Turk Kardiyol Dern Ars. 2014; 42(1): 55-60 | DOI: 10.5543/tkda.2014.88269

Association between endothelial nitric oxide synthase intron 4a/b polymorphism and aortic dissection

Ahmet Ekmekçi¹, Mahmut Uluganyan², Barış Güngör¹, Neslihan Abacı⁴, Kazım Serhan Özcan¹, Gokhan Ertaş¹, Aycan Zencirci¹, Ahmet Yavuz Balcı³, Sema Sırma Ekmekçi⁴, Nurten Sayar¹, Duran Ustek⁴, Mehmet Eren^1
1Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Training and Research Hospital, Istanbul
²Department of Cardiology, Kadirli State Hospital, Osmaniye
³Department of Cardiovasculary Surgery, Dr. Siyami Ersek Thoracic and Cardiovascular Surgery Center, Training and Research Hospital, İstanbul
⁴Department of Genetics, Istanbul University, Institute for Experimental Medical Research, Istanbul

OBJECTIVES
The genetic risk factors that contribute to the risk of developing aortic dissection (AD) have been studied. We assessed the association of endothelial nitric oxide synthase (eNOS) gene polymorphism with AD.

STUDY DESIGN
Patients who underwent surgery with the diagnosis of AD and survived after the operation in our center between May 2007 and June 2011 were recruited retrospectively. The eNOS intron 4a/b polymorphism was determined by polymerase chain reaction (PCR) using oligonucleotide primers (sense: 5’-AGGCCCTATGGTAGTGCCTTT-3’; antisense: 5’-TCTCTTAGTGCTGTGGTCAC-3’) that flank the region of the 27 bp VNTR in intron 4.

RESULTS
Thirty-nine patients (88%) had type A AD, while the remainder (12%) had type B AD. The distribution of eNOS4 a/b gene polymorphism differed significantly from the control group, with higher frequencies of eNOS 4a/a and 4a/b genotypes in the AD group (χ2=7.16, p=0.03).

CONCLUSION
In this study, the distribution of eNOS genotypes differed between the AD and control groups; however, this polymorphism was not found to be an independent factor for the development of AD.

Keywords: Aortic dissection, eNOS enzyme, genetic predisposition to disease; genotype; introns/genetics; nitric oxide; polymorphism, genetic.

---

CITE