Key result
Long-term VKA use linked to accelerated coronary artery calcification, whereas DOACs show no association.
Why the study?
Vitamin K antagonists may promote vascular calcification via inhibition of vitamin K-dependent proteins, prompting evaluation of the association of long-term VKA or DOAC therapy with coronary artery calcification progression.
Does long-term therapy with vitamin K antagonists or direct oral anticoagulants increase the progression of coronary artery calcification in adults without prior coronary revascularization?
Cohort (n=7,365)
Yes
Does long-term therapy with vitamin K antagonists or direct oral anticoagulants increase the progression of coronary artery calcification in adults without prior coronary revascularization?
Long-term use of vitamin K antagonists, but not direct oral anticoagulants, is associated with accelerated, duration-dependent progression of coronary artery calcification.
May warrant caution with prolonged vitamin K antagonists; extends observational evidence but leaves open need for randomized confirmation.
AIMS Vitamin K antagonists (VKAs) may promote vascular calcification through inhibition of vitamin K-dependent proteins. We aimed to examine the association between long-term anticoagulant therapy with VKA or direct oral anticoagulants (DOACs) and progression of coronary artery calcification (CAC) in a large, population-based cohort. METHODS We included men and women (<75 years) with two non-contrast CT scans for CAC ≥4 years apart, categorized into VKA, DOAC, mixed anticoagulant, and control groups. Cumulative treatment duration was calculated from prescription data. CAC progression was analysed using zero-inflated negative binomial and multinomial logistic regression, adjusting for traditional cardiovascular risk factors, baseline CAC and follow-up time. Sensitivity analyses excluded participants predisposed to vascular mineralization (statin use, mechanical valve, renal impairment). RESULTS 7,365 participants with similar risk profile were included. VKA therapy was significantly associated with CAC progression (incidence rate ratio (IRR) =1.004 per month of treatment (95% CI: 1.000-1.007)), showing a duration–response relationship. Long-term VKA therapy (>48months) was independently associated with higher CAC progression (IRR=1.43 (95% CI: 1.076-1.908)), and an increased risk of having severe CAC (CAC score ≥400) at follow-up (relative risk ratio (RRR) =1.012 per month of treatment (95% CI: 1.001-1.023)). In contrast, DOAC therapy was not associated with CAC progression. Sensitivity analyses confirmed that the association with VKA was not driven by high-risk subgroups. CONCLUSION In this large, real-world cohort, VKA - but not DOAC - therapy was associated with accelerated, duration-dependent CAC progression. These findings suggest that choice of anticoagulant may influence CAC, yet the clinical implications remain to be determined.
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Hasific et al. (2026) conducted a cohort in Coronary artery calcification (n=7,365). Vitamin K antagonists (VKAs) vs. No anticoagulant therapy (control) or DOACs was evaluated on Progression of coronary artery calcification (follow-up CAC score) (IRR 1.004 per month of treatment, 95% CI 1.000-1.007, p=0.033). Long-term exposure to vitamin K antagonists was associated with accelerated progression of coronary artery calcification (IRR 1.004 per month of treatment), whereas DOAC therapy showed no such association.
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