Why the study?
Whether low-attenuation epicardial adipose tissue affects intramyocardial fat and how it relates to anterior and posterior left atrial walls remains unclear.
Does the presence of low-attenuation epicardial adipose tissue correlate with intramyocardial fat burden and left atrial wall thickness heterogeneity in patients undergoing AF ablation?
Does the presence of low-attenuation epicardial adipose tissue correlate with intramyocardial fat burden and left atrial wall thickness heterogeneity in patients undergoing AF ablation?
In vivo CT imaging demonstrates that low-attenuation epicardial adipose tissue is associated with greater intramyocardial fat burden and left atrial wall thickness heterogeneity in patients undergoing AF ablation.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications for AF ablation; leaves open I-EAT's mechanistic role in LA remodeling.
Background Low-attenuation epicardial adipose tissue (I-EAT) has been implicated in atrial myopathy and AF severity. [1-3] Whether I-EAT affects intramyocardial fat (InFAT) and how it relates with anterior (AW) and posterior (PW) left atrial (LA) wall remains unclear. Purpose To investigate the relationship between I-EAT, InFAT (total, total%, and borderzone, BZ%) across AW and PW. Methods We retrospectively enrolled 22 consecutive patients undergoing pre-ablation cardiac CT. Images were processed with a dedicated software to quantify LA wall thickness, burden and distribution of intramyocardial fat (InFAT total% and InFAT BZ%, areas where InFAT intermingles with healthy myocardium), and presence of I-EAT. The LA was divided into segments according to a method previously described to ensure data comparability: segments 3–6 as the posterior wall (PW), segments 8–11 as the anterior wall (AW). [4] After excluding non-suitable segments, a segment-level analysis was performed on 174 segments (88 from AW and 86 from PW). Left atrial thickness heterogeneity (D-LAWT) was defined as the within-segment difference between the maximum and minimum wall thickness values. Predefined HU thresholds from prior literature were applied: I-EAT −96.6 to −45 HU; InFAT Total −194 to −5 HU; InFAT BZ −50 to −5 HU. Results Segments with I-EAT showed greater D-LAWT in both PW (2.5±0.9 vs 1.7±0.9 mm; p<0.001) and AW (2.5±0.9 vs 2.1±0.8 mm; p=0.049), and a higher InFAT burden (InFAT Total% 17.4±10.6 vs 11.6±8.9; InFAT BZ% 13.1±7.6 vs 8.5±5.8; both p<0.001) [Figure 1A] InFAT displayed an epicardial-to-endocardial gradient, with a greater InFAT burden in the more epicardial layers, InFAT BZ% gradient was stronger when I-EAT was present (Spearman’s Rho 0.6; p<0.001 when I-EAT was present vs 0.5; p<0.001, when I-EAT was absent, Z-score 3.5; p < 0.0001). [Figure 1B] I-EAT was more frequent in AW, whereas InFAT burden was greater in PW (BZ% 12.1±7.2 vs 7.8±5.8; Total% 17.5±10.9 vs 9.9±7.7; PW vs AW). D-LAWT correlated with InFAT BZ% in PW (p=0.006) but not in AW (p=0.069). [Figure 2] Conclusions In vivo CT suggests that I-EAT is associated with greater InFAT and higher D-LAWT. Intramyocardial fat showed to be more nuanced in the PW compared to the AW.
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Pistelli et al. (2026) studied this question.
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