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- Hüseyin Balcioğlu, Elif Fatma Özkan Pehlivanoğlu, Uğur Bilge, Kadir Uğur Mert, Muhammet Dural, Ebru Erzurumluoğlu Gökalp, Oğuz Çilingir, and Sevilhan Artan.
- Department of Family Medicine, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Turkiye.
- Turk J Med Sci. 2024 Jan 1; 54 (4): 682687682-687.
Background/AimWe aimed to determine the genetic risk factors in patients aged 45 years and below with a history of early myocardial infarction (MI), compared to individuals over 60 years of age with no history of MI.Materials And MethodsIn this study, we selected different age groups to more clearly distinguish genetic differences. Accordingly, we compared individuals who had experienced MI at an early age with those who were older and had not experienced any cardiovascular events. The patient group consisted of 99 volunteers under the age of 45 with a history of MI, while the control group included 99 volunteers aged 60 and over without a history of MI. MTHFR (C677T, A1298C), Factor V Leiden (G1691A), Prothrombin (G20210A), PAI (4G/5G), Factor XIII (V34L), APOA1 (rs670, rs1799837, rs5069), and APOB were studied using blood samples taken from the patients.ResultsIn the logistic regression analysis of thrombophilia markers and gene polymorphisms in the patient and control groups, no statistically significant increase was observed in markers other than APOA1 rs5069 gene polymorphism. APOA1 rs5069 gene polymorphism was found to be higher in the patient group than those without this polymorphism. The frequencies of homozygous MTHFR (C677T, A1298C) and heterozygous Factor XIII V34L were higher in the patient cohort compared to the controls.ConclusionIn our study, we found that prothrombotic gene variants and APOA1 rs5069 polymorphism were statistically significantly associated with coronary artery disease. Thus, prothrombotic gene variants and APOA1 rs5069 polymorphism may serve as predictors of early myocardial infarctions. Individuals with early family histories of coronary artery disease could be screened for these mutations.© TÜBİTAK.
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