Abstract

Introduction: Matrix Gla protein (MGP) is a vitamin K-dependent protein. Recently, the uncarboxylated (inactive, uc) form of MGP was associated with vascular tissue calcification. The aim of the present study was to investigate the relationship between a newly initiated oral anticoagulant treatment with the Vitamin-K antagonist phenprocoumon and serum levels of uncarboxylated MGP compared to a control group with aspirine therapy. Methods: We performed a prospective study in 43 non-dialyzed patients (mean age 61±10 years, 28 men) with newly initiated oral anticoagulant therapy with phenprocoumon (n=21) or aged-matched subjects with aspirine therapy (n=22). In all patients circulating ucMGP levels (in pM compared to synthetic ucMGP) were measured by a competitive ELISA-based assay (VitaK BV, Maastricht, The Netherlands) at baseline as well as after 1 month and 3 months follow-up. Results: At baseline, there were no significant differences in patient characteristics regarding cardiovascular risk factors and the prevalence of coronary artery disease between both groups. In addition, at baseline no significant difference in ucMGP levels between patients with newly initiated oral anticoagulant therapy (1003±526 pM) and control subjects with aspirine therapy (842±214 pM, p= 0.40) was detected. At 1 month follow-up, patients with oral anticoagulation therapy demonstrated significantly increased ucMGP levels (1904±402 pM) compared to the aspirine group (628±223 pM, p<0.001). At 3 months-follow up, a further increase in ucMGP levels in patients with oral anticoagulant treatment (2316±344 pM) compared to the aspirine group (685±378, p<0.001) as well as to study inclusion (1003±526 pM, p=0.003) was observed. Conclusion: The present study suggests that newly onset anticoagulation therapy with phenprocoumon is associated with increased serum levels of inactive, uncarboxylated MGP indicating calcification inhibitor deficiency compared to a reference population with aspirine therapy. Long-term follow-up data are needed to evaluate if newly onset oral anticoagulant therapy may be linked to an increased progression of coronary and valvular calcification.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.