Background: Epicardial adipose tissue represents a metabolically active visceral fat depot that is in direct contact with the left ventricular myocardium. While it is associated with coronary artery disease, little is known regarding its role in aortic stenosis. We sought to investigate the association of epicardial adipose tissue with aortic stenosis severity and progression, myocardial remodelling and function, and mortality in asymptomatic patients with aortic stenosis.
Methods: In a post hoc analysis of 124 patients with asymptomatic mild-to-severe aortic stenosis participating in a prospective clinical trial, baseline epicardial adipose tissue was quantified on CT angiography using fully automated deep learning-enabled software. Aortic stenosis disease severity was assessed at baseline and 1 year. The primary endpoint was all-cause mortality.
Results: Neither epicardial adipose tissue volume nor attenuation correlated with aortic stenosis severity or subsequent disease progression as assessed by echocardiography or CT (p>0.05 for all). Epicardial adipose tissue volume correlated with plasma cardiac troponin concentration (r=0.23, p=0.009), left ventricular mass (r=0.46, p<0.001), ejection fraction (r=-0.28, p=0.002), global longitudinal strain (r=0.28, p=0.017), and left atrial volume (r=0.39, p<0.001). During the median follow-up of 48 (IQR 26-73) months, a total of 23 (18%) patients died. In multivariable analysis, both epicardial adipose tissue volume (HR 1.82, 95% CI 1.10 to 3.03; p=0.021) and plasma cardiac troponin concentration (HR 1.47, 95% CI 1.13 to 1.90; p=0.004) were associated with all-cause mortality, after adjustment for age, body mass index and left ventricular ejection fraction. Patients with epicardial adipose tissue volume >90 mm had 3-4 times higher risk of death (adjusted HR 3.74, 95% CI 1.08 to 12.96; p=0.037).
Conclusions: Epicardial adipose tissue volume does not associate with aortic stenosis severity or its progression but does correlate with blood and imaging biomarkers of impaired myocardial health. The latter may explain the association of epicardial adipose tissue volume with an increased risk of all-cause mortality in patients with asymptomatic aortic stenosis.
Clinicaltrials: gov (NCT02132026).
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http://dx.doi.org/10.1136/heartjnl-2024-324925 | DOI Listing |
J Hum Hypertens
March 2025
Faculty of Medicine, Department of Cardiology, Karamanoğlu Mehmetbey University, Karaman Training and Research Hospital, Karaman, Turkey.
Epicardial adipose tissue is associated with the development of cardiovascular disease and its increase is positively correlated with blood pressure elevation in hypertensive individuals. In the literature, being physically active has been shown to be effective in the treatment of hypertension and reduction of epicardial adipose tissue thickness. The aim of this study was to evaluate the relationship between epicardial adipose tissue thickness and sedentary time, physical activity level and physical performance in patients with hypertension.
View Article and Find Full Text PDFEur Heart J
March 2025
Department of Cardiology, University Medical Centre Groningen, University of Groningen, Groningen, The Netherlands.
Front Cardiovasc Med
February 2025
Tianjin Key Laboratory of Cardiovascular Emergency and Critical Care, Tianjin Municipal Science and Technology Bureau, Tianjin, China.
Background: The mortality of patients with acute myocardial infarction (MI) raised rapidly in last decade and obesity are becoming the major cause to CAD progression, thus inducing heart failure preserved ejection fraction (HFpEF). However, why visceral adipocytes show different effects on healthy and ageing cardiomyocytes is less known.
Methods: GSE251971 was downloaded and Venn diagram between visceral adipocyte genes genes and DEGs was performed to obtain visceral adipocyte-associated DEGs in heart failure.
Med Sci Monit
March 2025
Department of Cardiology, Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
BACKGROUND Epicardial adipose tissue (EAT) and soluble suppression of tumorigenicity 2 (sST2) are valuable markers of myocardial fibrosis, but the relationship between EAT and sST2 remains controversial. This study aimed to evaluate the role of combined EAT measurements and levels of sST2 and the risk of major adverse cardiovascular events (MACEs) in patients with diagnosis of non-ST-elevation myocardial infarction (NSTEMI). MATERIAL AND METHODS This was a single-center retrospective observational study.
View Article and Find Full Text PDFCurr Cardiol Rep
March 2025
Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center El Paso, El Paso, TX, USA.
Purpose Of Review: This review evaluates the role of vascular inflammation in patients who develop myocardial infarction with non-obstructive coronary arteries (MINOCA). It also introduces pericoronary adipose tissue (PCAT) and epicardial adipose tissue (EAT) as possible biomarkers for risk prediction in patients with non-obstructive coronary artery disease (CAD).
Recent Findings: PCAT and EAT contribute to the development and progression of coronary artery inflammation and plaque vulnerability.
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