Patients with persistent atrial fibrillation and metabolic comorbidities have an altered inflammatory state of atrial epicardial adipose tissue, which is linked to CT-attenuation.
Meulendijks E, Fabrizi B, et al. • Cardiovascular diabetology • 2026
Patients with persistent versus paroxysmal AF exhibited increased EAT neutrophils and decreased anti-inflammatory macrophages, which is reflected by CT-EAT-attenuation, while AF recurrence, hypertension, and diabetes were associated with adipocyte hypertrophy suggesting a common underlying mechanism.
Key Findings
Results
Patients with persistent AF had significantly more EAT neutrophils compared to those with paroxysmal AF.
Neutrophil counts were 155[257] versus 63[106] cells/mm2 in persistent versus paroxysmal AF patients (p = 0.003).
113 of 134 included patients had a left atrial appendage available for (immuno)histochemistry.
The AUC for differentiating persistent from paroxysmal AF through neutrophil count was 0.75 (p < 0.001, CI 0.63–0.87).
Patients underwent thoracoscopic ablation for advanced AF, typically persistent with enlarged left atria and previous failed ablations.
Results
Patients with persistent AF had significantly fewer anti-inflammatory CD163+ macrophages in EAT compared to those with paroxysmal AF.
CD163+ macrophage counts were 126[134] versus 224[179] cells/mm2 in persistent versus paroxysmal AF patients (p = 0.03).
CD163+ macrophages are characterized as anti-inflammatory in the paper.
This finding indicates an altered inflammatory state in persistent AF beyond just neutrophil elevation.
Results
CT-EAT attenuation distinguished persistent from paroxysmal AF.
CT-EAT attenuation was -73.0 ± 4.6 HU in persistent AF versus -75.3 ± 5.3 HU in paroxysmal AF (p = 0.03).
Higher (less negative) attenuation values corresponded to persistent AF, indicating denser EAT.
Cardiac CT scans were performed before and 6 months after surgery.
Results
EAT neutrophil count was independently associated with CT-EAT attenuation in multivariable analysis.
Multivariable analysis showed expB 1.01 (CI 1.00–1.02, p = 0.04) for the relationship between neutrophil count and CT-EAT attenuation.
This finding links histological inflammatory cell content to a non-invasive CT-based measure.
CT-EAT attenuation (density) was used as a surrogate marker for EAT inflammation.
Results
Patients with AF recurrence after ablation had larger adipocytes in EAT compared to those without recurrence.
Multivariable analysis for adipocyte size and AF recurrence: ExpB 1.002 (CI 1.00–1.003, p = 0.02).
Patients with versus without recurrence had similar inflammatory cell counts.
Adipocyte hypertrophy rather than inflammatory cell infiltration was the distinguishing feature in AF recurrence.
Results
Hypertensive and diabetic patients also exhibited increased EAT adipocyte size.
Both hypertension and diabetes were associated with adipocyte hypertrophy in EAT.
This finding parallels the adipocyte hypertrophy observed in patients with AF recurrence.
The authors suggest this may imply a common mechanism underlying AF recurrence, hypertension, and diabetes.
Metabolic comorbidities (metabolic syndrome) were a primary focus of the study alongside AF type.
Methods
The study enrolled 134 patients undergoing thoracoscopic ablation for advanced AF with cardiac CT imaging before and after surgery.
134 patients were included in total; 113 had a left atrial appendage (LAA + EAT) available for (immuno)histochemistry.
Left atrial appendages were excised during ablation and stained for adipocytes and different inflammatory cells.
CT-EAT atrial volume and attenuation (density) were used for analyses.
The study population represented advanced AF, typically persistent, with enlarged left atria and previous failed ablations.
Meulendijks E, Fabrizi B, Bruns S, Eringa E, Hoebe R, van den Boogert T, et al.. (2026). Patients with persistent atrial fibrillation and metabolic comorbidities have an altered inflammatory state of atrial epicardial adipose tissue, which is linked to CT-attenuation.. Cardiovascular diabetology. https://doi.org/10.1186/s12933-025-02985-1