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Lipoprotein (a) Distribution in Aortic Stenosis Patients: Are Lp(a) Reducing Agents the Ultimate Solution?
Michael-Roy R Durr1, Ian G Burwash2, Lawrence Lau2
1Division of Internal Medicine, Department of Medicine, The Ottawa Hospital, Ottawa, Ontario, Canada.
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.
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