Epicardial Adipose Tissue Is Associated With Left Atrial Dysfunction in People Without Obstructive Coronary Artery Disease or Atrial Fibrillation |
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Authors: | Lei Zhao Danielle L. Harrop Arnold C.T. Ng William Y.S. Wang |
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Affiliation: | 1. Department of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China;2. Department of Cardiology, Princess Alexandra Hospital, Brisbane, Australia;3. Faculty of Medicine, The University of Queensland, Brisbane, Australia |
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Abstract: | BackgroundEpicardial adipose tissue (EAT) is a metabolically active visceral fat depot. Although EAT volume is associated with the incidence and burden of atrial fibrillation (AF), its role in subclinical left atrial (LA) dysfunction is unclear. This study aims to evaluate the relationships between EAT volumes, LA function, and LA global longitudinal strain.MethodsOne hundred and thirty people without obstructive coronary artery disease or AF were prospectively recruited into the study in Australia and underwent cardiac computed tomography and echocardiography. EAT volume was quantified from cardiac computed tomography. Echocardiographic 3-dimensional (3D) volumetric measurements and 2D speckle-tracking analysis were performed.ResultsUsing the overall median body surface area–indexed total EAT volume (EATi), the study cohort was divided into 2 groups of larger and smaller EATi volume. Subjects with larger EATi volume had significantly impaired LA reservoir function (3D LA ejection fraction, 46.1% ± 8.9% vs 49.0% ± 7.0%, P = 0.044) and reduced LA global longitudinal strain (37.6% ± 10.2% vs 44.1% ± 10.7%, P < 0.001). Total EATi volume was a predictor of impaired 2D LA global longitudinal strain (standardized β = ?0.204, P = 0.034), reduced 3D LA ejection fraction (standardized β = ?0.208, P = 0.036), and reduced 3D active LA ejection fraction (standardized β = ?0.211, P = 0.017). Total EATi volume, rather than LA EATi volume, was the more important predictor of LA dysfunction.ConclusionsIndexed EAT volume is independently associated with subclinical LA dysfunction and impaired global longitudinal strain in people without obstructive coronary artery disease or a history of AF. |
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Keywords: | Corresponding author: Dr William Y.S. Wang, Department of Cardiology, Princess Alexandra Hospital, The University of Queensland, 199 Ipswich Road, Woolloongabba, Brisbane 4102, Australia. Tel.: +61-7-3176-2111 fax: +61-7-3176-7630. |
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