Skip to content

Aortic Calcification and Vitamin K Antagonists

Aortic Calcification and Vitamin K Antagonists

Status
Completed
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT02823093
Acronym
AVKAL
Enrollment
73
Registered
2016-07-06
Start date
2016-04-19
Completion date
2021-03-18
Last updated
2026-06-12

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Vascular Calcification

Keywords

vascular calcification, aortic calcification, vitamin K antagonist, fluindione, warfarin, matrix gla protein

Brief summary

The vitamin K antagonists (VKA) are necessary drugs of prevention and treatment of thrombo-embolic disease. The AVKAL study assesses the impact of VKA treatment on the aortic calcifications development. This is a biomedical research without health product, transversal and monocentric study which compares the aortic calcifications levels of two populations : one treated by VKA and the other which has never been treated by VKA.

Detailed description

The vitamin K antagonists exercise their anticoagulant effect by preventing the vitamin K dependant gamma-carboxylation of coagulation II, VII, IX and X factors which forms the final step of their activation. They inhibit the vitamin K epoxide reductase VKORC1 enzyme, which is responsible of the vitamin K epoxide recycling in vitamin K hydroquinone (its reduced form). The carboxylation also can be inhibited by the Matrix Gla protein (MGP), inhibitor factor of vascular calcifications. Warfarin (the most used VKA at the word level) is employed on animal for produce vascular calcifications by inhibiting the MGP activation. Epidemiologic data indicate that warfarin could increase the calcifications of cardiac valves and coronary arteries. However, these studies were not interested in abdominal aorta's calcifications which are considered like an important marker of cardiovascular risk and did not concern the fluindione which is the most used VKA in France. Even if a class effect seems logical, the investigators can't dismiss the local effects, different to warfarin. In these studies, the calcifications assessment were rarely quantitative and the MGP levels were not measured. The vascular calcifications constitute a potential adverse effect of VKA which could limit their benefit in certain populations. In this work there is an assumption that the aortic calcifications levels are upper in patients receiving VKA than in patients who are not receiving VKA and the aortic calcifications increase is owed to the non-activation of MGP. The main objective is to assess if the taking of VKA is associated with the aortic calcifications development in patients receiving VKA. Investigators will compare 2 populations: one group treated by VKA treatment for at least 6 months and one focus group which have never been treated by VKA treatment.

Interventions

None listed

Sponsors

Centre Hospitalier Universitaire, Amiens
Lead SponsorOTHER

Study design

Observational model
CASE_CONTROL
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
Yes

Inclusion criteria

* patients having a abdominal scanner without injection planned at CHU Amiens * group treated by VKA: VKA treatment for at least 6 months * group not treated by VKA: no antecedent of AVK treatment

Exclusion criteria

* abdominal scanner contre indication * progressive cancer * scanner planned by emergency department * patient having had acute cardiovascular accident in the last 3 months

Design outcomes

Primary

MeasureTime frameDescription
Calcifications scoresat inclusionAgatston's method

Secondary

MeasureTime frameDescription
Plasmatic concentrations in dp-ucMGP12 monthsThe first measure of MGP is actually a measure of the dephosphorylated MGP \[ dpMGP \] performed by ELISA

Countries

France

Contacts

PRINCIPAL_INVESTIGATORCedric RENARD

CHU Amiens

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Jun 13, 2026