Evidence map›Paper›PMID 31345784›Full record

ArticleEBioMedicine2019

Early increase of specialized pro-resolving lipid mediators in patients with ST-elevation myocardial infarction.

Linn E Fosshaug, Romain A Colas, Anne K Anstensrud, Ida Gregersen, Ståle Nymo, Ellen L Sagen, Annika Michelsen, Leif E Vinge, Erik Øie, Lars Gullestad and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

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  9. Omega-3 (Nutrients · 2024
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  16. Molecular Pharmacology of Inflammation Resolution in Atherosclerosis.International journal of molecular sciences · 2022
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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

15 authors at 3 institutions in 2 countries.

Linn E FosshaugResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Department of Medicine, Diakonhjemmet Hospital, Oslo, Norway; Center for Heart Failure Research, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Norway. Electronic address: l.e.lillerud@medisin.uio.no.
Romain A ColasWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, UK.
Anne K AnstensrudCenter for Heart Failure Research, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Norway; Department of Cardiology, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Ida GregersenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Norway.
Ståle NymoResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Ellen L SagenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Norway.
Annika MichelsenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Norway.
Leif E VingeDepartment of Medicine, Diakonhjemmet Hospital, Oslo, Norway; Center for Heart Failure Research, Oslo University Hospital, Oslo, Norway; Surgical Research, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Erik ØieDepartment of Medicine, Diakonhjemmet Hospital, Oslo, Norway; Center for Heart Failure Research, Oslo University Hospital, Oslo, Norway.
Lars GullestadCenter for Heart Failure Research, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Norway; Department of Cardiology, Oslo University Hospital Rikshospitalet, Oslo, Norway; KG Jebsen Center for Cardiac Research, University of Oslo, Oslo, Norway.
Bente HalvorsenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Norway.
Trond V HansenSchool of Pharmacy, Department of Pharmaceutical Chemistry, University of Oslo, Oslo, Norway.
Pål AukrustResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Norway; School of Pharmacy, Department of Pharmaceutical Chemistry, University of Oslo, Oslo, Norway; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Jesmond DalliWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, UK; Centre for Inflammation and Therapeutic Innovation, Queen Mary University of London, London, UK.
Arne YndestadResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Center for Heart Failure Research, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Norway.
Oslo University Hospital · NOQueen Mary University of London · GBUniversity of Oslo · NO

Funding

European Research Council 677542
6 · The paper itself

Abstract

backgroundTermination of acute inflammation is an active process orchestrated by lipid mediators (LM) derived from polyunsaturated fatty acids, referred to as specialized pro-resolving mediators (SPM). These mediators also provide novel therapeutic opportunities for treating inflammatory disease. However, the regulation of these molecules following acute myocardial infarction (MI) remains of interest.

methodsIn this prospective observational study we aimed to profile plasma levels of SPMs in ST-elevation MI (STEMI) patients during the first week following MI. Plasma LM concentrations were measured in patients with STEMI (n = 15) at three time points and compared with stable coronary artery disease (CAD; n = 10) and healthy controls (n = 10).

findingsOur main findings were: (i) Immediately after onset of MI and before peak troponin T levels, STEMI patients had markedly increased levels of SPMs as compared with healthy controls and stable CAD patients, with levels of these mediators declining during follow-up. (ii) The increase in SPMs primarily reflected an increase in docosapentaenoic acid- and docosahexaenoic acid-derived protectins. (iii) Several individual protectins were correlated with the rapid increase in neutrophil counts, but not with CRP. (iv) A shift in 5-LOX activity from the leukotriene B

interpretationThe temporal regulation of SPMs indicates that resolution mechanisms are activated early during STEMI as part of an endogenous mechanism to initiate repair. Thus strategies to boost the activity and/or efficacy of these endogenous mechanisms may represent novel therapeutic opportunities for treatment of patients with MI. FUND: This work was supported by grants from the South-Eastern Norwegian regional health authority, the European Research Council under the European Union's Horizon 2020 research and innovation program, a Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society, and the Barts Charity.

Indexed as

AgedBiomarkersCase-Control StudiesCytokinesFemaleHumansInflammation MediatorsLipidsMaleMiddle AgedMyocardial InfarctionProspective StudiesST Elevation Myocardial InfarctionBiomarkersCytokinesInflammation MediatorsLipidsInflammationMyocardial infarctionPolyunsaturated fatty acidsResolutionSpecialized pro-resolving mediators

Identifiers

PMID31345784
PMCPMC6711324
OpenAlexW2963356053

What OpenQuestion holds

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Registered trials

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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.