Cihan ÖZTÜRK, Metin BUDAK, Gökay TAYLAN, Kenan YALTA

KORONER YAVAŞ AKIM FENOMENİ İLE ENDOTEL NİTRİK OKSİT SENTAZ'IN GLU298ASP VE T786-C GEN POLİMORFİZMLERI ARASINDAKİ İLİŞKİ

Giriş: Çalışmada Endotelyal Nitrik Oksit Sentaz Glu 298-Asp Ve T786- C gen polimorfizmleri ile koroner yavaş akım arasındaki ilişkinin belirlenmesi amaçlanmıştır. Yöntemler: Çalışmaya anginal yakınmalar, efor testi veya miyokard perfüzyon sintigrafisi sonucuna göre koroner anjiyografi yapılan 148 birey alındı. Koroner akım TIMI çerçeve sayısına göre hesaplandı. Hastalardan, gen analizi ve diğer biyokimyasal parametreler için venöz kan örneği alındı. Bulgular: Yapılan koroner anjiyografi işlemi sonucunda TIMI çerçeve sayısına göre koroner yavaş akım saptanan 74 birey hasta olarak ve normal koroner saptanan 74 birey kontrol grubu olarak alındı. Hasta ve kontrol grubunun genotipik polimorfizm incelemesinde T786-C polimorfizminde CC, CT ve TT genotipine sahip bireyler arasında (p=0.941) ve Glu298-Asp polimorfizminde GG, GT ve TT genotipine sahip bireyler arasında (p=0.070) anlamlı fark saptanmadı. Ayrıca koroner yavaş akımın tek damar tutulumu (LAD, CX veya RCA’dan yalnızca birinde) veya çok damar tutulumuna (LAD, CX veya RCA’dan en az iki veya daha fazlasında) göre dağılımı incelendiğinde T-786 C (p=0.220) ve Glu298-asp (p=0.378) polimorfizminin genotiplerinin dağılımı açısından istatiksel anlam bulunmadı. Sonuç: Çalışmamız, Türk toplumunda eNOS geninin T786-c ve Glu298-asp polimorfizmleri ile koroner yavaş akım fenomeni arasında ilişki olmadığını göstermiştir.

Anahtar Kelimeler:

Koroner yavaş akım, endoteliyal nitrik oksit sentaz, Genetik polimorfizim

THE RELATIONSHIP BETWEEN GLU298ASP AND T786-C GENE POLYMORPHISMS OF ENDOTHELIAL NITRIC OXIDE SYNTHASE AND CORONARY SLOW-FLOW PHENOMENON

Introduction: This study aims to determine the association between Glu 298-Asp and T786-C gene polymorphisms of endothelial nitric oxide synthase (eNOS) and coronary slow-flow (CSF) phenomenon. Methods: 148 individuals who underwent coronary angiogram (CAG) based on anginal symptoms, exercise testing, or myocardial perfusion scintigraphy were included in the study. Coronary flow was calculated based on TIMI frame counts (TFCs) on CAG. Venous blood samples were drawn from the patients for gene analysis and other biochemical parameters. Results: 74 patients with a CSF pattern based on TFCs were included as patients and 74 individuals with normal coronary arteries were included as the control group. In the genotypic polymorphism analysis of the patient and control groups, no significant difference was found among individuals with CC, CT, and TT genotypes in terms of T786- C polymorphism (p=0.941) and among individuals with GG, GT, and TT genotypes (p=0.070) in terms of Glu298Asp polymorphism. Also, there was no statistically significant difference with regard to the distribution of the T786-C (p=0.220) and Glu298Asp (p=0.378) polymorphisms between those with single (only one of LAD, CX, or RCA) and those with multi-vessel (at least two or more of LAD, CX, or RCA) CSF patterns. Conclusion: Our study demonstrated a null relationship between T786-C and Glu298Asp polymorphisms of the eNOS gene and CSF phenomenon in the Turkish population.

Keywords:

Coronary slow-flow, endothelial nitric oxide synthase, Genetic polymorphism,

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