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The Isolation and Culture of Primary Epicardial Cells Derived from Human Adult and Fetal Heart Specimens
Published on: April 24, 2018
Epicardial adipose tissue in patients with systemic sclerosis
Xu Wang1,2, Steele C Butcher1,3, Rinchyenkhand Myagmardorj4
1Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, Leiden 2333 ZA, The Netherlands.
Epicardial adipose tissue (EAT) is linked to impaired heart function and increased mortality in systemic sclerosis (SSc) patients. Higher EAT mass predicts worse outcomes, highlighting its role in SSc cardiovascular complications.
Area of Science:
- Cardiology
- Rheumatology
- Medical Imaging
Background:
- Epicardial adipose tissue (EAT) is implicated in cardiovascular disease pathogenesis.
- Systemic sclerosis (SSc) is associated with increased cardiovascular risk.
- The role of EAT in cardiac involvement in SSc requires further elucidation.
Purpose of the Study:
- To investigate the association between EAT and left ventricular (LV) function in SSc patients.
- To evaluate the prognostic significance of EAT in SSc.
- To determine if EAT is an independent predictor of mortality in SSc.
Main Methods:
- Prospective study including 230 SSc patients.
- Quantification of EAT mass using non-contrast thorax computed tomography.
- Assessment of LV function via echocardiography.
- Follow-up for all-cause mortality over a median of 8 years.
Main Results:
- Increased EAT mass (≥67g) was associated with impaired LV diastolic function.
- EAT mass remained independently associated with LV diastolic parameters after adjustment.
- Patients with higher EAT mass had a significantly higher rate of all-cause mortality (29% vs. 7%).
- EAT was an independent predictor of all-cause mortality in multivariable analysis.
Conclusions:
- Epicardial adipose tissue is independently associated with left ventricular diastolic dysfunction in SSc patients.
- Elevated EAT mass is a significant predictor of increased all-cause mortality in SSc.
- EAT may serve as a valuable biomarker for cardiovascular risk stratification in SSc.
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