Patients with persistent atrial fibrillation and metabolic comorbidities have an altered inflammatory state of atrial epicardial adipose tissue, which is linked to CT-attenuation
Year: 2025
Type: article
Study design: Observational Study
Abstract: BACKGROUND: Epicardial adipose tissue (EAT) is linked to both Atrial fibrillation (AF) and metabolic syndrome (MetS). Whether EAT inflammation relates to AF type, recurrence after ablation, or MetS, is incompletely known, likewise if it can be measured by CT angiography. AIM: To establish the link between (1) atrial EAT inflammatory composition and AF type, AF recurrence, and metabolic comorbidities. (2) EAT inflammation and EAT-volume or density. METHODS: Patients undergoing thoracoscopic ablation for advanced AF (that is, usually persistent, with enlarged left atria and previous failed ablations) with a cardiac CT-scan before and 6 months after surgery were enrolled. CT-EAT atrial volume and attenuation (density), were used for analyses. Patients' left atrial appendages (LAA + EAT) were excised during ablation and stained for adipocytes and different inflammatory cells. RESULTS: , (p = 0.003), and less anti-inflammatory CD163 + macrophages: 126[134] versus 224[179], (p = 0.03). The AUC curve for differentiating persistent from paroxysmal AF through neutrophil-count was 0.75 (p value < 0.001, CI 0.63-0.87). EAT neutrophil-count related to CT-EAT-attenuation (multivariable analysis: expB 1.01, CI 1.00-1.02, (p = 0.04)). CT-EAT-attenuation distinguished persistent from paroxysmal AF: - 73.0 ± 4.6 versus - 75.3 ± 5.3HU, (p = 0.03). Patients with versus without recurrence had similar inflammatory cell counts, but larger adipocytes, multivariable analysis: ExpB 1.002, CI 1.00-1.003, (p = 0.02). Hypertensive and diabetic patients also had an increased adipocyte size. CONCLUSION: Patients with persistent versus paroxysmal AF exhibited increased EAT neutrophils, which is reflected by CT-EAT-attenuation. Those with AF recurrence, hypertension and diabetes had adipocyte hypertrophy which may imply a common mechanism underlying these conditions.
Source: Cardiovascular Diabetology
Authors: Eva R. Meulendijks, Benedetta Fabrizi, Steffen Bruns, Etto C. Eringa, Ron Hoebe, Thomas van den Boogert, Robin Wesselink, Rushd F. M. Al-Shama, Tim A. C. de Vries, Auriane C. Ernault, H. W. M. Niessen, Wim J. P. van Boven, Antoine H. G. Driessen, I. Zbairi, Pietro Zappala, Damini Dey, Ivana Isgum, R. Nils Planken, Sébastien P. J. Krul, Joris R. de Groot
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $4,290
OpenAlex ID: W7117309236
