Evidence map›Paper›PMID 39457491›Full record

ArticleBiomedicines2024

Somatostatin Receptor Type 2 as a Potential Marker of Local Myocardial Inflammation in Myocardial Infarction: Morphologic Data on Distribution in Infarcted and Normal Human Myocardium.

Vyacheslav V Ryabov, Andrey A Trusov, Maria A Kercheva, Aleksandra E Gombozhapova, Julia N Ilyushenkova, Ivan V Stepanov, Mikhail V Fadeev, Anna G Syrkina, Svetlana I Sazonova

Abstract read
In one paragraph

Article in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

9 authors.

Vyacheslav V RyabovDepartment of Emergency Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk 634012, Russia.ORCID 0000-0002-4358-7329
Andrey A TrusovDepartment of Emergency Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk 634012, Russia.ORCID 0000-0003-4051-3196
Maria A KerchevaDepartment of Emergency Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk 634012, Russia.ORCID 0000-0003-1444-1037
Aleksandra E GombozhapovaDepartment of Emergency Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk 634012, Russia.ORCID 0000-0003-1281-3714
Julia N IlyushenkovaNuclear Medicine Department, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk 634012, Russia.
Ivan V StepanovDepartment of Pathology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk 634012, Russia.ORCID 0000-0002-8543-6027
Mikhail V FadeevDepartment of Pathology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk 634012, Russia.
Anna G SyrkinaDepartment of Emergency Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk 634012, Russia.
Svetlana I SazonovaNuclear Medicine Department, Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk 634012, Russia.

Funding

Russian Science Foundation 22-25-00234
6 · The paper itself

Abstract

Nuclear imaging modalities can detect somatostatin receptor type 2 (SSTR2) in vivo as a potential marker of local post-MI inflammation. SSTR2+ macrophages are thought to be the main substrate for SSTR-targeted radioimaging. However, the distribution of SSTR2+ cells in the MI patients' myocardium is unknown. Using immunohistochemistry, we investigated the distribution of SSTR2+ cells in the myocardium of patients who died during the MI inflammatory phase (n = 7) compared to the control group of individuals with fatal trauma (n = 3). Inflammatory cellular landscapes evolve in a wave front-like pattern, so we divided the myocardium into histological zones: the infarct core (IC), the border zone (BZ), the remote zone (RZ), and the peri-scar zone (PSZ). The number of SSTR2+ neutrophils (NPs), SSTR2+ monocytes/macrophages (Mos/MPs), and SSTR2+ vessels were counted. In the myocardium of the control group, SSTR2+ NPs and SSTR2+ Mos/MPs were occasional, SSTR2+ vessels were absent. In the RZ, the picture was similar to the control group, but there was a lower number of SSTR2+ Mos/MPs in the RZ. In the PSZ, SSTR2+ vessel numbers were highest in the myocardium. In the IC, the median number of SSTR2+ NPs was 200 times higher compared to the RZ or control group myocardium, which may explain the selective uptake of SSTR-targeted radiotracers in the MI area during the inflammatory phase of MI.

Indexed as

inflammationmacrophagesmolecular imagingmyocardial infarctionneutrophilspericytesPETSPECTSSTRSSTR-targeted radioimaging

Identifiers

PMID39457491
PMCPMC11504226

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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.