Epicardial Adipose Tissue Accumulation Confers Atrial Conduction Abnormality
Chrishan J Nalliah, James R Bell, Antonia JA Raaijmakers, Helen M Waddell, Simon P Wells, Gabriel B Bernasochi, Magdalene K Montgomery, Simon Binny, Troy Watts, Subodh B Joshi, Elaine Lui, Choon Boon Sim, Marco Larobina, Michael O'Keefe, John Goldblatt, Alistair Royse, Geoffrey Lee, Enzo R Porrello, Matthew J Watt, Peter M Kistler Show all
Journal of the American College of Cardiology | ELSEVIER SCIENCE INC | Published : 2020
BACKGROUND: Clinical studies have reported that epicardial adipose tissue (EpAT) accumulation associates with the progression of atrial fibrillation (AF) pathology and adversely affects AF management. The role of local cardiac EpAT deposition in disease progression is unclear, and the electrophysiological, cellular, and molecular mechanisms involved remain poorly defined. OBJECTIVES: The purpose of this study was to identify the underlying mechanisms by which EpAT influences the atrial substrate for AF. METHODS: Patients without AF undergoing coronary artery bypass surgery were recruited. Computed tomography and high-density epicardial electrophysiological mapping of the anterior right atriu..View full abstract
Awarded by National Health and Medical Research Council
Research support for this work has been provided by the National Health and Medical Research Council Project (NHMRC: 1099352 and 1125453 to Drs. Delbridge, Bell, and Kalman) and fellowship (1093830 to Dr. Nalliah; 1143224 to Dr. Montgomery) grants. Dr. Sanders has served on the Advisory Board of Biosense Webster, Medtronic, St. Jude Medical, and Boston Scientific; has received lecture and/or consulting fees from Biosense Webster, Medtronic, St. Jude Medical, and Boston Scientific; and has received research funding from Medtronic, St. Jude Medical, Boston Scientific, Biotronik, and Sorin. Dr. Kalman is the recipient of a Practitioner Fellowship (NHMRC: GNT1155084); has received research support from Biosense Webster, St. Jude Medical, and Medtronic; and has received research and fellowship funding from Medtronic, Abbott, Inc., and Biosense Webster. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.