Long-term vitamin-K antagonist use and coronary artery calcification
- PDF / 267,346 Bytes
- 6 Pages / 595 x 792 pts Page_size
- 94 Downloads / 204 Views
S. Ünlü1,3,4 · A. Şahinarslan1 · H. K. Kılıç2 · G. Gökalp1 · B. Sezenöz1 · G. Erbaş2 · R. M. Yalçın1 · M. Araç2 1
Faculty of Medicine, Department of Cardiology, Gazi University, Ankara, Turkey Faculty of Medicine, Department of Radiology, Gazi University, Ankara, Turkey 3 Institute of Health Sciences, Department of Pharmacology, Gazi University, Ankara, Turkey 4 Cardiology Department, Atatürk Chest Diseases and Chest Surgery Education and Research Hospital, Ankara, Turkey 2
Long-term vitamin-K antagonist use and coronary artery calcification Vitamin K antagonists (VKAs) have become the most widely prescribed anticoagulants around the world since their first use in 1954. However, VKAs have a very narrow therapeutic index and various unwanted side effects including fatal bleeding, which challenges the maintenance of the treatment [1]. Although the introduction of new oral anticoagulants lowered the rate of VKA use, patients with metal prosthetic valves are still prescribed these agents for optimal anticoagulation. VKAs inhibit the epoxide reductase enzyme, which plays an important role in coagulation factor synthesis in the liver by blocking carboxylation of glutamic acid residues. However, VKAs also block the matrix gamma-carboxyglutamate G1a-protein (MGP), which is not related to the coagulation system but needs vitamin K-dependent carboxylation to be activated with posttranslational modification. MGP deficiency has been shown to induce changes that lead to tissue calcification, in interaction with several proteins, such as bone morphogenic protein [2]. In animal studies, it has been shown that MGP deficiency can be induced by warfarinusage and itcanaggravate vascular calcification [3]. These studies mainly focused on calcification of the large arteries and reported that MGP-deficient Preliminary results of the study were presented as a poster at the European Society of Cardiology Congress 2015.
animals had extensively calcified aorta, carotid, and renal arteries. Apart from animal models, a small number of human studies (of which a few focused on coronary arteries) have evaluated the relationship between VKAs and arterial calcification [4]. There are conflicting data about the interaction between coronary artery calcification (CAC) and VKA use. To date, it is still unclear whether VKA use leads to CAC in a dose- and timedependent manner. We therefore conducted an observational study to compare the long-term effects of VKA treatment on CAC scores in patients who have a metallic prosthetic valve for at least 5 years with VKA-free patients.
Methods Study population We retrospectively screened all patients over the age of 18 years who had a metallic prosthetic valve and who presented to the Cardiology and Cardiovascular Departments of Gazi University Hospital Ankara between January 2012 and 2016 for coronary artery calcium score measurement with multislice computed tomography (CT). Patients who had undergone metallic prosthetic valve surgery more than 5 years before and had normal coronary arteries as diagnosed via presurgical an
Data Loading...
