Evidence map›Paper›PMID 26089856›Full record

ReviewJournal of geriatric cardiology : JGC2015

Systemic inflammatory response following acute myocardial infarction.

Lu Fang, Xiao-Lei Moore, Anthony M Dart, Le-Min Wang

Registry-linked trialAbstract readReview
In one paragraph

Review in Journal of geriatric cardiology : JGC, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03121911 (Effects of Interval Physical Training on Inflammatory Markers, Cardiac Autonomic Modulation at Rest, Expiratory Flow Limitation and Respiratory Efficiency in Recent Myocardial Infarction), which is not on this map. Cited by 120 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 2 pooled it
8.3field-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.

NCT03121911 nawithdrawnnot on this mapstarted 2019, after this paper: background citation

Effects of Interval Physical Training on Inflammatory Markers, Cardiac Autonomic Modulation at Rest, Expiratory Flow Limitation and Respiratory Efficiency in Recent Myocardial Infarction

TypeinterventionalSponsorFederal University of UberlandiaRan2019 to 2022Enrolled0ConditionsExpiratory Flow Limitation, Recent Myocardial InfarctionArmsInterval Training (IT), Inspiratory Muscle Training (IMT)
3 · Its place in the literature

Who cites it

120 citing papers in PubMed, 2 syntheses or guidelines pooled it, 141 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Simultaneous 3-D Adiabatic TNMR in biomedicine · 2026
    Article
  6. Cardioprotective Effects ofLife (Basel, Switzerland) · 2026
    Review
  7. Article
  8. Determinants of cancer mortality in patients after acute myocardial infarction.International journal of cardiology. Heart & vasculature · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Anti-inflammatory pharmacotherapy in patients with cardiovascular disease.European heart journal. Cardiovascular pharmacotherapy · 2025
    Review
  19. Review
  20. Article

60 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Lu FangBaker IDI Heart and Diabetes Institute, Melbourne, Vic, Australia.
Xiao-Lei MooreBaker IDI Heart and Diabetes Institute, Melbourne, Vic, Australia.
Anthony M DartBaker IDI Heart and Diabetes Institute, Melbourne, Vic, Australia ; Department of Cardiovascular Medicine, the Alfred Hospital, Commercial Road, Melbourne, Vic, Australia.
Le-Min WangDepartment of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China.
Baker Heart and Diabetes Institute · AUTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Inflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction (AMI). Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes (such as death, recurrent myocardial infarction, and heart failure) in patients with AMI.

Indexed as

Acute myocardial infarctionInflammatory markersLeukocytesSystemic inflammatory response

Identifiers

PMID26089856
PMCPMC4460175
OpenAlexW2236717664

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

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.