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Peer-reviewedCC BY-NC-ND 4.0European Journal of Haematology

Von Willebrand Factor and ADAMTS13 in Relation to Atherosclerosis in the General Population: The Rotterdam Study

  • Mitra Nekouei Shahraki1
  • Frank W. G. Leebeek2
  • Moniek P. M. de Maat2
  • Maryam Kavousi1
  • Daniel Bos1,3
  1. 1Department of Epidemiology Erasmus University Medical Center Rotterdam the Netherlands
  2. 2Department of Hematology Erasmus University Medical Centre Rotterdam the Netherlands
  3. 3Department of Radiology & Nuclear Medicine Erasmus University Medical Center Rotterdam the Netherlands
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Abstract

Background: Higher von Willebrand factor (VWF) levels and lower ADAMTS13 activity are linked to increased risk of atherosclerotic cardiovascular disease, but their association with atherosclerosis burden, a potential underlying mechanism, remains unclear. We investigated associations of these biomarkers with arterial calcification, a surrogate of atherosclerosis, in a general population.

Methods: In 2224 Rotterdam Study participants with measured VWF Antigen level (VWF:Ag) and ADAMTS13 activity (in percentage), computed tomography assessed calcification volume in the coronary arteries (CAC), aortic arch (AAC), and extracranial and intracranial carotid arteries (ECAC, ICAC) (mean age 69.5 ± 6.7 years; 51.5% female). Associations of VWF:Ag, ADAMTS13 activity, and their ratio (linear and quartiles) with calcification (linear and quartiles) were evaluated using multivariable linear and proportional odds logistic regression, adjusting for demographic and cardiovascular factors.

Results: Higher ADAMTS13 activity was significantly associated with lower volume of CAC (β [95% CI]: −0.04 [−0.08, −0.01]), AAC (−0.08 [−0.11, −0.03]), and ECAC (−0.05 [−0.09, −0.01]), but not in ICAC. A higher ADAMTS13:VWF ratio showed stronger inverse associations, extending to ICAC, suggesting a potential interplay between ADAMTS13 and VWF (β [95% CI]: CAC: −0.12 [−0.21, −0.02]; AAC: −0.20 [−0.30, −0.10]; ECAC: −0.08 [−0.18, −0.01]; ICAC: −0.11 [−0.21, −0.02]). The effect size of the ratio increased across quartiles at all artery‐specific locations, strengthening the observed relationship. Across levels of calcification, associations of the biomarkers remained generally unchanged.

Conclusions: Our findings support the potential relevance of ADAMTS13 activity in arterial calcification and, by extension, atherosclerosis. The observed associations may reflect both its balance with VWF and pathways independent of VWF. Future longitudinal and causal studies should determine whether ADAMTS13 influences the development and progression of arterial calcification through VWF‐dependent or VWF‐independent pathways, thereby clarifying its biological role and potentially identifying targets for preventive strategies against atherosclerotic vascular disease.

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Cite

BibTeXRIS
BibTeX
@article{shahraki2026willebrand,
  title = {{Von Willebrand Factor and ADAMTS13 in Relation to Atherosclerosis in the General Population: The Rotterdam Study}},
  author = {Mitra Nekouei Shahraki and Frank W. G. Leebeek and Moniek P. M. de Maat and Maryam Kavousi and Daniel Bos},
  journal = {European Journal of Haematology},
  year = {2026},
  month = aug,
  doi = {10.1111/ejh.70309},
  url = {https://doi.org/10.1111/ejh.70309},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Von Willebrand Factor and ADAMTS13 in Relation to Atherosclerosis in the General Population: The Rotterdam Study
AU  - Mitra Nekouei Shahraki
AU  - Frank W. G. Leebeek
AU  - Moniek P. M. de Maat
AU  - Maryam Kavousi
AU  - Daniel Bos
PY  - 2026
DA  - 2026/08/30
JO  - European Journal of Haematology
DO  - 10.1111/ejh.70309
UR  - https://doi.org/10.1111/ejh.70309
AB  - Background: Higher von Willebrand factor (VWF) levels and lower ADAMTS13 activity are linked to increased risk of atherosclerotic cardiovascular disease, but their association with atherosclerosis burden, a potential underlying mechanism, remains unclear. We investigated associations of these biomarkers with arterial calcification, a surrogate of atherosclerosis, in a general population.  Methods: In 2224 Rotterdam Study participants with measured VWF Antigen level (VWF:Ag) and ADAMTS13 activity (in percentage), computed tomography assessed calcification volume in the coronary arteries (CAC), aortic arch (AAC), and extracranial and intracranial carotid arteries (ECAC, ICAC) (mean age 69.5 ± 6.7 years; 51.5% female). Associations of VWF:Ag, ADAMTS13 activity, and their ratio (linear and quartiles) with calcification (linear and quartiles) were evaluated using multivariable linear and proportional odds logistic regression, adjusting for demographic and cardiovascular factors.  Results: Higher ADAMTS13 activity was significantly associated with lower volume of CAC (β [95% CI]: −0.04 [−0.08, −0.01]), AAC (−0.08 [−0.11, −0.03]), and ECAC (−0.05 [−0.09, −0.01]), but not in ICAC. A higher ADAMTS13:VWF ratio showed stronger inverse associations, extending to ICAC, suggesting a potential interplay between ADAMTS13 and VWF (β [95% CI]: CAC: −0.12 [−0.21, −0.02]; AAC: −0.20 [−0.30, −0.10]; ECAC: −0.08 [−0.18, −0.01]; ICAC: −0.11 [−0.21, −0.02]). The effect size of the ratio increased across quartiles at all artery‐specific locations, strengthening the observed relationship. Across levels of calcification, associations of the biomarkers remained generally unchanged.  Conclusions: Our findings support the potential relevance of ADAMTS13 activity in arterial calcification and, by extension, atherosclerosis. The observed associations may reflect both its balance with VWF and pathways independent of VWF. Future longitudinal and causal studies should determine whether ADAMTS13 influences the development and progression of arterial calcification through VWF‐dependent or VWF‐independent pathways, thereby clarifying its biological role and potentially identifying targets for preventive strategies against atherosclerotic vascular disease.
SN  - 0902-4441
SN  - 1600-0609
ER  -