Evidence map›Paper›PMID 23574969›Full record

Trial reportHeart (British Cardiac Society)2013

Cardiovascular effects of tumour necrosis factor α antagonism in patients with acute myocardial infarction: a first in human study.

Gareth J Padfield, Jehangir N Din, Elena Koushiappi, Nicholas L Mills, Simon D Robinson, Nicholas Le May Cruden, Andrew John Lucking, Stanley Chia, Scott A Harding, David E Newby

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

Trial report in Heart (British Cardiac Society), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 2 pooled it
4.2field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Pooled it
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  17. Imaging Inflammation Past, Present, and Future: Focus on Cardioimmunology.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2023
    Article
  18. Review
  19. Inflammatory biomarkers of ischemic stroke.Internal and emergency medicine · 2023
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Gareth J PadfieldBritish Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK. gareth.padfield@nhs.net
Jehangir N Din
Elena Koushiappi
Nicholas L Mills
Simon D Robinson
Nicholas Le May Cruden
Andrew John Lucking
Stanley Chia
Scott A Harding
David E Newby
University of Edinburgh · GBBritish Heart Foundation · GB

Funding

British Heart Foundation CH/09/002British Heart Foundation FS/10/024/28266British Heart Foundation PG/07/012British Heart Foundation PG/2001068British Heart Foundation SS/CH/92010Wellcome Trust
6 · The paper itself

Abstract

objectiveThe inflammatory cytokine, tumour necrosis factor α (TNF-α), exerts deleterious cardiovascular effects. We wished to determine the effects of TNF-α antagonism on endothelial function and platelet activation in patients with acute myocardial infarction. DESIGN AND SETTING AND PATIENTS: A double-blind, parallel group, randomised controlled trial performed in a tertiary referral cardiac centre. 26 patients presenting with acute myocardial infarction randomised to receive an intravenous infusion of etanercept (10 mg) or saline placebo.

main outcome measuresLeucocyte count, plasma cytokine concentrations, flow cytometric measures of platelet activation and peripheral vasomotor and fibrinolytic function were determined before and 24 h after study intervention.

resultsConsistent with effective conjugation of circulating TNF-α, plasma TNF-α concentrations increased in all patients following etanercept (254 ± 15 vs 0.12 ± 0.02 pg/ml; p < 0.0001), but not saline infusion. Etanercept treatment reduced neutrophil (7.4 ± 0.6 vs 8.8 ± 0.6 × 10(9) cells/l; p = 0.03) and plasma interleukin-6 concentrations (5.8 ± 2.0 vs 10.6 ± 4.0 pg/ml; p = 0.012) at 24 h but increased platelet-monocyte aggregation (30 ± 5 vs 20 ± 3%; p = 0.02). Vasodilatation in response to substance P, acetylcholine and sodium nitroprusside, and acute tissue plasminogen activator release were unaffected by either treatment (p > 0.1 for all).

conclusionsFollowing acute myocardial infarction, etanercept reduces systemic inflammation but increases platelet activation without affecting peripheral vasomotor or fibrinolytic function. We conclude that TNF-α antagonism is unlikely to be a beneficial therapeutic strategy in patients with acute myocardial infarction.

Indexed as

Cardiovascular SystemCytokinesDouble-Blind MethodEndothelium, VascularEtanerceptFemaleFlow CytometryHumansImmunoglobulin GLeukocyte CountMaleMiddle AgedMyocardial InfarctionPlatelet ActivationReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alphaCytokinesEtanerceptImmunoglobulin GReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alphaMYOCARDIAL ISCHAEMIA AND INFARCTION (IHD)

Identifiers

PMID23574969
PMCPMC3756454
OpenAlexW2104334596

What OpenQuestion holds

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LicenceCC BY-NC
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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.