作者: Sammy Elmariah , Emile R. Mohler
DOI: 10.1007/S11886-010-0089-6
关键词: Calcification 、 Internal medicine 、 Arteriosclerosis 、 Aortic valve 、 Statin 、 Medicine 、 Stenosis 、 Aortic valve stenosis 、 Pathogenesis 、 Calcinosis 、 Cardiology
摘要: 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 AS. However, two randomized trials, SALTIRE SEAS study, showed no benefit with statin therapy for These shed doubt over efficacy AS, although their at early stages valve disease remains possible. In this article, we review pathophysiology fibrocalcific AS discuss future directions its nonsurgical management in post-SEAS era.