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Aim: To investigate how the inflammatory response after out-of-hospital cardiac arrest (OHCA) is modulated by blocking IL-6-mediated signalling with tocilizumab, and to relate induced changes to clinical status, myocardial- and brain injury. Methods: This is a preplanned substudy of the IMICA trial (ClinicalTrials.gov, NCT03863015). Upon admission 80 comatose OHCA patients were randomized to infusion of tocilizumab or placebo. Inflammation was characterized by a cytokine assay, CRP, and leukocyte differential count; myocardial injury by TnT and NT-proBNP; brain injury by neuron-specific enolase (NSE) and Neurofilament Light chain (NFL), while sequential organ assessment (SOFA) score and Vasoactive-Inotropic Score (VIS) represented overall clinical status. Results: Responses for IL-5, IL-6, IL-17, neutrophil as well as monocyte counts, and VIS were affected by tocilizumab treatment (all p < 0.05), while there was no effect on levels of NFL. IL-5 and IL-6 were substantially increased by tocilizumab, while IL-17 was lowered. Neutrophils and monocytes were lower at 24 and 48 hours, and VIS was lower at 24 hours, for the tocilizumab group compared to placebo. Multiple correlations were identified for markers of organ injury and clinical status versus inflammatory markers; this included correlations of neutrophils and monocytes with TnT, NSE, NFL, SOFA- and VIS score for the tocilizumab but not the placebo group. NT-proBNP, NFL and SOFA score correlated with CRP in both groups. Conclusions: Treatment with tocilizumab after OHCA modulated the inflammatory response with notable increases for IL-5, IL-6, and decreases for neutrophils and monocytes, as well as reduced vasopressor and inotropy requirements.

Aims Resuscitated out-of-hospital cardiac arrest (OHCA) patients who remain comatose after hospital arrival are at high risk of mortality due to anoxic brain injury. MicroRNA are small–non-coding RNA molecules ultimately involved in gene-silencing. They show promise as biomarkers, as they are stable in body fluids. The microRNA 9-3p (miR-9-3p) is associated with neurological injury in trauma and subarachnoid haemorrhage. Methods and results This post hoc analysis considered all 171 comatose OHCA patients from a single centre in the target temperature management (TTM) trial. Patients were randomized to TTM at either 33°C or 36°C for 24 h. MicroRNA-9-3p (miR-9-3p) was measured in plasma sampled at admission and at 28, 48, and 72 h. There were no significant differences in age, gender, and pre-hospital data, including lactate level at admission, between miR-9-3p level quartiles. miR-9-3p levels changed markedly following OHCA with a peak at 48 h. Median miR-9-3p levels between TTM 33°C vs. 36°C were not different at any of the four time points. Elevated miR-9-3p levels at 48 h were strongly associated with an unfavourable neurological outcome [OR: 2.21, 95% confidence interval (CI): 1.64–3.15, P Conclusion MiR-9-3p is strongly associated with neurological outcome following OHCA, and the levels of miR-9-3p are peaking 48 hours following cardiac arrest.

Hypothermia or Normothermia after Cardiac ArrestThis trial randomly assigned patients with coma after out-of-hospital cardiac arrest to undergo targeted hypothermia at 33 degrees C or normothermia with treatment of fever. At 6 months, there were no significant between-group differences regarding death or functional outcomes.BackgroundTargeted temperature management is recommended for patients after cardiac arrest, but the supporting evidence is of low certainty.MethodsIn an open-label trial with blinded assessment of outcomes, we randomly assigned 1900 adults with coma who had had an out-of-hospital cardiac arrest of presumed cardiac or unknown cause to undergo targeted hypothermia at 33 degrees C, followed by controlled rewarming, or targeted normothermia with early treatment of fever (body temperature, >= 37.8 degrees C). The primary outcome was death from any cause at 6 months. Secondary outcomes included functional outcome at 6 months as assessed with the modified Rankin scale. Prespecified subgroups were defined according to sex, age, initial cardiac rhythm, time to return of spontaneous circulation, and presence or absence of shock on admission. Prespecified adverse events were pneumonia, sepsis, bleeding, arrhythmia resulting in hemodynamic compromise, and skin complications related to the temperature management device.ResultsA total of 1850 patients were evaluated for the primary outcome. At 6 months, 465 of 925 patients (50%) in the hypothermia group had died, as compared with 446 of 925 (48%) in the normothermia group (relative risk with hypothermia, 1.04; 95% confidence interval [CI], 0.94 to 1.14; P=0.37). Of the 1747 patients in whom the functional outcome was assessed, 488 of 881 (55%) in the hypothermia group had moderately severe disability or worse (modified Rankin scale score >= 4), as compared with 479 of 866 (55%) in the normothermia group (relative risk with hypothermia, 1.00; 95% CI, 0.92 to 1.09). Outcomes were consistent in the prespecified subgroups. Arrhythmia resulting in hemodynamic compromise was more common in the hypothermia group than in the normothermia group (24% vs. 17%, PConclusionsIn patients with coma after out-of-hospital cardiac arrest, targeted hypothermia did not lead to a lower incidence of death by 6 months than targeted normothermia. (Funded by the Swedish Research Council and others; TTM2 ClinicalTrials.gov number, .)

Acute myocardial infarction complicated by cardiogenic shock (AMICS) comprises a heterogeneous population with high mortality. Insight in timing and cause of death may improve understanding of the condition and aid individualization of treatment. This was assessed in a retrospective, multicenter observational cohort study based on 1,716 patients with AMICS treated during the period of 2010 to 2017, of whom 904 died before hospital discharge. Patients with AMICS were identified through national registries and review of individual patients charts. In 904 patients with AMICS who died before hospital discharge (median age 72 years [interquartile range (IQR) 63 to 79], 70% men), 342 (38%) had suffered out-of-hospital cardiac arrest. The most frequent cause of death was primary cardiac (54%), whereas 24% died of neurologic injury, and 20% of multiorgan failure (MOF). Time to death was 13 hours (IQR 5 to 43) for heart failure; 140 hours (IQR 95 to 209) in neurologic injury; and 137 hours (IQR 59 to 321) in MOF, p

INTRODUCTION: Cardiac arrest patients presenting with back pain are at risk of not receiving the appropriate help when calling emergency medical services. In telephone consultations regarding patients with back pain preceding an out-of-hospital cardiac arrest, we investigated how communication between caller and call-taker influenced the call-taker's interpretation of back pain descriptions and decision-making about choice of response.METHOD: The study was conducted using 20 recorded phone calls from 17 patients who contacted the Copenhagen Emergency Medical Services (Denmark) reporting back pain up to 24 hours before an out-of-hospital cardiac arrest. Qualitative content analysis was applied.RESULTS: Two main categories emerged: (1) reasons, including subcategories: reported conditions, descriptions of conditions, patient's interpretation of condition and patient's own remedial actions; and (2) considerations, including subcategories: assessment of the severity, call-taker's interpretation of the condition, arguments for chosen response and conditions not facilitating further communication by the call-taker.CONCLUSION: In telephone consultations regarding patients with back pain preceding an out-of-hospital cardiac arrest the communication was influenced by the communicative preconditions of the call-taker. Communication in consultations where ambulances were not dispatched was characterized by complex descriptions of symptoms not easily fitting into the health system's interpretations of conditions warranting an urgent response.

International audience; Purpose: Prognostication of hypoxic-ischaemic brain injury after resuscitation from cardiac arrest is based on a multimodal approach including biomarker assays. Our goal was to assess whether plasma NSE helps to predict day-90 death or poor neurological outcome in patients resuscitated from cardiac arrest in non-shockable rhythm. Methods: All included patients participated in the randomised multicentre HYPERION trial. Serum blood samples were taken 24, 48, and 72 h after randomisation; pre-treated, aliquoted, and frozen at −80 °C at the study sites; and shipped to a central biology laboratory, where the NSE assays were performed. Primary outcome was neurological status at day 90 assessed by Cerebral Performance Category (1 or 2 versus. 3, 4 or 5). Results: NSE was assayed in 235 assessable blood samples from 101 patients. In patients with good versus poor outcomes, median NSE values at 24, 48, and 72 h were 22.6 [95%CI, 14.6;27.3] ng/mL versus 33.6 [20.5;90.0] ng/mL (p < 0.04), 18.1 [11.7;29.7] ng/mL versus 76.8 [21.5;206.6] ng/mL (p < 0.0029), and 9 [6.1;18.6] ng/mL versus 80.5 [22.9;236.1] ng/mL (p < 0.001), respectively. NSE at 48 and 72 h predicted the neurological outcome with areas under the receiver-operating curve of 0.79 [95%CI, 0.69;0.96] and 0.9 [0.81;0.96], respectively. NSE levels did not differ significantly between the groups managed at 33°C and 37°C (p = 0.59). Conclusions: Data from a multicentre trial on cardiac arrest with a non-shockable rhythm due to any cause confirm that NSE values at 72 h are associated with 90-day outcome. NSE levels did not differ significantly according to the targeted temperature. Registration Identifier: ClinicalTrial NCT02722473.

OBJECTIVES: To investigate the effects of the glucagon-like peptide-1 analog exenatide on blood glucose, lactate clearance, and hemodynamic variables in comatose, resuscitated out-of-hospital cardiac arrest patients. DESIGN: Predefined post hoc analyzes from a double-blind, randomized clinical trial. SETTING: The ICU of a tertiary heart center. PATIENTS: Consecutive sample of adult, comatose patients undergoing targeted temperature management after out-of-hospital cardiac arrest from a presumed cardiac cause, irrespective of the initial cardiac rhythm. INTERVENTIONS: Patients were randomized 1:1 to receive 6 hours and 15 minutes of infusion of either 17.4 μg of the glucagon-like peptide-1 analog exenatide (Byetta; Lilly) or placebo within 4 hours from sustained return of spontaneous circulation. The effects of exenatide were examined on the following prespecified covariates within the first 6 hours from study drug initiation: lactate level, blood glucose level, heart rate, mean arterial pressure, and combined dosage of norepinephrine and dopamine. MEASUREMENTS AND MAIN RESULTS: The population consisted of 106 patients receiving either exenatide or placebo. During the first 6 hours from study drug initiation, the levels of blood glucose and lactate decreased 17% (95% CI, 8.9-25%; p = 0.0004) and 21% (95% CI, 6.0-33%; p = 0.02) faster in patients receiving exenatide versus placebo, respectively. Exenatide increased heart rate by approximately 10 beats per minute compared to placebo (p < 0.0001). There was no effect of exenatide on other hemodynamic variables. CONCLUSIONS: In comatose out-of-hospital cardiac arrest patients, infusion with exenatide lowered blood glucose and resulted in increased clearance of lactate as well as increased heart rate. The clinical importance of these physiologic effects remains to be investigated.

Aim: To detect and quantify gasping during cardiopulmonary resuscitation (CPR) in out-of-hospital cardiac arrest (OHCA) patients and to investigate whether gasping is associated with increased return of spontaneous circulation (ROSC). Materials and methods: A prospective observational study in patients resuscitated and mechanically or manually ventilated for OHCA by emergency physicians of Ghent University Hospital. After intubation, pressure catheters were inserted in the endotracheal tube (ETT) and pressures were measured at the proximal and distal ends of the ETT. Gasping was analysed with custom-developed software and volumes were calculated based on pressure differences between the catheters. Data are expressed as median (interquartile range). Results: Data were collected in 292 resuscitated patients of whom 36.2% achieved ROSC. Seventy-six of 292 (26.0%) patients showed gasping on the pressure curves during resuscitation. The median gasping volume was 274 ml (196-434). The median gasping rate was 3.7 gasps/min (1.5-7.3). Gasping occurred significantly more in patients displaying ventricular fibrillation as the initial rhythm compared to patients with pulseless electrical activity, pulseless ventricular tachycardia or asystole. The median gasping rate was significantly higher in the ROSC group compared to the non-ROSC group (11.8 gasps/min (95% CI [4.2, 13.9]) and 2.8 gasps/min (95% CI [1.7, 3.9]) respectively (P < 0.001)). A gasping rate of > 7.3 gasps/min appeared to be the optimal criterion value to herald ROSC. Deeper negative pressures were associated with an increased incidence of ROSC (P = 0.011). There was no significant difference in ROSC between patients with gasping and those without. Conclusion: The occurrence of gasping during CPR was high. Significant gasping volumes were measured. The presence or absence of gasping was not associated with ROSC, but higher gasping rate and deeper negative pressures were. (C) 2017 Elsevier B.V. All rights reserved.