 pg/mL in TLV versus control at 3 hours after resuscitation, respectively), but not after rewarming (752±563 versus 741±219 pg/mL in TLV versus control at 6 hours after resuscitation, respectively). In vitro assays confirmed the high temperature sensitivity of interleukin-6 secretion. Conversely, TLV did not modify circulating high-mobility group box 1 levels or immune cell recruitment into the peripheral circulation. The link between interleukin-6 early transcripts (<8 hours) and neurological outcome in a subpopulation of the previously described Epo-ACR-02 (High Dose of Erythropoietin Analogue After Cardiac Arrest) trial confirmed the importance of this cytokine at the early stages as compared with delayed stages (>8 hours). Conclusions The neuroprotective effect of hypothermic TLV was associated with a mitigation of humoral interleukin-6 response. A temperature-dependent attenuation of immune cell reactivity during the early phase of the post-cardiac arrest syndrome could explain the potent effect of rapid hypothermia. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT00999583.

Cardiac arrest (CA) is a leading cause of death and there is a necessity for animal models that accurately represent human injury severity. We evaluated a rat model of severe CA injury by comparing plasma metabolic alterations to human patients. Plasma was obtained from adult human control and CA patients post-resuscitation, and from male Sprague-Dawley rats at baseline and after 20 min CA followed by 30 min cardiopulmonary bypass resuscitation. An untargeted metabolomics evaluation using UPLC-QTOF-MS/MS was performed for plasma metabolome comparison. Here we show the metabolic commonality between humans and our severe injury rat model, highlighting significant metabolic dysfunction as seen by similar alterations in (1) TCA cycle metabolites, (2) tryptophan and kynurenic acid metabolites, and (3) acylcarnitine, fatty acid, and phospholipid metabolites. With substantial interspecies metabolic similarity in post-resuscitation plasma, our long duration CA rat model metabolically replicates human disease and is a suitable model for translational CA research.

Natriuretic peptides (NPs) regulate blood pressure and fluid homeostasis and exert various effects on the cardiovascular system. Recently, the relationship between NPs and the energy metabolism has been reported, and using a cell culture experiment system, we previously showed that NP activated brown cells in a low temperature environment while also suppressing a decrease in the cell temperature. However, few reports have described the secretion of NPs in cold environments, and there have been almost no studies of B-type natriuretic peptide (BNP) in humans. We investigated how NPs respond to cold environments in 21 patients who underwent therapeutic hypothermia (TH) after cardiac arrest. The plasma BNP levels were significantly increased (more than fivefold) during TH (logarithmically from 1.98 ± 0.79 to 2.63 ± 0.59, P < 0.01). During TH, diastolic pulmonary artery pressure (PAP) significantly decreased, and there were no significant changes in the stroke volume index (SVI). This increase of BNP was not associated with any hemodynamic changes. In contrast to our findings for BNP, the change in A-type NP (ANP) was quite small. We detected a significant increase in the plasma BNP levels during TH, unrelated to hemodynamics. This elevation of BNP levels seems to be potential influenced by hypothermia.

Introduction: Elevated plasma levels of asymmetric dimethylarginine (ADMA), an inhibitor of NO synthase, are associated with adverse outcome. There is no data available, whether ADMA levels are associated with arrhythmic death (AD) in patients with ischemic cardiomyopathy (ICM) or non-ischemic, dilated cardiomyopathy (DCM)., Methods and Results: A total of 110 ICM, 52 DCM and 30 control patients were included. Primary outcome parameter of this prospective study was arrhythmic death (AD) or resuscitated cardiac arrest (RCA). Plasma levels of ADMA were significantly higher in ICM (p < 0.001) and in DCM (p < 0.001) patients compared to controls. During a median follow-up of 7.0 years, 62 (32.3%) patients died. AD occurred in 26 patients and RCA was observed in 22 patients. Plasma levels of ADMA were not associated with a significantly increased risk of AD or RCA in ICM (hazard ratio (HR) = 1.37, p = 0.109) or in DCM (HR = 1.06, p = 0.848) patients. No significant association was found with overall mortality in ICM (HR = 1.39, p = 0.079) or DCM (HR = 1.10, p = 0.666) patients. Stratified Kaplan-Meier curves for ADMA levels in the upper tertile (>0.715 µmol/l) or the two lower tertiles (≤0.715 µmol/l) did not show a higher risk for AD or RCA (p = 0.221) or overall mortality (p = 0.548). In patients with left ventricular ejection fraction ≤ 35%, ADMA was not associated with AD or RCA (HR = 1.35, p = 0.084) or with overall mortality (HR = 1.24, p = 0.162)., Conclusions: Plasma levels of ADMA were elevated in patients with ICM or DCM as compared to controls, but were not significantly predictive for overall mortality or the risk for arrhythmic death., (Copyright © 2020 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.)

Outcome prognostication after cardiac arrest (CA) is challenging. Current multimodal prediction approaches would benefit from new biomarkers. MicroRNAs constitute a novel class of disease markers and circulating levels of brain-enriched ones have been associated with outcome after CA. To determine whether these levels reflect the extent of brain damage in CA patients, we assessed their correlation with neuron-specific enolase (NSE), a marker of brain damage. Blood samples taken 48 h after return of spontaneous circulation from two groups of patients from the Targeted Temperature Management trial were used. Patients were grouped depending on their neurological outcome at six months. Circulating levels of microRNAs were assessed by sequencing. NSE was measured at the same time-point. Among the 673 microRNAs detected, brain-enriched miR9-3p, miR124-3p and miR129-5p positively correlated with NSE levels (all p < 0.001). Interestingly, these correlations were absent when only the good outcome group was analyzed ( p > 0.5). Moreover, these correlations were unaffected by demographic and clinical characteristics. All three microRNAs predicted neurological outcome at 6 months. Circulating levels of brain-enriched microRNAs are correlated with NSE levels and hence can reflect the extent of brain injury in patients after CA. This observation strengthens the potential of brain-enriched microRNAs to aid in outcome prognostication after CA.

Background This study investigated whether levosimendan, an inotropic calcium sensitizer, when combined with moderate therapeutic hypothermia, may exert synergistic benefits on post-cardiac arrest myocardial dysfunction and improve outcomes. Methods and Results After 9.5-minute asphyxia-induced cardiac arrest and resuscitation, 48 rats were randomized equally into 4 groups following return of spontaneous circulation (ROSC), including normothermia, hypothermia, normothermia-levosimendan, and hypothermia-levosimendan groups. For the normothermia group, the target temperature was 37°C while for the hypothermia group, the target temperature was 32°C, both of which were to be maintained for 4 hours after ROSC. Levosimendan was administered after ROSC with a loading dose of 10 μg/kg and then infused at 0.1 μg/kg per min for 4 hours. In the hypothermia-levosimendan group, left ventricular systolic function and cardiac output increased significantly, whereas the heart rate and systemic vascular resistance decreased significantly compared with the normothermia group. Also, the concentrations of interleukin 1β at 4 hours post-ROSC and the production of NO between 1 hour and 4 hours post-ROSC were reduced significantly in the hypothermia-levosimendan group compared with the normothermia group. The 72-hour post-ROSC survival and neurological recovery were also significantly better in the hypothermia-levosimendan group compared with the normothermia group (survival, 100% versus 50%, χ 2 test, P =0.006). Conclusions Compared with normothermia, only combined moderate therapeutic hypothermia and levosimendan treatment could consistently improve post-cardiac arrest myocardial dysfunction and decrease the release of pro-inflammatory molecules, thereby improving survival and neurological outcomes. These findings suggest synergistic benefits between moderate therapeutic hypothermia and levosimendan.

Background: Cardiac arrest is a tragic event that causes 1 death roughly every 90 seconds worldwide. Survivors generally undergo a workup to identify the cause of arrest. However, 5% to 10% of cardiac arrests remain unexplained. Because cardiac arrhythmias underlie most cardiac arrests and increasing evidence strongly supports the involvement of autoantibodies in arrhythmogenesis, a large-panel autoantibody screening was performed in patients with cardiac arrest., Methods: This is an observational, cross-sectional study of patients from the Montreal Heart Institute hospital cohort, a single-center registry of participants. A peptide microarray was designed to screen for immunoglobulin G targeting epitopes from all known cardiac ion channels with extracellular domains. Plasma samples from 23 patients with unexplained cardiac arrest were compared with those from 22 patients with cardiac arrest cases of ischemic origin and a group of 29 age-, sex-, and body mass index-matched healthy subjects. The false discovery rate, least absolute shrinkage and selection operator logistic regression, and random forest methods were carried out jointly to find significant differential immunoglobulin G responses., Results: The autoantibody against the pore domain of the L-type voltage-gated calcium channel was consistently identified as a biomarker of idiopathic cardiac arrest ( P =0.002; false discovery rate, 0.007; classification accuracies ≥0.83). Functional studies on human induced pluripotent stem cell-derived cardiomyocytes demonstrated that the anti-L-type voltage-gated calcium channel immunoglobulin G purified from patients with idiopathic cardiac arrest is proarrhythmogenic by reducing the action potential duration through calcium channel inhibition., Conclusions: The present report addresses the concept of autoimmunity and cardiac arrest. Hitherto unknown autoantibodies targeting extracellular sequences of cardiac ion channels were detected. Moreover, the study identified an autoantibody signature specific to patients with cardiac arrest.

Objective: After cardiac arrest (CA), epileptiform EEG, occurring in about 1/3 of patients, often but not invariably heralds poor prognosis. We tested the hypothesis that a combination of specific EEG features identifies patients who may regain consciousness despite early epileptiform patterns., Methods: We retrospectively analyzed a registry of comatose patients post-CA (2 Swiss centers), including those with epileptiform EEG. Background and epileptiform features in EEGs 12-36 hours or 36-72 hours from CA were scored according to the American Clinical Neurophysiology Society nomenclature. Best Cerebral Performance Category (CPC) score within 3 months (CPC 1-3 vs 4-5) was the primary outcome. Significant EEG variables were combined in a score assessed with receiver operating characteristic curves, and independently validated in a US cohort; its correlation with serum neuron-specific enolase (NSE) was also tested., Results: Of 488 patients, 107 (21.9%) had epileptiform EEG <72 hours; 18 (17%) reached CPC 1-3. EEG 12-36 hours background continuity ≥50%, absence of epileptiform abnormalities ( p < 0.00001 each), 12-36 and 36-72 hours reactivity ( p < 0.0001 each), 36-72 hours normal background amplitude ( p = 0.0004), and stimulus-induced discharges ( p = 0.0001) correlated with favorable outcome. The combined 6-point score cutoff ≥2 was 100% sensitive (95% confidence interval [CI], 78%-100%) and 70% specific (95% CI, 59%-80%) for CPC 1-3 (area under the curve [AUC], 0.98; 95% CI, 0.94-1.00). Increasing score correlated with NSE (ρ = -0.46, p = 0.0001). In the validation cohort (41 patients), the score was 100% sensitive (95% CI, 60%-100%) and 88% specific (95% CI, 73%-97%) for CPC 1-3 (AUC, 0.96; 95% CI, 0.91-1.00)., Conclusion: Prognostic value of early epileptiform EEG after CA can be estimated combining timing, continuity, reactivity, and amplitude features in a score that correlates with neuronal damage., (© 2020 American Academy of Neurology.)

Background: Systemic inflammation is an important feature of post-cardiac arrest syndrome (PCAS). This study was designed to determine whether the plasma concentrations of some circulating pro-inflammatory cytokines (interleukin-17 [IL-8], IL-22, IL-23 and IL-33) are of value in predicting the outcome of patients after return of spontaneous circulation (ROSC) during the post-cardiac arrest period., Methods: This was a prospective observational clinical study. In total, 21 patients (survivors, n = 10; non-survivors, n = 11) who experienced cardiac arrest and successful ROSC with expected survival of at least 7 days were consecutively enrolled from January 2016 to December 2017. Of the 21 enrolled patients, ten survived were designated "survivors". The other eleven patients died between 2 days and 1 months post ROSC. Venous blood was drawn at three time-points: baseline (< 1 h post ROSC), 2 days post ROSC and 7 days post ROSC. Plasma IL-8, IL-22, IL-23 and IL-33 were determined using commercial enzyme-linked immunosorbent assays., Results: Plasma creatinine levels, but aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, were elevated in non-survivors compared with survivors. Plasma levels of IL-17, IL-22, IL-23 and IL-33 of the 21 total patients did not change at 2 or 7 days post ROSC compared to baseline. In survivors, the plasma levels of IL-17 and IL-23 at 2 or 7 days post ROSC were lower than baseline. In non-survivors, plasma levels of IL-17 increased compared with baseline. Receiver operating characteristic curve analysis showed that the plasma levels of IL-17 and IL-23 at 2 or 7 days post ROSC were able to predict the mortality of PCAS patients, and positively correlated with Acute Physiology and Chronic Health Evaluation (APACHE)-II score and time to ROSC., Conclusion: These results provide the first evidence that the elevated plasma IL-17 and IL-23 levels are associated with poor outcome in PCAS patients. The role of IL-17/IL-23 axis post ROSC is worth paying attention to in PCAS patients., Trial Registration: Clinicaltrial.govNCT02297776, 2014-11-21.

This study aims to quantify the extent of electrolyte (potassium, magnesium, and phosphorus) and blood glucose changes during targeted temperature management (TTM), with insight on electrolyte replacements and insulin administration. This was a 3-year retrospective study of patients who underwent TTM via Arctic Sun. Electrolyte and blood glucose values in addition to electrolyte replacements and insulin administrations were collected before, during, and post-TTM. The primary analysis assessed changes in electrolyte and blood glucose values during and after TTM, and the secondary analysis assessed changes before and during, and before and after TTM. The secondary analysis also incorporated amount of electrolyte replacements and insulin administrations patients received before, during, and post-TTM. Sixty patients were included for analysis. Comparing levels during to after TTM, there was a significant increase in potassium (3.7 [0.7]-4.4 [0.7] mmol/L, p  < 0.001) and decrease in blood glucose (192 [135]-134 [55] mg/dL, p  = 0.001). Comparing levels before to during TTM, there was a significant decrease in potassium (4.3 [0.7]-3.7 [0.7] mmol/L, p  < 0.001) and phosphorus (4.8 [3.2]-3.4 [1.5] mg/dL, p  = 0.003). Comparing levels before to after TTM, there was a significant decrease in phosphorus (4.5 [2.9]-3.3 [1.2] mmol/L, p  = 0.026) and blood glucose (219 [35]-134 [55] mg/dL, p  < 0.001). Patients received on average potassium 102 mEq, magnesium 1.9 g, phosphorus 9 mmol, and insulin 94 units. Potassium significantly decreased during and significantly increased after TTM. Phosphorus significantly decreased during TTM and blood glucose significantly decreased after TTM. There were no significant changes in magnesium during the defined time period.

Introduction: Post-cardiac arrest syndrome (PCAS) is characterized by systemic ischemia/reperfusion injury, anoxic brain injury, and post-arrest myocardial dysfunction superimposed on a precipitating pathology. The role of inflammatory cytokines in cardiac arrest remains unclear., Aims: We aimed to describe, with an emphasis on clinical applications, what is known about the role of inflammatory cytokines in cardiac arrest., Data Sources: A PubMed literature review was performed for relevant articles. Only articles in English that studied cytokines in patients with cardiac arrest were included., Results: Cytokines play a crucial role in the pathogenesis of PCAS. Following cardiac arrest, the large release of circulating cytokines mediates the ischemia/reperfusion injury, brain dysfunction, and myocardial dysfunction seen. Interleukins, tumor necrosis factor, and matrix metalloproteinases all play a unique prognostic role in PCAS. High levels of inflammatory cytokines have been associated with mortality and/or poor neurologic outcomes. Interventions to modify the systemic inflammation seen in PCAS continue to be heavily studied. Currently, the only approved medical intervention for comatose patients following cardiac arrest is targeted temperature management. Medical agents, including minocycline and sodium sulfide, have demonstrated promise in animal models., Conclusions: The role of inflammatory cytokines for both short- and long-term outcomes is an important area for future investigation.

Background: Resuscitation guidelines list acidaemia as a potentially reversible cause of cardiac arrest without specifying the threshold defining acidaemia. We examined the association between early intra-arrest arterial blood gas (ABG) data and outcomes of in-hospital cardiac arrest (IHCA)., Methods: This single-centred retrospective study reviewed patients with IHCA between 2006 and 2015. Early intra-arrest ABG data were measured within 10 min of initiating cardiopulmonary resuscitation. The ABG analysis included measurements of blood pH, PaCO 2 , and HCO 3 - ., Results: Among the 1065 included patients, 60 (5.6%) achieved neurologically intact survival. Mean blood pH was 7.2. Mean PaCO 2 and HCO 3 - levels were 59.7 mmHg and 22.1 mmol/L, respectively. A blood pH of 7.2 was identified by a generalised additive models plot to define severe acidaemia. The PaCO 2 level was higher in patients with severe acidaemia (mean: 74.5 vs. 44.1 mmHg) than in those without. Multivariable logistic regression analyses indicated that blood pH > 7.2 was associated with a favourable neurological recovery (odds ratio [OR]: 2.79, 95% confidence interval [CI]: 1.43-5.46; p-value = 0.003) and blood pH was positively associated with survival at hospital discharge (OR: 5.80, 95% CI: 1.62-20.69; p-value = 0.007)., Conclusion: Early intra-arrest blood pH was associated with IHCA outcomes, while levels of PaCO 2 and HCO 3 - were not. A blood pH of 7.2 could be used as the threshold defining severe acidaemia during arrest and help profile patients with IHCA. Innovative interventions should be developed to improve the outcomes of patients with severe acidaemia, such as novel ventilation methods., (Copyright © 2019 Formosan Medical Association. Published by Elsevier B.V. All rights reserved.)