Yannick Kaiser (Netherlands)
Amsterdam UMC Vascular MedicineAuthor Of 2 Presentations
Live Q&A (ID 1551)
O061 - Lipoprotein(a) is not associated with active calcification assessed with 18F-NaF PET/CT in patients with mild to moderate aortic valve stenosis (ID 1450)
Abstract
Background and Aims
Lipoprotein [Lp(a)] has emerged as a causal risk factor for aortic valve stenosis (AVS). 18F-NaF is a surrogate marker for active calcification and disease progression. We hypothesized that AVS patients with elevated Lp(a) levels are characterized by increased valvular 18F-NaF-uptake.
Methods
We performed 18F-NaF PET/CT in patients with mild to moderate AVS, and high versus low Lp(a) levels (> versus <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 (TBR) with a most diseased segment (MDS) approach to compare 18F-NaF-uptake between groups.
Results
A total of 52 individuals were included in the analysis. Mean age was 66.4±5.5 years, 44 (84.6%) were men, and mean aortic valve velocity was 2.80±0.49 m/s. Median Lp(a) was 79 [64-117] and 7 [5-11] mg/dL in the high and low Lp(a) group, respectively. Systolic blood pressure and LDL-C (corrected for Lp(a)) were significantly higher in the low Lp(a) group (141±12 vs 128±12 mmHg, 2.5±1.1 vs 1.9±0.8 mmol/L). We found no difference in valvular 18F-NaF-uptake between 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 18F-NaF-uptake (β=0.63; 95%CI:0.38-0.88 per 1,000 AU increase, p<0.001). Lp(a) was not significantly associated with 18F-NaF uptake (β=0.17; 95%CI:-0.44;0.88, p=0.305 for the high Lp(a) group).
Conclusions
Among patients with mild to moderate AVS, active calcification is predominantly determined by established calcium burden. The results do not support our hypothesis that Lp(a) is associated with valvular 18F-NaF uptake.
Presenter of 2 Presentations
Live Q&A (ID 1551)
O061 - Lipoprotein(a) is not associated with active calcification assessed with 18F-NaF PET/CT in patients with mild to moderate aortic valve stenosis (ID 1450)
Abstract
Background and Aims
Lipoprotein [Lp(a)] has emerged as a causal risk factor for aortic valve stenosis (AVS). 18F-NaF is a surrogate marker for active calcification and disease progression. We hypothesized that AVS patients with elevated Lp(a) levels are characterized by increased valvular 18F-NaF-uptake.
Methods
We performed 18F-NaF PET/CT in patients with mild to moderate AVS, and high versus low Lp(a) levels (> versus <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 (TBR) with a most diseased segment (MDS) approach to compare 18F-NaF-uptake between groups.
Results
A total of 52 individuals were included in the analysis. Mean age was 66.4±5.5 years, 44 (84.6%) were men, and mean aortic valve velocity was 2.80±0.49 m/s. Median Lp(a) was 79 [64-117] and 7 [5-11] mg/dL in the high and low Lp(a) group, respectively. Systolic blood pressure and LDL-C (corrected for Lp(a)) were significantly higher in the low Lp(a) group (141±12 vs 128±12 mmHg, 2.5±1.1 vs 1.9±0.8 mmol/L). We found no difference in valvular 18F-NaF-uptake between 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 18F-NaF-uptake (β=0.63; 95%CI:0.38-0.88 per 1,000 AU increase, p<0.001). Lp(a) was not significantly associated with 18F-NaF uptake (β=0.17; 95%CI:-0.44;0.88, p=0.305 for the high Lp(a) group).
Conclusions
Among patients with mild to moderate AVS, active calcification is predominantly determined by established calcium burden. The results do not support our hypothesis that Lp(a) is associated with valvular 18F-NaF uptake.