Only 1 in 4 aortic stenosis patients has high Lp(a), limiting how many could benefit from future Lp(a)-lowering therapies, 162-patient Canadian valve clinic study finds (JACC Adv 2025)

Original title: Lipoprotein (a) Distribution in Aortic Stenosis Patients: Are Lp(a) Reducing Agents the Ultimate Solution?

JACC Adv · 21 March 2025 · 7

Durr MR, Burwash IG, Lau L, Alfraidi H, Mulloy A, Tavoosi A, Arangalage D, Chan V, Lakhani M, Aljamaan A, Prosperi-Porta G, Gauda R et al.

This cross-sectional study measured Lp(a) in 162 unselected aortic stenosis (AS) patients (mean age 75, 43% female, mean pressure gradient 29 mm Hg) seen at a specialised Canadian valve clinic, to characterise how many might benefit from Lp(a)-lowering therapies now under evaluation for slowing AS progression, using the Canadian Cardiovascular Society threshold of 100 nmol/L for high Lp(a). Mean Lp(a) was 69 nmol/L (median 24, IQR 19-91), and 39 patients (24%) had a high Lp(a) level, with no significant differences in mean Lp(a) or the proportion with high Lp(a) by sex, age, or AS severity (all P > 0.20). The authors conclude that in this unselected valve-clinic population, only about 1 in 4 AS patients has significantly elevated Lp(a), suggesting future Lp(a)-lowering therapies would have limited applicability to most AS patients, and highlighting the need for research into other therapeutic pathways for the majority whose AS is not Lp(a)-driven.

Original abstract

Background: There is currently no medical therapy that can slow down/stop the progression of aortic stenosis (AS). Novel drugs lowering lipoprotein(a) (Lp[a]), a proinflammatory particle linked to AS development, are currently under evaluation, but the proportion of patients with AS and elevated Lp(a) who might benefit from such therapy is not known.

Objectives: The authors sought to characterize the prevalence of high Lp(a) in patients with AS to determine the role of future Lp(a)-lowering therapies.

Methods: In a nonselected Canadian population of AS patients seen in our specialized valve clinic, we assessed Lp(a) levels. High Lp(a) level was defined as an Lp(a) ≥100 nmol/L as per the Canadian Cardiovascular Society's Lipid Guidelines.

Results: Lp(a) levels were measured in 162 patients (mean age: 75 ± 10 years, 43% female, mean pressure gradient: 29 ± 14 mm Hg). Mean Lp(a) was 69 ± 79 nmol/L (median: 24 nmol/L, IQR: 19-91 nmol/L), and 39 patients (24%) had a high Lp(a) level. There were no differences in the mean Lp(a) or in the proportion of high Lp(a) levels with respect to sex, age, or AS severity (all P > 0.20).

Conclusions: In this cross-sectional series of unselected AS patients followed in a valve clinic, only 1 in every 4 patients had a significantly elevated Lp(a) level. Novel Lp(a)-lowering therapies may have limited applicability to most patients with AS and highlight the need for further research into understanding the pathophysiology of AS and developing medical therapies targeting different pathways.

Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.