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Epicardial Adipose Tissue in Arrhythmogenic Cardiomyopathy
Davide Lapolla1, Luca Canovi1, Maria Letizia Berloni1
1Cardiology Unit, Azienda Ospedaliero Universitaria of Ferrara, 44124 FE, Italy.
Insights
Arrhythmogenic cardiomyopathy (ACM) patients show increased epicardial adipose tissue (EAT). This EAT amount appears to correlate with disease progression, suggesting a role in ACM pathogenesis.
Area of Science:
- Cardiology
- Genetics
- Medical Imaging
Background:
- Arrhythmogenic cardiomyopathy (ACM) is an inherited cardiac condition marked by fibrofatty myocardial replacement.
- Sudden cardiac death is a primary presentation in 16-23% of ACM patients.
- Epicardial fat's role in cardiac disease is increasingly recognized, yet its specific involvement in ACM remains under-explored.
Purpose of the Study:
- To investigate epicardial adipose tissue (EAT) volume in patients with arrhythmogenic cardiomyopathy.
- To determine if EAT volume differs between ACM patients and healthy controls.
- To explore the relationship between EAT volume and ACM disease progression.
Main Methods:
- Cardiac magnetic resonance (CMR) imaging was utilized to quantify EAT volume.
- ACM patients and a control group were included in the study.
- Statistical analyses were performed to compare EAT volumes and assess correlations.
Main Results:
- Patients with ACM exhibited significantly higher EAT volumes compared to control subjects.
- A positive correlation was observed between EAT volume and the clinical progression of ACM.
- Fibrofatty infiltration, a hallmark of ACM, was assessed via CMR.
Conclusions:
- Elevated epicardial adipose tissue is a characteristic feature of arrhythmogenic cardiomyopathy.
- Increased EAT may play a pathogenic role in ACM and its progression.
- CMR is a valuable tool for assessing both myocardial and epicardial fat in ACM.
Abstract:
Arrhythmogenic cardiomyopathy (ACM) is an inherited heart disease characterized by fibrofatty replacement of the ventricular myocardium, with an estimated prevalence of 1:5000 people in the general population. Sudden cardiac death is the first manifestation of this disease in 16-23% of patients with ACM. Fibrofatty infiltration can be identified with noninvasive cardiac magnetic resonance. Studies of epicardial fat deposits have suggested pathogenic roles of epicardial fats in mediating cardiac diseases and arrhythmias. Although myocardial fat infiltration has been well described in ACM, changes in epicardial fat deposits with this disease have not been well investigated. Our study shows that patients with ACM have a higher amount of EAT compared to controls. Additionally, the EAT amount seems to increase with the evolution of the disease.
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