Evidence map›Paper›PMID 30010800›Full record

SynthesisCardiovascular research2018

Immunomodulatory interventions in myocardial infarction and heart failure: a systematic review of clinical trials and meta-analysis of IL-1 inhibition.

Mona Panahi, Angelos Papanikolaou, Azam Torabi, Ji-Gang Zhang, Habib Khan, Ali Vazir, Muneer G Hasham, John G F Cleland, Nadia A Rosenthal, Sian E Harding and 1 more

Open access · hybridAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Cardiovascular research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. PAF Triggered Pyroptotic NETosis Aggravates Myocardial Ischemia/Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

11 authors at 4 institutions in 2 countries.

Mona PanahiNational Heart and Lung Institute, Imperial College London, Du Cane Road, London, UK.
Angelos PapanikolaouNational Heart and Lung Institute, Imperial College London, Du Cane Road, London, UK.
Azam TorabiRoyal Brompton Hospital, Royal Brompton and Harefield NHS Foundation Trust, Sydney Street, London, UK.
Ji-Gang ZhangThe Jackson Laboratory, 600 Main Street, Bar Harbor, USA.
Habib KhanRoyal Brompton Hospital, Royal Brompton and Harefield NHS Foundation Trust, Sydney Street, London, UK.
Ali VazirRoyal Brompton Hospital, Royal Brompton and Harefield NHS Foundation Trust, Sydney Street, London, UK.
Muneer G HashamThe Jackson Laboratory, 600 Main Street, Bar Harbor, USA.
John G F ClelandNational Heart and Lung Institute, Imperial College London, Du Cane Road, London, UK.
Nadia A RosenthalNational Heart and Lung Institute, Imperial College London, Du Cane Road, London, UK.
Sian E HardingNational Heart and Lung Institute, Imperial College London, Du Cane Road, London, UK.
Susanne SattlerNational Heart and Lung Institute, Imperial College London, Du Cane Road, London, UK.
Imperial College London · GBJackson Laboratory · USRoyal Brompton & Harefield NHS Foundation Trust · GBRoyal Brompton Hospital · GB

Funding

British Heart Foundation PG/16/93/32345British Heart Foundation RG/14/1/30588Medical Research Council MR/L012618/1
6 · The paper itself

Abstract

Following a myocardial infarction (MI), the immune system helps to repair ischaemic damage and restore tissue integrity, but excessive inflammation has been implicated in adverse cardiac remodelling and development towards heart failure (HF). Pre-clinical studies suggest that timely resolution of inflammation may help prevent HF development and progression. Therapeutic attempts to prevent excessive post-MI inflammation in patients have included pharmacological interventions ranging from broad immunosuppression to immunomodulatory approaches targeting specific cell types or factors with the aim to maintain beneficial aspects of the early post-MI immune response. These include the blockade of early initiators of inflammation including reactive oxygen species and complement, inhibition of mast cell degranulation and leucocyte infiltration, blockade of inflammatory cytokines, and inhibition of adaptive B and T-lymphocytes. Herein, we provide a systematic review on post-MI immunomodulation trials and a meta-analysis of studies targeting the inflammatory cytokine Interleukin-1. Despite an enormous effort into a significant number of clinical trials on a variety of targets, a striking heterogeneity in study population, timing and type of treatment, and highly variable endpoints limits the possibility for meaningful meta-analyses. To conclude, we highlight critical considerations for future studies including (i) the therapeutic window of opportunity, (ii) immunological effects of routine post-MI medication, (iii) stratification of the highly diverse post-MI patient population, (iv) the potential benefits of combining immunomodulatory with regenerative therapies, and at last (v) the potential side effects of immunotherapies.

Indexed as

Anti-Inflammatory AgentsClinical Trials as TopicHeart FailureHumansImmunosuppressive AgentsInflammation MediatorsInterleukin-1Myocardial InfarctionRisk FactorsSignal TransductionTreatment OutcomeAnti-Inflammatory AgentsImmunosuppressive AgentsInflammation MediatorsInterleukin-1

Identifiers

PMID30010800
PMCPMC6106100
OpenAlexW2884458063

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.