Heart, Lung and Circulation

Cardiac Computed Tomography-Based Epicardial Adipose Tissue Assessment Reveals Association With Electroanatomical Voltage Mapping in Patients With Atrial Fibrillation

Published:August 10, 2022DOI:


      Epicardial adipose tissue (EAT) around the left atrium (LA) can change the electric conduction of the LA, potentially leading to atrial fibrillation (AF).


      The aim of this study was to evaluate whether an association existed between EAT and the electrophysiological properties of adjacent atrial myocardium in patients with AF.


      A total of 201 consecutive patients referred for initial AF catheter ablation were prospectively included. A preprocedural computed tomography scan was performed to assess total and LA-EAT parameters. Detailed point-by-point voltage mapping using an electroanatomical mapping system was realised to assess the LA low-voltage zone (LVZ), defined as an area with bipolar electrograms ≤0.5 mV during sinus rhythm.


      Ninety-one (91) patients (45.3%) presented at least one LVZ. They had a significantly more severe AF pattern (p=0.04) than patients without LVZ, and little difference existed with regard to other clinical variables. Patients with LVZ presented significantly more total EAT volume (162.4±71.3 mL vs 135.5±57.2 mL; p=0.03) and LA-EAT volume (26.4±15.9 mL vs 20.9±10.5 mL; p<0.01) than no-LVZ patients. Multivariable logistic regression analyses revealed total EAT volume index to be an independent predictor of the presence of LVZ (odds ratio [OR] 1.01; 95% confidence interval [CI] 1.01–1.04; p<0.01) and LA-EAT percentage to be an independent predictor of severe LVZ (OR 1.34; 95% CI 1.18–1.64; p<0.001).


      The EAT volume and its distribution around the LA may indicate the presence and severity of LVZ. The assessment of the volume of EAT and its distribution may lead to better risk stratification in patients with AF.


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      Linked Article

      • What is the Relationship Between Epicardial Adipose Tissue, Left Atrial Low Voltage Zones and Atrial Fibrillation?
        Heart, Lung and CirculationVol. 31Issue 11
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          The pathophysiology of atrial fibrillation (AF) is complex and remains incompletely understood. Structural and electrophysiological remodelling of the left atrium have shown to create substrates leading to the development of AF, with atrial fibrotic changes demonstrated to be both present [1] and pathological [2]. Catheter ablation, primarily as pulmonary vein isolation (PVI), has become the core part of the ablation therapy for AF. However, persistent pulmonary vein electrical isolation remains difficult to achieve, and early recurrence of AF post ablation remains a major limiting factor [3].
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