title: Impact of obesity on cardiac metabolism, fibrosis, and function.
abstract: Obesity is a global pandemic with a huge burden on the healthcare system. Obesity is not only linked to the development of risk factors for atherosclerotic vascular disease but also has a strong association with ventricular hypertrophy, heart failure, atrial fibrillation, and stroke. Recent experimental and clinical studies have demonstrated that obesity is associated with cardiac dysfunction, adipokine dysregulation, and activation of the pro-fibrotic signaling pathways leading to cardiac fibrosis, which is a key structural change responsible for atrial fibrillation. Importantly, these also have been shown to be reversible with weight reduction strategies. This review discusses the alterations in cardiac metabolism and function due to obesity. In addition, it addresses the complex and not yet fully understood mechanisms underlying cardiac fibrosis, with a focus on atrial substrate predisposing to atrial fibrillation in obesity.
authors.affiliation: Centre for Heart Rhythm Disorders (CHRD), South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia.
authors.forename: Rajiv
authors.initials: R
authors.lastname: Mahajan
authors.affiliation: Centre for Heart Rhythm Disorders (CHRD), South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia.
authors.forename: Dennis H
authors.initials: DH
authors.lastname: Lau
authors.affiliation: Centre for Heart Rhythm Disorders (CHRD), South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia. Electronic address: prash.sanders@adelaide.edu.au.
authors.forename: Prashanthan
authors.initials: P
authors.lastname: Sanders
mesh_terms: D001281:Atrial Fibrillation / Q000209:etiology* / Q000503:physiopathology; D003324:Coronary Artery Disease / Q000209:etiology* / Q000503:physiopathology; D004719:Endomyocardial Fibrosis / Q000209:etiology* / Q000503:physiopathology; D006321:Heart / Q000502:physiology; D006801:Humans; D009765:Obesity / Q000150:complications* / Q000503:physiopathology