Evidence map›Paper›PMID 39375494›Full record

ArticleScientific reports2024

Myocardial inflammatory cells in cardiac amyloidosis.

Philip Simon, Hans-Michael Behrens, Arnt Kristen, Christoph Röcken

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Observational
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Current cardiology reports · 2025
    Review
  13. 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

4 authors.

Philip SimonDepartment of Pathology, University Hospital Schleswig-Holstein, Christian-Albrechts-University, Arnold-Heller-Str. 3, Building U33, 24105, Kiel, Germany.
Hans-Michael BehrensDepartment of Pathology, University Hospital Schleswig-Holstein, Christian-Albrechts-University, Arnold-Heller-Str. 3, Building U33, 24105, Kiel, Germany.
Arnt KristenDepartment of Cardiology, Angiology, Respiratory Medicine, Medical University of Heidelberg, Heidelberg, Germany.
Christoph RöckenDepartment of Pathology, University Hospital Schleswig-Holstein, Christian-Albrechts-University, Arnold-Heller-Str. 3, Building U33, 24105, Kiel, Germany. christoph.roecken@uksh.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmunoglobulin derived AL amyloidosis and transthyretin derived ATTR amyloidosis are the most common forms of cardiac amyloidosis. Both may present with cardiac arrhythmias, heart failure, and extracardiac symptoms. Disease outcome is often fatal. Recently, it was proposed that amyloid may cause cardiac inflammation. Here we tested the hypothesis that immune cell infiltration in cardiac tissue correlates with clinicopathological patient characteristics. PATIENTS AND

methodsMyocardial biopsies from 157 patients with cardiac amyloidosis (46.5% AL, 53.3% ATTR) were immunohistochemically assessed for the presence and amount of T lymphocytes (CD3), macrophages (CD68) and neutrophils (MPO). Amyloid load, cardiomyocyte diameter, apoptosis (Caspase 3), necrosis (complement 9), and various clinical parameters were assessed and correlated with immune cell density.

resultsMyocardial tissue was infiltrated with T lymphocytes (CD3), macrophages (CD68) and neutrophils (MPO) with variable amounts. Significant correlations were found between the number of macrophages and NYHA class. No correlations were found between the presence and amount of T lymphocytes, neutrophils and clinicopathological patient characteristics.

conclusionThe significant correlation between cardiac macrophage density and heart failure points towards a significant role of macrophages in disease pathology.

Indexed as

MacrophagesMyocardiumNeutrophilsAgedAged, 80 and overAmyloidosisCardiomyopathiesFemaleHumansImmunoglobulin Light-chain AmyloidosisInflammationMaleMiddle AgedT-LymphocytesAmyloidAmyloidosisCaspase 3Cell deathComplement 9Inflammation

Identifiers

PMID39375494
PMCPMC11458899

What Socratic holds

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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 Socratic graph.