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Vitamin K Antagonists, Non–Vitamin K Antagonist Oral Anticoagulants, and Vascular Calcification in Patients with Atrial Fibrillation

Background  Vitamin K antagonists (VKAs) are associated with coronary artery calcification in low-risk populations, but their effect on calcification of large arteries remains uncertain. The effect of non–vitamin K antagonist oral anticoagulants (NOACs) on vascular calcification is unknown. We inves...

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Autores principales: Peeters, Frederique E. C. M., Dudink, Elton A. M. P., Kimenai, Dorien M., Weijs, Bob, Altintas, Sibel, Heckman, Luuk I. B., Mihl, Casper, Schurgers, Leon J., Wildberger, Joachim E., Meex, Steven J. R., Kietselaer, Bas L. J. H., Crijns, Harry J. G. M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Georg Thieme Verlag KG 2018
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6524908/
https://www.ncbi.nlm.nih.gov/pubmed/31249966
http://dx.doi.org/10.1055/s-0038-1675578
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author Peeters, Frederique E. C. M.
Dudink, Elton A. M. P.
Kimenai, Dorien M.
Weijs, Bob
Altintas, Sibel
Heckman, Luuk I. B.
Mihl, Casper
Schurgers, Leon J.
Wildberger, Joachim E.
Meex, Steven J. R.
Kietselaer, Bas L. J. H.
Crijns, Harry J. G. M.
author_facet Peeters, Frederique E. C. M.
Dudink, Elton A. M. P.
Kimenai, Dorien M.
Weijs, Bob
Altintas, Sibel
Heckman, Luuk I. B.
Mihl, Casper
Schurgers, Leon J.
Wildberger, Joachim E.
Meex, Steven J. R.
Kietselaer, Bas L. J. H.
Crijns, Harry J. G. M.
author_sort Peeters, Frederique E. C. M.
collection PubMed
description Background  Vitamin K antagonists (VKAs) are associated with coronary artery calcification in low-risk populations, but their effect on calcification of large arteries remains uncertain. The effect of non–vitamin K antagonist oral anticoagulants (NOACs) on vascular calcification is unknown. We investigated the influence of use of VKA and NOAC on calcification of the aorta and aortic valve. Methods  In patients with atrial fibrillation without a history of major adverse cardiac or cerebrovascular events who underwent computed tomographic angiography, the presence of ascending aorta calcification (AsAC), descending aorta calcification (DAC), and aortic valve calcification (AVC) was determined. Confounders for VKA/NOAC treatment were identified and propensity score adjusted logistic regression explored the association between treatment and calcification (Agatston score > 0). AsAC, DAC, and AVC differences were assessed in propensity score–matched groups. Results  Of 236 patients (33% female, age: 58 ± 9 years), 71 (30%) used VKA (median duration: 122 weeks) and 79 (34%) used NOAC (median duration: 16 weeks). Propensity score–adjusted logistic regression revealed that use of VKA was significantly associated with AsAC (odds ratio [OR]: 2.31; 95% confidence interval [CI]: 1.16–4.59; p  = 0.017) and DAC (OR: 2.38; 95% CI: 1.22–4.67; p  = 0.012) and a trend in AVC (OR: 1.92; 95% CI: 0.98–3.80; p  = 0.059) compared with non-anticoagulation. This association was absent in NOAC versus non-anticoagulant (AsAC OR: 0.51; 95% CI: 0.21–1.21; p  = 0.127; DAC OR: 0.80; 95% CI: 0.36–1.76; p  = 0.577; AVC OR: 0.62; 95% CI: 0.27–1.40; p  = 0.248). A total of 178 patients were propensity score matched in three pairwise comparisons. Again, use of VKA was associated with DAC ( p  = 0.043) and a trend toward more AsAC ( p  = 0.059), while use of NOAC was not (AsAC p  = 0.264; DAC p  = 0.154; AVC p  = 0.280). Conclusion  This cross-sectional study shows that use of VKA seems to contribute to vascular calcification. The calcification effect was not observed in NOAC users.
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spelling pubmed-65249082019-06-27 Vitamin K Antagonists, Non–Vitamin K Antagonist Oral Anticoagulants, and Vascular Calcification in Patients with Atrial Fibrillation Peeters, Frederique E. C. M. Dudink, Elton A. M. P. Kimenai, Dorien M. Weijs, Bob Altintas, Sibel Heckman, Luuk I. B. Mihl, Casper Schurgers, Leon J. Wildberger, Joachim E. Meex, Steven J. R. Kietselaer, Bas L. J. H. Crijns, Harry J. G. M. TH Open Background  Vitamin K antagonists (VKAs) are associated with coronary artery calcification in low-risk populations, but their effect on calcification of large arteries remains uncertain. The effect of non–vitamin K antagonist oral anticoagulants (NOACs) on vascular calcification is unknown. We investigated the influence of use of VKA and NOAC on calcification of the aorta and aortic valve. Methods  In patients with atrial fibrillation without a history of major adverse cardiac or cerebrovascular events who underwent computed tomographic angiography, the presence of ascending aorta calcification (AsAC), descending aorta calcification (DAC), and aortic valve calcification (AVC) was determined. Confounders for VKA/NOAC treatment were identified and propensity score adjusted logistic regression explored the association between treatment and calcification (Agatston score > 0). AsAC, DAC, and AVC differences were assessed in propensity score–matched groups. Results  Of 236 patients (33% female, age: 58 ± 9 years), 71 (30%) used VKA (median duration: 122 weeks) and 79 (34%) used NOAC (median duration: 16 weeks). Propensity score–adjusted logistic regression revealed that use of VKA was significantly associated with AsAC (odds ratio [OR]: 2.31; 95% confidence interval [CI]: 1.16–4.59; p  = 0.017) and DAC (OR: 2.38; 95% CI: 1.22–4.67; p  = 0.012) and a trend in AVC (OR: 1.92; 95% CI: 0.98–3.80; p  = 0.059) compared with non-anticoagulation. This association was absent in NOAC versus non-anticoagulant (AsAC OR: 0.51; 95% CI: 0.21–1.21; p  = 0.127; DAC OR: 0.80; 95% CI: 0.36–1.76; p  = 0.577; AVC OR: 0.62; 95% CI: 0.27–1.40; p  = 0.248). A total of 178 patients were propensity score matched in three pairwise comparisons. Again, use of VKA was associated with DAC ( p  = 0.043) and a trend toward more AsAC ( p  = 0.059), while use of NOAC was not (AsAC p  = 0.264; DAC p  = 0.154; AVC p  = 0.280). Conclusion  This cross-sectional study shows that use of VKA seems to contribute to vascular calcification. The calcification effect was not observed in NOAC users. Georg Thieme Verlag KG 2018-11-10 /pmc/articles/PMC6524908/ /pubmed/31249966 http://dx.doi.org/10.1055/s-0038-1675578 Text en https://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Peeters, Frederique E. C. M.
Dudink, Elton A. M. P.
Kimenai, Dorien M.
Weijs, Bob
Altintas, Sibel
Heckman, Luuk I. B.
Mihl, Casper
Schurgers, Leon J.
Wildberger, Joachim E.
Meex, Steven J. R.
Kietselaer, Bas L. J. H.
Crijns, Harry J. G. M.
Vitamin K Antagonists, Non–Vitamin K Antagonist Oral Anticoagulants, and Vascular Calcification in Patients with Atrial Fibrillation
title Vitamin K Antagonists, Non–Vitamin K Antagonist Oral Anticoagulants, and Vascular Calcification in Patients with Atrial Fibrillation
title_full Vitamin K Antagonists, Non–Vitamin K Antagonist Oral Anticoagulants, and Vascular Calcification in Patients with Atrial Fibrillation
title_fullStr Vitamin K Antagonists, Non–Vitamin K Antagonist Oral Anticoagulants, and Vascular Calcification in Patients with Atrial Fibrillation
title_full_unstemmed Vitamin K Antagonists, Non–Vitamin K Antagonist Oral Anticoagulants, and Vascular Calcification in Patients with Atrial Fibrillation
title_short Vitamin K Antagonists, Non–Vitamin K Antagonist Oral Anticoagulants, and Vascular Calcification in Patients with Atrial Fibrillation
title_sort vitamin k antagonists, non–vitamin k antagonist oral anticoagulants, and vascular calcification in patients with atrial fibrillation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6524908/
https://www.ncbi.nlm.nih.gov/pubmed/31249966
http://dx.doi.org/10.1055/s-0038-1675578
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