Background: Among 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.
Objective: The 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.
Methods: Patients 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.
Results: Among 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).
Conclusion: In 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.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10881203 | PMC |
| http://dx.doi.org/10.1016/j.hrthm.2023.08.033 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
NLRP3 inflammasome-modulated angiogenic function of EPC via PI3K/ Akt/mTOR pathway in diabetic myocardial infarction.
Cardiovasc Diabetol
January 2025
Department of Clinical Pharmacy, School of Preclinical Medicine and Clinical Pharmacy, China Pharmaceutical University, 24 Tong jia Lane, Nanjing, 210009, People's Republic of China.
Background: Inflammatory diseases impair the reparative properties of endothelial progenitor cells (EPC); however, the involvement of diabetes in EPC dysfunction associated with myocardial infarction (MI) remains unknown.
Methods: A model was established combining high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic mice with myocardial infarction. The therapeutic effects of transplanted wild-type EPC, Nlrp3 knockout EPC, and Nlrp3 overexpression EPC were evaluated.
The effects of gender-affirming hormone therapy on myocardial, hepatic, pancreatic lipid content, body fat distribution and other cardiometabolic risk factors: A magnetic resonance-based study in transgender individuals.
J Clin Transl Endocrinol
March 2025
Department of Internal Medicine III, Clinical Division of Endocrinology and Metabolism, Gender Medicine Unit, Medical University of Vienna, General Hospital Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.
Purpose: We aimed to assess the changes in body fat distribution, intraorgan lipid accumulation, and cardiometabolic risk factors after 6 months of gender-affirming hormone therapy (GAHT) in transgender men (TM) and transgender women (TW).
Methods: Conducted at the Medical University of Vienna between 2019 and 2022, the study included 15 TW and 20 TM. We conducted magnetic resonance imaging and spectroscopy to determine the visceral (VAT) and subcutaneous adipose tissue (SAT) amounts, the VAT/SAT ratio, and the intraorgan lipid content (liver, pancreas, myocardium), bloodwork, and an oral glucose tolerance test at baseline and after 6 months of GAHT.
Adipocyte-derived small extracellular vesicles exacerbate diabetic ischemic heart injury by promoting oxidative stress and mitochondrial-mediated cardiomyocyte apoptosis.
Redox Biol
December 2024
Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA, USA; Department of Biomedical Engineering, UAB, Birmingham, AL, USA. Electronic address:
Background: Diabetes increases ischemic heart injury via incompletely understood mechanisms. We recently reported that diabetic adipocytes-derived small extracellular vesicles (sEV) exacerbate myocardial reperfusion (MI/R) injury by promoting cardiomyocyte apoptosis. Combining in vitro mechanistic investigation and in vivo proof-concept demonstration, we determined the underlying molecular mechanism responsible for diabetic sEV-induced cardiomyocyte apoptosis after MI/R.
View Article and Find Full Text PDFLipomatous Metaplasia Facilitates Ventricular Tachycardia in Patients With Nonischemic Cardiomyopathy.
JACC Clin Electrophysiol
November 2024
Cardiovascular Medicine Division, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA. Electronic address:
Article Synopsis
- The study investigates the role of lipomatous metaplasia (LM) as a critical anatomical feature in the pathways that lead to ventricular tachycardia (VT) in patients with nonischemic cardiomyopathy (NICM).
- Researchers analyzed cardiac MRI and electroanatomical maps from 49 patients, revealing that VT corridors had significantly higher volumes of LM.
- The findings suggest that these VT corridors not only contain more LM but also show lower variability in current amplitude, indicating that LM may help stabilize electrical signaling during VT episodes.
Sexual dimorphism in the relationships between intramyocardial fat, myocardial fibrosis, and exercise intolerance in heart failure with preserved ejection fraction.
Eur J Heart Fail
September 2024
Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!