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Fibrocalcific aortic stenosis (AS) results from an active process similar to atherosclerosis that involves basement membrane disruption, lipid deposition, inflammatory cell infiltration, and calcification. Consequently, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have been extensively studied as potential therapeutic agents capable of slowing the progression of AS. However, two randomized trials, SALTIRE and the SEAS study, showed no benefit with statin therapy for AS. These results have shed doubt over the efficacy of statin therapy for AS, although their potential efficacy at early stages of aortic valve disease remains possible. In this article, we review the pathophysiology of fibrocalcific AS and discuss future directions for its nonsurgical management in the post-SEAS era.

The Pathogenesis and Treatment of the Valvulopathy of Aortic Stenosis: Beyond the SEAS