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Blood, 15 November 2004, Vol. 104, No. 10, pp. 3231-3232. Prepublished online as a Blood First Edition Paper on July 20, 2004; DOI 10.1182/blood-2004-04-1277. This Article Full Text (PDF) All Versions of this Article: 2004-04-1277v1 104/10/3231    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Schurgers, L. J Articles by Janzen, J. Search for Related Content PubMed PubMed Citation Articles by Schurgers, L. J Articles by Janzen, J. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 9, 2004 Accepted July 6, 2004 Oral Anticoagulant Treatment: Friend or Foe in Cardiovascular Disease? Leon J Schurgers*, Hermann Aebert, Cees Vermeer, Burkhard Bueltmann, and Jan Janzen Department of Biochemistry and Cardiovascular Research Institute, University Maastricht, Maastricht, The Netherlands Department of Surgery, Tuebingen University, Tuebingen, Germany Department of Pathology, Tuebingen University, Tuebingen, Germany * Corresponding author; email: l.schurgers{at}bioch.unimaas.nl. Calcification is a common complication in cardiovascular disease and may affect both arteries and heart valves. Matrix Gla-protein (MGP) is a potent inhibitor of vascular calcification the activity of which is regulated by vitamin K. In animal models, vitamin K-antagonists (oral anticoagulants, OAC) were shown to induce arterial calcification. To investigate whether also in man long term OAC treatment may induce calcification, we have measured the grade of aortic valve calcification in patients with and without pre-operative OAC treatment. OAC-treated subjects were matched with non-treated ones for age, gender and disease. Calcifications in patients receiving pre-operative OAC treatment were significantly (2-fold) larger than in non-treated patients. These observations suggest that OAC, which are widely used for anti-thrombotic therapy, may induce cardiovascular calcifications as an adverse side effect. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. C McCann and B. N Ames Vitamin K, an example of triage theory: is micronutrient inadequacy linked to diseases of aging? Am. J. Clinical Nutrition, October 1, 2009; 90(4): 889 - 907. [Abstract] [Full Text] [PDF] A. Y.-M. Wang VASCULAR AND OTHER TISSUE CALCIFICATION IN PERITONEAL DIALYSIS PATIENTS Perit. Dial. Int., February 1, 2009; 29(Supplement_2): S9 - S14. [Abstract] [Full Text] [PDF] J. Danziger Vitamin K-dependent Proteins, Warfarin, and Vascular Calcification Clin. J. Am. Soc. Nephrol., September 1, 2008; 3(5): 1504 - 1510. [Abstract] [Full Text] [PDF] L. L. Demer and Y. Tintut Vascular Calcification: Pathobiology of a Multifaceted Disease Circulation, June 3, 2008; 117(22): 2938 - 2948. [Full Text] [PDF] M. Teichert, L.E. Visser, R.H.N. van Schaik, A. Hofman, A.G. Uitterlinden, P.A.G. M. De Smet, J.C.M. Witteman, and B.H.Ch. Stricker Vitamin K Epoxide Reductase Complex Subunit 1 (VKORC1) Polymorphism and Aortic Calcification: The Rotterdam Study Arterioscler Thromb Vasc Biol, April 1, 2008; 28(4): 771 - 776. [Abstract] [Full Text] [PDF] Y. Yao, A. F. Zebboudj, A. Torres, E. Shao, and K. Bostrom Activin-like kinase receptor 1 (ALK1) in atherosclerotic lesions and vascular mesenchymal cells Cardiovasc Res, May 1, 2007; 74(2): 279 - 289. [Abstract] [Full Text] [PDF] E. Sconce, H. Wynne, and F. Kamali Vitamin K supplementation during oral anticoagulation: no real cause for concern Blood, April 15, 2007; 109(8): 3607 - 3607. [Full Text] [PDF] E. Sconce, H. Wynne, and F. Kamali Response: vitamin K supplementation during oral anticoagulation: no real cause for concern Blood, April 15, 2007; 109(8): 3607 - 3608. [Full Text] [PDF] L. J. Schurgers, H. M. H. Spronk, B. A. M. Soute, P. M. Schiffers, J. G. R. DeMey, and C. Vermeer Regression of warfarin-induced medial elastocalcinosis by high intake of vitamin K in rats Blood, April 1, 2007; 109(7): 2823 - 2831. [Abstract] [Full Text] [PDF] C. J. O'Donnell, M. K. Shea, P. A. Price, D. R. Gagnon, P. W. F. Wilson, M. G. Larson, D. P. Kiel, U. Hoffmann, M. Ferencik, M. E. Clouse, et al. Matrix Gla Protein Is Associated With Risk Factors for Atherosclerosis but not With Coronary Artery Calcification Arterioscler Thromb Vasc Biol, December 1, 2006; 26(12): 2769 - 2774. [Abstract] [Full Text] [PDF] Y. Yao, A. F. Zebboudj, E. Shao, M. Perez, and K. Bostrom Regulation of Bone Morphogenetic Protein-4 by Matrix GLA Protein in Vascular Endothelial Cells Involves Activin-like Kinase Receptor 1 J. Biol. Chem., November 10, 2006; 281(45): 33921 - 33930. [Abstract] [Full Text] [PDF] L. L. Demer and Y. Tintut Pitting Phosphate Transport Inhibitors Against Vascular Calcification Circ. Res., April 14, 2006; 98(7): 857 - 859. [Full Text] [PDF] L. J. Schurgers, K. J.F. Teunissen, M. H.J. Knapen, M. Kwaijtaal, R. van Diest, A. Appels, C. P. Reutelingsperger, J. P.M. Cleutjens, and C. Vermeer Novel Conformation-Specific Antibodies Against Matrix {gamma}-Carboxyglutamic Acid (Gla) Protein: Undercarboxylated Matrix Gla Protein as Marker for Vascular Calcification Arterioscler Thromb Vasc Biol, August 1, 2005; 25(8): 1629 - 1633. [Abstract] [Full Text] [PDF]

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