Özet:

The patient population with a typical angina, found ischemic in non-invasive tests and with normal epicardal coronary arteries in coronary angiography is defined as Heart Syndrome X (KSX). A rise in the levels of CRP and other inflammatory indicators in KSX patients indicates that the disease has a pathogenesis through inflammation. CYP2J2, the enzyme of cytokrom P450, is a member of the both protein family, which is expressed at high levels in coronary artery endotels, flat muscle cells and cardiomyocytes. The main task of CYP2J2 is to ensure the conversion of researchonic acid into 4 different types of epoxy-icotrienoic acids (EET), including 5,6- 8,9- 11,12- 14,15. These EETs undermine the formation of inflammatory response by reducing the endotelial expression of VCAM-1, stimulated by TNF-α, and also by inhibiting NF-κB, reduce the adhesion of leukocytes to the vascular wall. CYP2J2 gene -76G>T polymorphism causes a decrease in the expression of CYP2J2 and its metabolites within the cell. In this study, we aimed at studying the connection between the known CYP2J2 gene -76G>T polymorphism that has been considered to be effective in the pathophysology of the inflammatory processes and the KSX disease that is considered to be effective in the inflammatory path. Material and Method: We compared the control group consisting of 125 KSX patients and 125 healthy individuals in terms of CYP2J2 gene -76G>T polymorphism. Genotyplemic of the CYP2J2 gene -76G>T polymorphism from DNA samples was made using the real-time PCR method. Results: When the genotypes TT, GT and GG were studied in patients and control groups, no statistically significant difference was observed (p>0,05). The result: This situation suggests that CYP2J2 gene -76G>T polymorphism, which causes an increase in inflammation, does not play an important role in the pathogenesis of the KSX disease.