TY - JOUR
T1 - Lipoprotein(a) is associated with the onset but not the progression of aortic valve calcification
AU - Kaiser, Yannick
AU - van der Toorn, Janine E.
AU - Singh, Sunny S.
AU - Zheng, Kang H.
AU - Kavousi, Maryam
AU - Sijbrands, Eric J. G.
AU - Stroes, Erik S. G.
AU - Vernooij, Meike W.
AU - de Rijke, Yolanda B.
AU - Boekholdt, S. Matthijs
AU - Bos, Daniel
N1 - © The Author(s) 2022. Published by Oxford University Press on behalf of European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
PY - 2022/10/14
Y1 - 2022/10/14
N2 - Aim: Lipoprotein(a) [Lp(a)] is a potential causal factor in the pathogenesis of aortic valve disease. However, the relationship of Lp(a) with new onset and progression of aortic valve calcium (AVC) has not been studied. The purpose of the study was to assess whether high serum levels of Lp(a) are associated with AVC incidence and progression. Methods and results: A total of 922 individuals from the population-based Rotterdam Study (mean age 66.0±4.2 years, 47.7% men), whose Lp(a) measurements were available, underwent non-enhanced cardiac computed tomography imaging at baseline and after a median follow-up of 14.0 [interquartile range (IQR) 13.9-14.2] years. New-onset AVC was defined as an AVC score >0 on the follow-up scan in the absence of AVC on the first scan. Progression was defined as the absolute difference in AVC score between the baseline and follow-up scan. Logistic and linear regression analyses were performed to evaluate the relationship of Lp(a) with baseline, new onset, and progression of AVC. All analyses were corrected for age, sex, body mass index, smoking, hypertension, dyslipidaemia, and creatinine. AVC progression was analysed conditional on baseline AVC score expressed as restricted cubic splines. Of the 702 individuals without AVC at baseline, 415 (59.1%) developed new-onset AVC on the follow-up scan. In those with baseline AVC, median annual progression was 13.5 (IQR = 5.2-37.8) Agatston units (AU). Lipoprotein(a) concentration was independently associated with baseline AVC [odds ratio (OR) 1.43 for each 50 mg/dL higher Lp(a); 95% confidence interval (CI) 1.15-1.79] and new-onset AVC (OR 1.30 for each 50 mg/dL higher Lp(a); 95% CI 1.02-1.65), but not with AVC progression (β:-71 AU for each 50 mg/dL higher Lp(a); 95% CI-117; 35). Only baseline AVC score was significantly associated with AVC progression (P < 0.001). Conclusion: In the population-based Rotterdam Study, Lp(a) is robustly associated with baseline and new-onset AVC but not with AVC progression, suggesting that Lp(a)-lowering interventions may be most effective in pre-calcific stages of aortic valve disease.
AB - Aim: Lipoprotein(a) [Lp(a)] is a potential causal factor in the pathogenesis of aortic valve disease. However, the relationship of Lp(a) with new onset and progression of aortic valve calcium (AVC) has not been studied. The purpose of the study was to assess whether high serum levels of Lp(a) are associated with AVC incidence and progression. Methods and results: A total of 922 individuals from the population-based Rotterdam Study (mean age 66.0±4.2 years, 47.7% men), whose Lp(a) measurements were available, underwent non-enhanced cardiac computed tomography imaging at baseline and after a median follow-up of 14.0 [interquartile range (IQR) 13.9-14.2] years. New-onset AVC was defined as an AVC score >0 on the follow-up scan in the absence of AVC on the first scan. Progression was defined as the absolute difference in AVC score between the baseline and follow-up scan. Logistic and linear regression analyses were performed to evaluate the relationship of Lp(a) with baseline, new onset, and progression of AVC. All analyses were corrected for age, sex, body mass index, smoking, hypertension, dyslipidaemia, and creatinine. AVC progression was analysed conditional on baseline AVC score expressed as restricted cubic splines. Of the 702 individuals without AVC at baseline, 415 (59.1%) developed new-onset AVC on the follow-up scan. In those with baseline AVC, median annual progression was 13.5 (IQR = 5.2-37.8) Agatston units (AU). Lipoprotein(a) concentration was independently associated with baseline AVC [odds ratio (OR) 1.43 for each 50 mg/dL higher Lp(a); 95% confidence interval (CI) 1.15-1.79] and new-onset AVC (OR 1.30 for each 50 mg/dL higher Lp(a); 95% CI 1.02-1.65), but not with AVC progression (β:-71 AU for each 50 mg/dL higher Lp(a); 95% CI-117; 35). Only baseline AVC score was significantly associated with AVC progression (P < 0.001). Conclusion: In the population-based Rotterdam Study, Lp(a) is robustly associated with baseline and new-onset AVC but not with AVC progression, suggesting that Lp(a)-lowering interventions may be most effective in pre-calcific stages of aortic valve disease.
KW - Aged
KW - Aortic Valve Stenosis/epidemiology
KW - Aortic Valve/diagnostic imaging
KW - Calcinosis
KW - Calcium
KW - Creatinine
KW - Female
KW - Humans
KW - Lipoprotein(a)
KW - Male
KW - Middle Aged
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85137809809&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/35869873
U2 - https://doi.org/10.1093/eurheartj/ehac377
DO - https://doi.org/10.1093/eurheartj/ehac377
M3 - Article
C2 - 35869873
SN - 0195-668X
VL - 43
SP - 3960
EP - 3967
JO - European Heart journal
JF - European Heart journal
IS - 39
ER -