This process triggers inflammation and oxidative stress that lead progressively to valve calcification. Lipid deposition into intima cusps with subsequent oxidation constitutes the primary mechanism of pathogenesis of degenerative AS. This editorial describes the pathophysiology and management strategies of AS, with a particular focus on the recent extension of TAVR to low-risk patients. Iterations in TAVR technologies and bioprosthetic valves’ design have expanded TAVR indications to patients across the spectrum of surgical risk. Historically, surgical aortic valve replacement (SAVR) has been the mainstay therapy in most patients, while transcatheter aortic valve replacement (TAVR) has been limited to those at high risk for surgery. In addition to medical therapy, aortic valve replacement is often needed to limit disease progression, improve prognosis, and enhance the quality of life. ![]() As a result of this decrease in cardiac output, patients complain of decreased exercise capacity that might progress to heart failure or even death if left untreated. The progressive fibrosis and calcification of the aortic valve obstruct blood flow from the left ventricle to the ascending aorta during systole. bicuspid aortic valve) and rheumatic heart disease, can lead to AS, although degenerative processes directly related to aging are the most common. 1,2 Several etiologies, including congenital abnormalities (i.e. ![]() Aortic valve stenosis (AS) is the most common form of valvular heart disease in developed countries, with a prevalence that increases exponentially with advancing age.
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