Aortic stenosis (AS) is the most common valvular heart disease in industrialized countries, with a prevalence that increases with age, and represents an important cause of morbidity, hospitalization and death in the elderly population.
It is widely recognized that AS is a progressive and active process that leads to calcific degeneration of the aortic valve, involving complex and multifactorial pathological mechanisms, and including triggering factors which lead to inflammation. In the last decades, several pieces of evidence have suggested a pathogenetic role of the epicardial adipose tissue (EAT), the cardiac visceral fat depot, in the development and progression of AS. EAT contributes to the inflammatory burden of AS through the secretion of numerous pro-inflammatory and pro-atherogenic cytokines. Therefore, this review aims to explore the potential role of EAT in the pathogenesis of AS and the potential therapeutic perspectives to slower AS progression.