Aortic Calcification and Vitamin K Antagonists

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.