Author/Authors :
Leggio, Massimo Department of Medicine and Rehabilitation - Cardiac Rehabilitation Operative Unit - San Filippo Neri Hospital – Salus Infirmorum Clinic - Rome - Italy , Severi, Paolo Department of Medicine and Rehabilitation - Cardiac Rehabilitation Operative Unit - San Filippo Neri Hospital – Salus Infirmorum Clinic - Rome-Italy; Physical Medicine and Neurorehabilitation Operative Unit - Salus Infirmorum Clinic - Rome - Italy , D’emidio, Stefania Physical Medicine and Neurorehabilitation Operative Unit - Salus Infirmorum Clinic - Rome - Italy , Mazza, Andrea Division of Cardiology - Santa Maria della Stella Hospital - Orvieto - Italy
Abstract :
Epicardial adipose tissue, a specialised visceral adipose
tissue, produces numerous pro-inflammatory and pro-atherogenic mediators that promote the initiation and progression
of coronary atherosclerosis (1). Increased epicardial adipose
tissue is related to the presence and angiographic severity of
coronary artery disease and coronary plaque vulnerability and
independently predicts major adverse cardiovascular events
(2). Furthermore, in visceral obesity, the epicardial adipose tissue undergoes conformational and functional changes, leading
to the secretin of pro-inflammatory and pro-atherogenic adipokines (e.g., interleukin-6, tumor necrosis factor α, adiponectin,
leptin, and plasminogen activator inhibitor) (2), which are involved in a causal relationship between inflammation and atrial
fibrillation (3). Consequently, beyond classical cardiovascular
risk factors, a causative link between the epicardial adipose
tissue and atrial fibrillation has also been suggested because
of the structural and functional interplay between atrial fibrillation and the epicardial adipose tissue and the existing evidence of abnormal atrial architecture, adipocyte infiltration,
and atrial fibrosis that predispose the myocardial tissue to arrhythmic genesis (4).
