Aortic stenosis (AS) is a dynamic degenerative process that shares many pathophysiological features with atherogenesis, from initial proinflammatory calcification and focal thickening of the valve leaflets to obstruction of left ventricular outflow due to superimposed of severe calcification and immobilization of the valve leaflets. As the prevalence increases with age, AS is expected to become one of the most common heart diseases worldwide. In both obese and nonobese patients, persistent thickening of epicardial adipose tissue (EAT) is associated with a shift in its normal metabolic functions toward a dysmetabolic and proatherogenic phenotype that may impair the physiology of adjacent coronary arteries and promote the occurrence of coronary atherosclerosis. In tight analogy with atherosclerosis, recent clinical evidence indicates that EAT may also exert a deleterious role in promoting AS and contributing to myocardial dysfunction, leading to increased health risk for elderly patients with AS and an economic burden on the health care system. This review discusses the clinical and pathologic evidence for the association between EAT and AS and concomitant left ventricular hypertrophy, and provides new insights for the future direction of AS diagnosis and treatment.
Keywords: Aortic stenosis; Calcification, epicardial adipose tissue; Inflammation; Left ventricular remodeling.
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