Evidence map›Paper›PMID 37640127›Full record

ArticleHeart rhythm2023

Association of epicardial and intramyocardial fat with ventricular arrhythmias.

Maryam Mojarrad Sani, Eric Sung, Marc Engels, Usama A Daimee, Natalia Trayanova, Katherine C Wu, Jonathan Chrispin

Registry-linked trialAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heart rhythm, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01076660 (Left Ventricular Structural Predictors of Sudden Cardiac Death [Substudy of), which is not on this map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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.

NCT01076660 recruitingnot on this map

Left Ventricular Structural Predictors of Sudden Cardiac Death [Substudy of: Functional Energetics and Imaging for Phenotypic Characterization of Patients at Risk for Sudden Cardiac Death, See Also NCT000181233]

TypeobservationalSponsorJohns Hopkins UniversityRan2003 to 2030Enrolled400ConditionsIschemic Cardiomyopathy, Nonischemic Cardiomyopathy
3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Review
  2. CK2α Deficiency Drives Myocardial Fibrosis via Desmin-Induced Mitochondrial Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Review
  4. Computer-aided characterization of the arrhythmogenic substrate after myocardial infarction.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Maryam Mojarrad SaniDepartment of Medicine, Division of Cardiology, Johns Hopkins Hospital, Baltimore, Maryland.
Eric SungDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland.
Marc EngelsDepartment of Medicine, Division of Cardiology, Johns Hopkins Hospital, Baltimore, Maryland.
Usama A DaimeeDepartment of Medicine, Division of Cardiology, Johns Hopkins Hospital, Baltimore, Maryland.
Natalia TrayanovaDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland.
Katherine C WuDepartment of Medicine, Division of Cardiology, Johns Hopkins Hospital, Baltimore, Maryland.
Jonathan ChrispinDepartment of Medicine, Division of Cardiology, Johns Hopkins Hospital, Baltimore, Maryland. Electronic address: chrispin@jhmi.edu.

Funding

Cardiac MR to Improve Clinical Risk Prediction in Defibrilator PatientsR01HL132181 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI TOMASELLI, GORDON FRANK, WU, KATHERINE C · 2017 to 2020
$3.1M
NHLBI NIH HHS R01 HL132181
6 · The paper itself

Abstract

backgroundAmong patients with ischemic cardiomyopathy (ICM) and nonischemic cardiomyopathy (NICM), myocardial fibrosis is associated with an increased risk for ventricular arrhythmia (VA). Growing evidence suggests that myocardial fat contributes to ventricular arrhythmogenesis. However, little is known about the volume and distribution of epicardial adipose tissue and intramyocardial fat and their relationship with VAs.

objectiveThe purpose of this study was to assess the association of contrast-enhanced computed tomography (CE-CT)-derived left ventricular (LV) tissue heterogeneity, epicardial adipose tissue volume, and intramyocardial fat volume with the risk of VA in ICM and NICM patients.

methodsPatients enrolled in the PROSE-ICD registry who underwent CE-CT were included. Intramyocardial fat volume (voxels between -180 and -5 Hounsfield units [HU]), epicardial adipose tissue volume (between -200 and -50 HU), and LV tissue heterogeneity were calculated. The primary endpoint was appropriate ICD shocks or sudden arrhythmic death.

resultsAmong 98 patients (47 ICM, 51 NICM), LV tissue heterogeneity was associated with VA (odds ratio [OR] 1.10; P = .01), particularly in the ICM cohort. In the NICM subgroup, epicardial adipose tissue and intramyocardial fat volume were associated with VA (OR 1.11, P = .01; and OR = 1.21, P = .01, respectively) but not in the ICM patients (OR 0.92, P =.22; and OR = 0.96, P =.19, respectively).

conclusionIn ICM patients, increased fat distribution heterogeneity is associated with VA. In NICM patients, an increased volume of intramyocardial fat and epicardial adipose tissue is associated with a higher risk for VA. Our findings suggest that fat's contribution to VAs depends on the underlying substrate.

Indexed as

CardiomyopathiesMyocardial IschemiaTachycardia, VentricularArrhythmias, CardiacHumansMyocardiumContrast-enhanced computed tomographyEpicardial fatIntramyocardial fatIschemic cardiomyopathyLeft ventricular tissue heterogeneityNonischemic cardiomyopathyVentricular arrhythmia

Identifiers

PMID37640127
PMCPMC10881203

What Socratic holds

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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 Socratic graph.