Evidence map›Paper›PMID 35327407›Full record

ArticleBiomedicines2022

Association of Plasma Methylglyoxal Increase after Myocardial Infarction and the Left Ventricular Ejection Fraction.

Stefan Heber, Paul M Haller, Attila Kiss, Bernhard Jäger, Kurt Huber, Michael J M Fischer

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Dicarbonyl Stress in Diabetic Vascular Disease.International journal of molecular sciences · 2022
    Review
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

6 authors at 4 institutions in 2 countries.

Stefan HeberInstitute of Physiology, Center for Physiology and Pharmacology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-3398-0442
Paul M HallerDepartment of Cardiology, University Heart & Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Attila KissCenter for Biomedical Research and Translational Surgery, Ludwig Boltzmann Institute for Cardiovascular Research, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-4652-1998
Bernhard Jäger3rd Department of Medicine, Cardiology and Intensive Care Medicine, Klinik Ottakring, 1016 Vienna, Austria.
Kurt Huber3rd Department of Medicine, Cardiology and Intensive Care Medicine, Klinik Ottakring, 1016 Vienna, Austria.
Michael J M FischerInstitute of Physiology, Center for Physiology and Pharmacology, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-3811-7066
Medical University of Vienna · ATLudwig Boltzmann Institute for Cardiovascular Research · ATSigmund Freud Privatuniversität Wien · ATUniversität Hamburg · DE

Funding

Association for Research on Arteriosclerosis, Thrombosis and Vascular Biology No specific numberLudwig Boltzmann Institute for Cardiovascular Research No specific numberMedical Scientific Fund of the Mayor of the City of Vienna 17091
6 · The paper itself

Abstract

Background: Preclinical studies suggest that methylglyoxal (MG) increases within the myocardium upon acute myocardial infarction (AMI) and thereafter contributes to adverse postinfarct remodeling. The aims of this study were to test whether MG increases in plasma of humans after AMI and whether this increase is related to the left ventricular ejection fraction (LVEF). Methods: The plasma samples of 37 patients with ST elevation AMI undergoing primary percutaneous coronary intervention (pPCI) acquired in a previously conducted randomized controlled trial testing remote ischemic conditioning (RIC) were analyzed by means of high-performance liquid chromatography. Time courses of the variables were analyzed by means of mixed linear models. Multiple regression analyses served to explore the relationship between MG levels and the LVEF. Results: Compared to the MG levels upon admission due to AMI, the levels were increased 2.4-fold (95% CI, 1.6−3.6) 0.5 h after reperfusion facilitated by pPCI, 2.6-fold (1.7−4.0) after 24 h and largely returned to the baseline after 30 d (1.1-fold, 0.8−1.5). The magnitude of the MG increase was largely independent of that of cardiac necrosis markers. Overall, the highest MG values within 24 h after AMI were associated with the lowest LVEF after 4 d. While markers of myocardial necrosis and stretch quantified within the first 24 h explained 52% of the variance of the LVEF, MG explained additional 23% of the variance (p < 0.001). Conclusions: Considering these observational data, it is plausible that the preclinical finding of MG generation after AMI negatively affecting the LVEF also applies to humans. Inhibition of MG generation or MG scavenging might provide a novel therapeutic strategy to target post-AMI myocardial remodeling and dysfunction.

Indexed as

acute myocardial infarctioncardiac functionmethylglyoxalremodeling

Identifiers

PMID35327407
PMCPMC8945522
OpenAlexW4220890251

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.