Investigation of serum afamine, vitamin E and OX-LDL levels in coronary heart disease

Coronary artery disease is one of the most important diseases of our age. At least half of the deaths in developed western countries are due to cardiovascular diseases. Coronary artery disease occurs as a result of atherosclerosis. Atherosclerosis occurs with the accumulation of lipids in the arterial intima. The oxidative modification hypothesis arose from the conclusion that cultured macrophages transform into lipid-laden cells in the presence of chemically modified LDL (Ox-LDL). Modified LDL has been shown to increase the synthesis of monocyte chemotactic protein-1 in smooth muscle cells and endothelial cells in vitro. Ox-LDL is chemotactic for monocytes and lymphocytes. It has been shown to proliferate Ox-LDL smooth muscle cells. Ox-LDL causes endothelial dysfunction and damage. Vitamin E protects LDL from oxidative damage. It has a high level of binding to LDL. Afamin is also a protein that has the ability to bind vitamin E and transport it in the blood. Therefore, our study will examine the relationship between afamin, vitamin E and ox-LDL. Fifty patients and 40 healthy volunteers followed in Dicle University Medical Faculty Hospital, cardiology clinics and polyclinic were included. Samples were collected from all participants. Serum afamin, vitamin E and ox-LDL levels were measured by ELISA method. There was significant difference between serum afamin, vitamin E and ox-LDL concentrations between the patient and control groups. Afamin levels were found to be significantly higher in the patient group. Vitamin E was found to be high in patients. Ox-LDL levels were found to be low in the patients. A strong positive correlation was found between afamin and vitamin E. As a result, afamin, ox-LDL and vitamin E levels in coronary artery patients indicate that oxidative stress plays a role in the pathogenesis of the disease. Key words: Coronary artery disease, Afamin, Vitamin E, oxidized LD