Evidence map›Paper›PMID 34838662›Full record

ArticleResuscitation2022

The inflammatory response is related to circulatory failure after out-of-hospital cardiac arrest: A prospective cohort study.

Halvor Langeland, Jan Kristian Damås, Tom Eirik Mollnes, Judith Krey Ludviksen, Thor Ueland, Annika E Michelsen, Magnus Løberg, Daniel Bergum, Trond Nordseth, Nils Kristian Skjærvold and 1 more

Registry-linked trialAbstract read
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In one paragraph

Article in Resuscitation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02648061 (Transitions Between Clinical Circulatory States After Out-of-hospital Cardiac Arrest), which is not on this map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT02648061 completednot on this map

Transitions Between Clinical Circulatory States After Out-of-hospital Cardiac Arrest

TypeobservationalSponsorNorwegian University of Science and TechnologyRan2016 to 2017Enrolled50ConditionsOut-of-Hospital Cardiac Arrest
3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Halvor LangelandDepartment of Anaesthesiology and Intensive Care Medicine, St. Olav's University Hospital, Trondheim, Norway; Institute of Circulation and Medical Imaging, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway. Electronic address: halvor.langeland@ntnu.no.
Jan Kristian DamåsGemini Center for Sepsis Research, Norwegian University of Science and Technology (NTNU), Trondheim, Norway; Centre of Molecular Inflammation Research, Institute for Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway; Department of Infectious Diseases, St. Olav's University Hospital, Trondheim, Norway.
Tom Eirik MollnesCentre of Molecular Inflammation Research, Institute for Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway; Department of Immunology, Oslo University Hospital and University of Oslo, Oslo, Norway; Research Laboratory, Nordland Hospital, Bodø, Norway; K. G. Jebsen Thrombosis Research and Expertise Center, University of Tromsø, Tromsø, Norway.
Judith Krey LudviksenResearch Laboratory, Nordland Hospital, Bodø, Norway.
Thor UelandK. G. Jebsen Thrombosis Research and Expertise Center, University of Tromsø, Tromsø, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Research Institute of Internal Medicine, Oslo University Hospital (Rikshospitalet), Oslo, Norway.
Annika E MichelsenInstitute of Clinical Medicine, University of Oslo, Oslo, Norway; Research Institute of Internal Medicine, Oslo University Hospital (Rikshospitalet), Oslo, Norway.
Magnus LøbergClinical Effectiveness Research Group, Institute of Health and Society, University of Oslo, Oslo, Norway; Department of Transplantation Medicine, Oslo University Hospital, Oslo, Norway.
Daniel BergumDepartment of Anaesthesiology and Intensive Care Medicine, St. Olav's University Hospital, Trondheim, Norway.
Trond NordsethDepartment of Anaesthesiology and Intensive Care Medicine, St. Olav's University Hospital, Trondheim, Norway; Institute of Circulation and Medical Imaging, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway; Department of Anaesthesia, Molde Hospital, Molde, Norway.
Nils Kristian SkjærvoldDepartment of Anaesthesiology and Intensive Care Medicine, St. Olav's University Hospital, Trondheim, Norway; Institute of Circulation and Medical Imaging, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
Pål KlepstadDepartment of Anaesthesiology and Intensive Care Medicine, St. Olav's University Hospital, Trondheim, Norway; Institute of Circulation and Medical Imaging, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWhole body ischemia and reperfusion injury after cardiac arrest leads to the massive inflammation clinically manifested in the post-cardiac arrest syndrome. Previous studies on the inflammatory effect on circulatory failure after cardiac arrest have either investigated a selected patient group or a limited part of the inflammatory mechanisms. We examined the association between cardiac arrest characteristics and inflammatory biomarkers, and between inflammatory biomarkers and circulatory failure after cardiac arrest, in an unselected patient cohort.

methodsThis was a prospective study of 50 consecutive patients with out-of-hospital cardiac arrest. Circulation was invasively monitored from admission until day five, whereas inflammatory biomarkers, i.e. complement activation, cytokines and endothelial injury, were measured daily. We identified predictors for an increased inflammatory response, and associations between the inflammatory response and circulatory failure.

resultsWe found a marked and broad inflammatory response in patients after cardiac arrest, which was associated with clinical outcome. Long time to return of spontaneous circulation and high lactate level at admission were associated with increased complement activation (TCC and C3bc), pro-inflammatory cytokines (IL-6, IL-8) and endothelial injury (syndecan-1) at admission. These biomarkers were in turn significantly associated with lower mean arterial blood pressure, lower cardiac output and lower systemic vascular resistance, and increased need of circulatory support in the initial phase. High levels of TCC and IL-6 at admission were significantly associated with increased 30-days mortality.

conclusionInflammatory biomarkers, including complement activation, cytokines and endothelial injury, were associated with increased circulatory failure in the initial period after cardiac arrest.

Indexed as

Out-of-Hospital Cardiac ArrestPost-Cardiac Arrest SyndromeShockBiomarkersCohort StudiesHumansProspective StudiesBiomarkersBiomarkersHaemodynamicInflammationOut-of-hospital cardiac arrestPost-cardiac arrest syndrome

Identifiers

PMID34838662

What OpenQuestion holds

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.