# Lipoprotein(a) and Aortic Valve Stenosis: From Pathophysiology to Emerging Pharmacological Agents

## TL;DR

This paper explores how lipoprotein(a) contributes to aortic valve disease and reviews new drugs that may slow its progression.

## Contribution

The paper highlights emerging pharmacological agents targeting lipoprotein(a) as a novel therapeutic approach for aortic valve stenosis.

## Key findings

- Lipoprotein(a) is identified as a causal factor linking lipid metabolism and valve calcification in aortic valve stenosis.
- Emerging therapies like antisense oligonucleotides and siRNA-based agents show promise in lowering lipoprotein(a) levels.
- Lipoprotein(a) levels are genetically determined and stable, making them a viable target for therapeutic intervention.

## 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.