Lipoprotein(a) has no major impact on calcification activity in patients with mild to moderate aortic valve stenosis

Objective To assess whether patients with aortic valve stenosis (AS) with elevated lipoprotein(a) (Lp(a)) are characterised by increased valvular calcification activity compared with those with low Lp(a). Methods We performed F-18-sodium fluoride (F-18-NaF) positron emission tomography/CT in patients with mild to moderate AS (peak aortic jet velocity between 2 and 4 m/s) and high versus low Lp(a) (>50 mg/dL vs <50 mg/dL, respectively). Subjects were matched according to age, gender, peak aortic jet velocity and valve morphology. We used a target to background ratio with the most diseased segment approach to compare F-18-NaF uptake. Results 52 individuals (26 matched pairs) were included in the analysis. The mean age was 66.4 +/- 5.5 years, 44 (84.6%) were men, and the mean aortic valve velocity was 2.80 +/- 0.49 m/s. The median Lp(a) was 79 (64-117) mg/dL and 7 (5-11) mg/dL in the high and low Lp(a) groups, respectively. Systolic blood pressure and low-density-lipoprotein cholesterol (corrected for Lp(a)) were significantly higher in the low Lp(a) group (141 +/- 12 mm Hg vs 128 +/- 12 mm Hg, 2.5 +/- 1.1 mmol/L vs 1.9 +/- 0.8 mmol/L). We found no difference in valvular F-18-NaF uptake between the high and low Lp(a) groups (3.02 +/- 1.26 vs 3.05 +/- 0.96, p=0.902). Linear regression analysis showed valvular calcium score to be the only significant determinant of valvular F-18-NaF uptake (beta=0.63; 95% CI 0.38 to 0.88 per 1000 Agatston unit increase, p<0.001). Lp(a) was not associated with F-18-NaF uptake (beta=0.17; 95% CI -0.44 to 0.88, p=0.305 for the high Lp(a) group). Conclusion Among patients with mild to moderate AS, calcification activity is predominantly determined by established calcium burden. The results do not support our hypothesis that Lp(a) is associated with valvular F-18-NaF uptake.

Automated summary

In patients with mild to moderate aortic valve stenosis, calcification activity is mainly determined by established calcium burden rather than elevated lipoprotein(a) levels. The study's results do not support the hypothesis that Lp(a) is associated with valvular F-18-NaF uptake.