Aortic stenosis
Lp(a)-lowering agents could become the first pharmacological therapy for aortic valve stenosis, review argues (J Clin Med 2025)
Original title: Lipoprotein(a) and Aortic Valve Stenosis: From Pathophysiology to Emerging Pharmacological Agents
This review surveys the evidence linking lipoprotein(a) to aortic valve stenosis (AVS), the most common valvular disease in developed countries and one with no approved pharmacological therapy today. It summarises how Lp(a), largely genetically determined and stable across life, causally links lipid metabolism, inflammation and valve calcification, and reviews its diagnostic and prognostic role in AVS. The authors argue that emerging Lp(a)-targeted therapies, antisense oligonucleotides and siRNA-based agents among them, could become the first pharmacological option to slow AVS progression in selected high-risk patients, pending outcomes-trial confirmation. A synthesis of existing evidence and ongoing trials rather than new data, useful as a current state-of-the-field reference on the AVS indication.
Original abstract
Aortic valve stenosis (AVS) is the most common valvular disease in developed countries, and no pharmacological therapy is currently available. Increasing evidence identifies lipoprotein(a) [Lp(a)] as a causal factor linking lipid metabolism, inflammation, and valve calcification. Lp(a) levels are largely genetically determined and remain stable throughout life, making them a potential therapeutic target. This review summarizes the current evidence on Lp(a) and AVS pathophysiology, the diagnostic and prognostic role of Lp(a), and the therapeutic potential of Lp(a)-lowering agents. Emerging Lp(a)-targeted therapies, including antisense oligonucleotides and siRNA-based agents, could reshape AVS management by providing the first pharmacological option to slow disease progression in selected high-risk patients.
aortic stenosismechanismstherapy
Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.