Evidence map›Paper›PMID 41692740›Full record

ArticleCardiovascular diabetology2026

Epicardial fat remodeling in end-stage heart failure with reduced ejection fraction.

Maciej Mączewski, Marta Załęska-Kocięcka, Maksymilian Nowakowski, Maciej Mazuruk, Łukasz Nogajski, Hanna Czerwińska, Igor Gronek, Mateusz Smoliński, Aleksandra Świstak, Mikołaj Kurpias and 8 more

Abstract read
In one paragraph

Article in Cardiovascular diabetology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. 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

18 authors.

Maciej Mączewski *Department of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Marta Załęska-Kocięcka *Heart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Maksymilian NowakowskiDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Maciej MazurukDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Łukasz NogajskiDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Hanna CzerwińskaDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Igor GronekDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Mateusz SmolińskiDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Aleksandra ŚwistakDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Mikołaj KurpiasDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Oliwia ŁuniewskaDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Marta KacperskaDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Filip PilzakDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Zuzanna WojdyńskaHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Ilona MichałowskaDepartment of Radiology, National Institute of Cardiology, Warsaw, Poland.
Michał MączewskiDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland. michal.maczewski@cmkp.edu.pl.
Aleksandra Paterek *Department of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Przemysław Leszek *Heart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.

Funding

Agencja Badań Medycznych KPOD.07.07-IW.07-0149/24Narodowe Centrum Nauki 2024/55/D/NZ4/01538
6 · The paper itself

Abstract

backgroundEpicardial adipose tissue (EAT) transformation in heart failure with reduced ejection fraction (HFrEF) is poorly understood, which limits its potential as a therapeutic target and prognostic factor. The aim of our study was to characterize EAT in patients with HFrEF at the histological, computed tomography (CT) imaging and radiomic level to better understand its transformation in HFrEF.

methodsWe enrolled 70 patients with HFrEF who were scheduled for implantation of a left ventricular assist device (LVAD) or orthotopic heart transplantation (OHT). Fifty non-heart failure (HF) subjects served as controls. All participants underwent contrast- or non-contrast-enhanced chest CT imaging for EAT analysis. Left ventricular myocardial cones with overlying EAT were obtained from LVAD patients during surgery, from explanted OHT hearts, and from 20 unused healthy donor hearts for histological analysis.

resultsWhile total EAT volume did not differ between non-HF and HFrEF subjects, its density assessed in CT images, was higher in HFrEF. Moreover, periventricular EAT exhibited density gradient, with the densest voxels immediately adjacent to the myocardium (over up to 1 mm). This density gradient was extended to almost 3 mm in LV EAT in HFrEF patients. Histological analysis showed that adipocytes also exhibited a characteristic cell size gradient, with smaller cells adjacent to the myocardium, more pronounced than in non-HF subjects; moreover, median LV EAT adipocyte size was smaller in HFrEF vs. non-HF patients. However, EAT fibrosis and blood vessel density did not differ between non-HF and HFrEF subjects. Both histological analysis and radiomic analysis of CT images revealed that EAT was more heterogeneous in HFrEF than in non-HF subjects. These changes were most pronounced in LV EAT, but other EAT depots (RV and periatrial) were also affected.

conclusionsLV EAT in HFrEF contains smaller adipocytes and has higher density in CT images, exhibits pronounced cell size/density gradient and is more heterogeneous than in non-HF subjects. Thus LV EAT undergoes complex remodeling in HFrEF. Further studies are needed to elucidate the mechanisms driving this remodeling, determine whether it can be therapeutically targeted, and assess which parameters may have prognostic value in patients with HFrEF.

Indexed as

AdiposityEpicardial Adipose TissueHeart FailureStroke VolumeVentricular Function, LeftVentricular RemodelingAdipocytesAdultAgedCase-Control StudiesFemaleFibrosisHeart-Assist DevicesHeart TransplantationHumansMaleAdipose tissue, adipocytesComputed tomography imagingEpicardial fatHeart failure with reduced ejection fraction

Identifiers

PMID41692740
PMCPMC13011763

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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.