Key result
Emerging Lp(a)-targeted therapies show potential to slow aortic valve stenosis progression in high-risk patients.
Why the study?
Aortic valve stenosis is the most common valvular disease without available pharmacological therapy, and lipoprotein(a) has emerged as a potential therapeutic target linking lipid metabolism, inflammation, and valve calcification.
Do Lp(a)-targeted therapies slow disease progression in patients with aortic valve stenosis?
Do Lp(a)-targeted therapies slow disease progression in patients with aortic valve stenosis?
Lp(a)-lowering therapies represent a promising emerging pharmacological strategy to potentially slow the progression of aortic valve stenosis.
May support Lp(a) lowering to slow AVS progression; hypothesis-generating pending randomized trials.
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.
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Agnello et al. (2025) studied this question. Emerging Lp(a)-targeted therapies, such as antisense oligonucleotides, have potential to slow aortic valve stenosis progression in selected high-risk patients.
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