Calcific aortic valve stenosis (CAVS) is the most frequent valve disorder in adults, with a steadily increasing incidence as the population ages. Currently, there are no effective treatments that prevent or delay disease progression. In addition to the progressive calcification, there is increasing recognition of the underlying roles of oxidative stress, chronic inflammation, lipoprotein deposition and induction of osteogenic signaling in driving progression of the valve calcification characteristic of CAVS. Although traditional markers of CAVS progression, such as increased valve gradients and reduced areas, are currently utilized to guide clinical decisions regarding valve replacement, these measures may not capture progression of early, potentially modifiable disease. Hence, there is a need for more sensitive markers such as AV calcification, to monitor disease progression in CAVS. We review the current understanding of the pathogenesis and progression of CAVS, highlight the unmet need for newer medical therapies, discuss emerging therapies and novel techniques to assess disease progression and therapeutic response.
Editors
Editor-in-Chief
Harlan M. Krumholz, MD, SM, FACC
CME Editor
Ragavendra R. Baliga, MD
Author
Milind Desai, MD
Eugene Braunwald, MD
Important Dates
Date of Release: August 25, 2025
Term of Approval/Date of CME/MOC Expiration: August 24, 2026