(P240) LIPOPROTEIN(A) DISTRIBUTION IN AORTIC STENOSIS PATIENTS SEEN AT A SPECIALISED VALVE CLINIC: ARE LP(A) REDUCING AGENTS THE ULTIMATE SOLUTION?

Background: Aortic stenosis (AS) is the most common form of valvular disease in developed countries with no available therapies to stop progression. Lipoprotein A (Lp(a)) is a pro-inflammatory biomarker linked to calcification and the development of AS. Lowering Lp(a) might therefore provide a non-invasive preventative treatment for AS. Current lipid-lowering therapies do not lower Lp(a), thus, novel drugs targeting Lp(a) are under evaluation. The proportion of patients with AS and elevated Lp(a) who might benefit from such therapy is not yet known.

METHODS AND RESULTS: We prospectively and routinely measured Lp(a) levels in AS patients in a specialised valve clinic to determine its distribution. A significantly elevated Lp(a) level was defined as an Lp(a) ≥ 100nmol/L as per the Canadian Cardiovascular Society’s Lipid Guidelines. 162 patients had an Lp(a) level measured (mean age 75 years, 43% female, 25% known coronary artery disease, 65% hypertension, 25% diabetes mellitus, 50% on active treatment for hypercholesterolemia, 46% active or former smokers, 12% abnormal left ventricular ejection fraction, 9% moderate or worse valvular insufficiency of any valve). Baseline AS mean gradient was 29±14 mmHg and aortic valve area (AVA) was 1.05±0.27 cm2.

Mean ± standard deviation and median [interquartile] Lp(a) were 68.6 ±79 nmol/L and 24 [19-90.9] nmol/L. 39 patients (24%) had a clinically significant elevated Lp(a) level. There were no differences in the mean Lp(a) or in the proportion of clinically elevated Lp(a) with respect to age (age ≥70years 72±84 nmol/L, 25%; age < 70years 59±65 nmol/L, 21%; p=0.530, X2 p=0.551) or sex (men 65±75 nmol/L, 22%; women 73±86 nmol/L, 28%; p=0.829, X2 p=0.375). Patients without severe AS (AVA≥1.0cm2) at baseline did not differ in terms of mean Lp(a) and or proportion of clinically significant Lp(a) levels compared to patients with baseline severe AS (AVA < 1.0cm2) (non-severe AS 75±83 nmol/L, 29%; severe AS 58±73 nmol/L, 15%; p=0.217, X2 p=0.098).

Conclusion: In this prospective cohort of AS patients followed in a specialized valve clinic, only 1 in 4 patients had a significantly elevated Lp(a) level. There were no significant differences based on age, sex, or valve disease severity. Novel Lp(a)-lowering therapies may have limited applicability to most patients with AS, underlying the need for further research into the understanding of AS pathophysiology and the development of medical therapies which target different pathways.