The present cross-sectional clinical study aimed to examine the connection between statin exposure, coronary artery calcification (CAC), and vitamin K-dependent proteins (VKDPs) in patients with cardiovascular (CV) conditions. Two groups of patients were studied: patients with established CV disease (CVD) and healthy patients at moderate risk for CVD (a control group). The groups were also split into statin users and non-users. The following VKDPs were measured in plasma: uncarboxylated Matrix Gla-protein (ucMGP), undercarboxylated (ucOC), and carboxylated osteocalcin (cOC), Gla-rich protein (GRP).CAC score (CACS) was determined by multislice computed tomography. Among all the participants in the study, CACS was more pronounced in statin users compared to nonusers; the same was found also among the CVD patients and among the controls. While the levels of ucMGP and GRP did not differ between statin users and non-users, ucOC and ucOC/cOC were significantly elevated in statin users, indicating vitamin K deficiency.There was a positive correlation between the levels of ucOC and CACS in the entire population and in the group of statin users, but not in statin non-users. No association was found between ucMGP or GRP and CACS. Statins had also an impact on the international normalized ratio and interacted with vitamin K antagonists (VKAs). Our results are in agreement with the existing evidence about positive association between statins and vascular calcification. They enlighten to a certain extent the possible mechanisms through which statins may enhance calcium accumulation in arterial wall, namely, by inhibition of vitamin K dependent proteins and functions involved in vascular protection.
Objectives
Matrix Gla protein (MGP) is a calcification inhibitor that plays a role in preventing soft tissue calcification and local mineralization of the vascular wall. The present study aimed to assess the expression of MGP in Peripheral Blood Mononuclear Cells (PBMC) in adult patients with CVD pathologies and its association with the presence and severity of coronary artery calcium score (CACS) and conventional CVD risk factors.
Methods
MGP expression was measured in 87 individuals using real time qPCR. Subgrouping was performed according etiologic and metabolic CVD risk factors.
Results
A clear trend for a decreased MGP expression was observed in all subgroups with high CVD risk. This decrease was significant in abdominally obese hypertensive individuals and in those with dyslipidemia. MGP expression was significantly lower in patients representing high Total cholesterol and LDL cholesterol levels. A positive correlation between MGP expression and smoking status in patients with coronary calcium and in the CVD group was established. Atrial hypertension duration correlated negatively with MGP expression in the group without coronary calcium deposits.
Conclusions
The current study supports the hypothesis that MGP expression in PBMC probably reflects CVD pathology and is related to lipid metabolism dysregulation.
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