Abstract

Atherosclerotic coronary artery disease is a major health problem worldwide. Endothelial dysfunction in atherosclerosis is considered a precursor phenomenon of atherosclerosis. In this inflammatory process, many mediators interact with each other and influence the formation of atherosclerosis in the vascular bed. Asymmetric dimethylarginine (ADMA) appears to cause vascular damage by reducing nitric oxide (NO) amounts. Oxidized-low-density lipoprotein (LDL) induces the protein arginine methyl transferase enzyme, which enables ADMA synthesis; it also increases ADMA levels by inhibiting the enzyme dimethylarginine dimethylaminohydrolase, which breaks down ADMA, thus indirectly reducing NO synthesis. Ox-LDL is formed through the process of lipid peroxidation, and measurement of malondialdehyde (MDA) in biological material is used as an indicator of lipid peroxide levels. In our study, the relationship between the levels of the mentioned enzymes and coronary artery disease was examined.

In our study, ADMA and symmetric dimethylarginine (SDMA), high-pressure liquid chromatography (HPLC) method (Eureka kit); Ox-LDL, ELISA method (Immunodiagnostic kit); and MDA levels were measured by HPLC (Immuchrom kit)-spectrophotometric methods. The relationship of these parameters both between the groups and with each other was evaluated. The patient population was selected from patients who presented to the cardiology outpatient clinic with chest pain and were found to have evidence of ischemia on a non-invasive stress test.

The low total cholesterol and LDL values in the severe coronary artery disease (CAD) group were attributed to the effect of statin use. It is possible that statin-type drugs used in severe CAD groups reduce lipid levels as well as ADMA levels. We think that low ADMA levels will be effective in reducing the negative effects of ADMA on the vascular bed. This hypothesis needs to be supported by larger-scale studies.

According to the statistical results of the study, in terms of ADMA, SDMA, Ox-LDL and MDA levels; there was no statistically significant difference between the control group with normal coronary arteries and the groups with minimal and severe coronary artery disease (p>0.05).