Evidence map›Paper›PMID 29424484›Full record

Trial reportESC heart failure2018

Acute heart failure following myocardial infarction: complement activation correlates with the severity of heart failure in patients developing cardiogenic shock.

Hilde L Orrem, Per H Nilsson, Søren E Pischke, Guro Grindheim, Peter Garred, Ingebjørg Seljeflot, Trygve Husebye, Pål Aukrust, Arne Yndestad, Geir Ø Andersen and 2 more

Open access · goldAbstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in ESC heart failure, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 46 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 3 countries.

Hilde L OrremDepartment of Immunology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Per H NilssonDepartment of Immunology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Søren E PischkeDepartment of Immunology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Guro GrindheimDivision of Emergencies and Critical Care, Department of Anesthesiology, Rikshospitalet, Oslo University Hospital, Oslo, Norway.
Peter GarredLaboratory of Molecular Medicine, Department of Clinical Immunology, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Ingebjørg SeljeflotCenter for Clinical Heart Research, Oslo University Hospital, Ullevål, Oslo, Norway.
Trygve HusebyeDepartment of Cardiology, Oslo University Hospital, Ullevål, Oslo, Norway.
Pål AukrustK.G. Jebsen Inflammatory Research Centre, University of Oslo, Oslo, Norway.
Arne YndestadK.G. Jebsen Inflammatory Research Centre, University of Oslo, Oslo, Norway.
Geir Ø AndersenCenter for Clinical Heart Research, Oslo University Hospital, Ullevål, Oslo, Norway.
Andreas Barratt-DueDepartment of Immunology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Tom E MollnesDepartment of Immunology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Oslo University Hospital · NOUniversity of Oslo · NONorwegian University of Science and Technology · NORigshospitalet · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsHeart failure (HF) is an impending complication to myocardial infarction. We hypothesized that the degree of complement activation reflects severity of HF following acute myocardial infarction. METHODS AND

resultsThe LEAF trial (LEvosimendan in Acute heart Failure following myocardial infarction) evaluating 61 patients developing HF within 48 h after percutaneous coronary intervention-treated ST-elevation myocardial infarction herein underwent a post hoc analysis. Blood samples were drawn from inclusion to Day 5 and at 42 day follow-up, and biomarkers were measured with enzyme immunoassays. Regional myocardial contractility was measured by echocardiography as wall motion score index (WMSI). The cardiogenic shock group (n = 9) was compared with the non-shock group (n = 52). Controls (n = 44) were age-matched and sex-matched healthy individuals. C4bc, C3bc, C3bBbP, and sC5b-9 were elevated in patients at inclusion compared with controls (P < 0.01). The shock group had higher levels compared with the non-shock group for all activation products except C3bBbP (P < 0.05). At Day 42, all products were higher in the shock group (P < 0.05). In the shock group, sC5b-9 correlated significantly with WMSI at baseline (r = 0.68; P = 0.045) and at Day 42 (r = 0.84; P = 0.036). Peak sC5b-9 level correlated strongly with WMSI at Day 42 (r = 0.98; P = 0.005). Circulating endothelial cell activation markers sICAM-1 and sVCAM-1 were higher in the shock group during the acute phase (P < 0.01), and their peak levels correlated with sC5b-9 peak level in the whole HF population (r = 0.32; P = 0.014 and r = 0.30; P = 0.022, respectively).

conclusionsComplement activation discriminated cardiogenic shock from non-shock in acute ST-elevation myocardial infarction complicated by HF and correlated with regional contractility and endothelial cell activation, suggesting a pathogenic role of complement in this condition.

Indexed as

Acute DiseaseAgedAnterior Wall Myocardial InfarctionComplement ActivationEchocardiographyFemaleHeart FailureHumansMaleMiddle AgedPercutaneous Coronary InterventionSeverity of Illness IndexShock, CardiogenicAcute heart failureCardiogenic shockComplement activationInflammationMyocardial infarctionWall motion score index

Identifiers

PMID29424484
PMCPMC5933968
OpenAlexW2790221546

What OpenQuestion holds

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Registered trials

None linked

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.