作者: Liv Vossen , Leon Schurgers , Bernard van Varik , Bas Kietselaer , Cees Vermeer
DOI: 10.3390/NU7115443
关键词: Clinical endpoint 、 Pathogenesis 、 Vitamin 、 Calcification 、 Matrix gla protein 、 Coronary artery disease 、 Vitamin K2 、 Arterial calcification 、 Medicine 、 Internal medicine 、 Cardiology 、 Pathology
摘要: Coronary artery calcification (CAC) develops early in the pathogenesis of atherosclerosis and is a strong independent predictor cardiovascular disease (CVD). Arterial caused by an imbalance regulatory mechanisms. An important inhibitor vitamin K-dependent matrix Gla protein (MGP). Both preclinical clinical studies have shown that inhibition K-cycle K antagonists (VKA) results elevated uncarboxylated MGP (ucMGP) subsequently extensive arterial calcification. This led us to hypothesize supplementation may slow down progression To test this, we designed VitaK-CAC trial which analyses effects menaquinone-7 (MK-7) on CAC. The double-blind, randomized, placebo-controlled including patients with coronary (CAD). Patients baseline Agatston CAC-score between 50 400 will be randomized intervention-group (360 microgram MK-7) or placebo group. Treatment duration 24 months. primary endpoint difference both groups. Secondary endpoints include changes structure function, associations biomarkers. We treatment MK-7 arrest CAC this lead option for vascular subsequent CVD.