Extent of arterial calcification by conventional vitamin K antagonist treatment.
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2020
2020
Historique:
received:
03
06
2020
accepted:
14
10
2020
entrez:
29
10
2020
pubmed:
30
10
2020
medline:
22
12
2020
Statut:
epublish
Résumé
Vitamin K antagonists (VKA) remain the most frequently prescribed oral anticoagulants worldwide despite the introduction of non-vitamin K antagonist oral anticoagulants (NOAC). VKA interfere with the regeneration of Vitamin K1 and K2, essential to the activation of coagulation factors and activation of matrix-Gla protein, a strong inhibitor of arterial calcifications. This study aimed to clarify whether VKA treatment was associated with the extent of coronary artery calcification (CAC) in a population with no prior cardiovascular disease (CVD). We collected data on cardiovascular risk factors and CAC scores from cardiac CT scans performed as part of clinical examinations (n = 9,672) or research studies (n = 14,166) in the period 2007-2017. Data on use of anticoagulation were obtained from the Danish National Health Service Prescription Database. The association between duration of anticoagulation and categorized CAC score (0, 1-99, 100-399, ≥400) was investigated by ordered logistic regression adjusting for covariates. The final study population consisted of 17,254 participants with no prior CVD, of whom 1,748 and 1,144 had been treated with VKA or NOAC, respectively. A longer duration of VKA treatment was associated with higher CAC categories. For each year of VKA treatment, the odds of being in a higher CAC category increased (odds ratio (OR) = 1.032, 95%CI 1.009-1.057). In contrast, NOAC treatment duration was not associated with CAC category (OR = 1.002, 95%CI 0.935-1.074). There was no significant interaction between VKA treatment duration and age on CAC category. Adjusted for cardiovascular risk factors, VKA treatment-contrary to NOAC-was associated to higher CAC category.
Sections du résumé
BACKGROUND AND AIMS
Vitamin K antagonists (VKA) remain the most frequently prescribed oral anticoagulants worldwide despite the introduction of non-vitamin K antagonist oral anticoagulants (NOAC). VKA interfere with the regeneration of Vitamin K1 and K2, essential to the activation of coagulation factors and activation of matrix-Gla protein, a strong inhibitor of arterial calcifications. This study aimed to clarify whether VKA treatment was associated with the extent of coronary artery calcification (CAC) in a population with no prior cardiovascular disease (CVD).
METHODS
We collected data on cardiovascular risk factors and CAC scores from cardiac CT scans performed as part of clinical examinations (n = 9,672) or research studies (n = 14,166) in the period 2007-2017. Data on use of anticoagulation were obtained from the Danish National Health Service Prescription Database. The association between duration of anticoagulation and categorized CAC score (0, 1-99, 100-399, ≥400) was investigated by ordered logistic regression adjusting for covariates.
RESULTS
The final study population consisted of 17,254 participants with no prior CVD, of whom 1,748 and 1,144 had been treated with VKA or NOAC, respectively. A longer duration of VKA treatment was associated with higher CAC categories. For each year of VKA treatment, the odds of being in a higher CAC category increased (odds ratio (OR) = 1.032, 95%CI 1.009-1.057). In contrast, NOAC treatment duration was not associated with CAC category (OR = 1.002, 95%CI 0.935-1.074). There was no significant interaction between VKA treatment duration and age on CAC category.
CONCLUSIONS
Adjusted for cardiovascular risk factors, VKA treatment-contrary to NOAC-was associated to higher CAC category.
Identifiants
pubmed: 33119722
doi: 10.1371/journal.pone.0241450
pii: PONE-D-20-16893
pmc: PMC7595268
doi:
Substances chimiques
Anticoagulants
0
Vitamin K
12001-79-5
Types de publication
Journal Article
Multicenter Study
Observational Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0241450Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
Références
Clin Epidemiol. 2012;4:303-13
pubmed: 23204870
Clin Epidemiol. 2014 Dec 31;7:53-64
pubmed: 25657592
PLoS One. 2012;7(8):e43229
pubmed: 22952653
J Cell Mol Med. 2010 Sep;14(9):2203-10
pubmed: 20716128
Arthritis Care Res (Hoboken). 2015 May;67(6):848-54
pubmed: 25418360
Int J Cardiol. 2018 Jun 1;260:11-15
pubmed: 29530620
Adv Cardiol. 2007;44:234-244
pubmed: 17075212
Ann Intern Med. 2009 May 5;150(9):604-12
pubmed: 19414839
BMJ Open. 2017 Dec 10;7(12):e017493
pubmed: 29229652
JACC Cardiovasc Imaging. 2018 Sep;11(9):1315-1323
pubmed: 28734922
BMJ Open. 2018 Aug 23;8(8):e022019
pubmed: 30139903
JACC Cardiovasc Imaging. 2017 Aug;10(8):858-866
pubmed: 28797406
J Am Heart Assoc. 2016 Feb 22;5(2):
pubmed: 26903006
Eur Heart J. 2012 May;33(10):1201-13
pubmed: 22547221
Blood. 2010 Jun 17;115(24):5121-3
pubmed: 20354170
Nutrients. 2015 Oct 28;7(11):8905-15
pubmed: 26516910
Circ Cardiovasc Imaging. 2017 Dec;10(12):
pubmed: 29222121
Eur Heart J. 2011 Oct;32(20):2555-62
pubmed: 21775389
Am Heart J. 2019 Jun;212:129-133
pubmed: 31002997
J Cardiovasc Electrophysiol. 2018 May;29(5):707-714
pubmed: 29478291
Am Heart J. 2018 Dec;206:127-130
pubmed: 30227941
BMJ Open. 2018 Mar 3;8(3):e018391
pubmed: 29502085
Arterioscler Thromb Vasc Biol. 2013 Nov;33(11):2618-24
pubmed: 23990204
Nature. 1997 Mar 6;386(6620):78-81
pubmed: 9052783
Vasc Health Risk Manag. 2008;4(2):315-24
pubmed: 18561507
Trials. 2015 Dec 05;16:554
pubmed: 26637993
J Am Coll Cardiol. 1990 Mar 15;15(4):827-32
pubmed: 2407762
Herz. 2020 Sep;45(6):580-585
pubmed: 30276478
Vasc Health Risk Manag. 2009;5(1):185-97
pubmed: 19436645
Arterioscler Thromb Vasc Biol. 1998 Sep;18(9):1400-7
pubmed: 9743228