Atrial Fibrillation and Adipokines: A Pathophysiological Perspective

Abstract

Atrial fibrillation (AF) is a prevalent cardiac arrhythmia characterized by irregular and frequently rapid electrical activity in the atria. Adipokines are bioactive molecules that are secreted by adipose tissue, and exert diverse effects on health and disease. Obesity is a complex condition influenced by multiple interconnected factors, and the specific mechanisms linking obesity to AF may vary among individuals. Obesity contributes to the development of atrial arrhythmia. Moreover, obesity plays major roles in the pathophysiology of AF and its associated complications by inducing systemic changes, including altered hemodynamics, heightened sympathetic tone, and a persistent low-grade inflammatory state. Although the associations between overweight or obesity and elevated risk of AF have been established, the underlying mechanisms remain incompletely characterized. This article highlights the pathophysiological aspects of adipokines, such as Angiopoietin-like protein 2, Fibroblast growth factor 21, Lipocalin, Vaspin, Visfatin, and Nesfatin-1, in AF and concludes that adipokines play major roles in AF pathogenesis.