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Clinical Chemistry 52: 53-58, 2006. First published November 10, 2005; 10.1373/clinchem.2005.057950
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(Clinical Chemistry. 2006;52:53-58.)
© 2006 American Association for Clinical Chemistry, Inc.

Molecular Diagnostics and Genetics

Hyperhomocysteinemia, Endothelial Nitric Oxide Synthase Polymorphism, and Risk of Coronary Artery Disease

Mohsen Kerkeni1,2,3,a, Faouzi Addad2, Maryline Chauffert3, Anne Myara3, Mohamed Ben Farhat2, Abdelhedi Miled4, Khira Maaroufi1 and François Trivin3,4,5

1 Research Unit 03/UR/08-14, Faculty of Pharmacy, Monastir, Tunisia.
2 Department of Cardiology, CHU Fattouma Bourguiba, Monastir, Tunisia.
3 Department of Biochemistry, Hospital Saint-Joseph, Paris, France.
4 Department of Biochemistry and Toxicology, CHU Hached, Sousse, Tunisia.
5 Department of Clinical Biochemistry, François Rabelais University, Tours, France.

aAddress correspondence to this author at: Department of Biochemistry, Hospital Saint-Joseph, 185 rue Raymond Losserand, 75674 Paris cedex 14, France. Fax 33-14-4123244; e-mail m.kerkeni{at}belgique.com or ftrivin{at}hopital-saint-joseph.org.

Background: Hyperhomocysteinemia is an independent, graded risk factor for coronary artery disease (CAD). The G894T variant of endothelial nitric oxide synthase (eNOS) was postulated to be associated with hyperhomocysteinemia and could influence individual susceptibility to CAD. The aims of this study were to investigate (a) the relationship of the eNOS G894T polymorphism with the presence and the severity of CAD and (b) the possible relationship between hyperhomocysteinemia and the eNOS G894T variant for the risk of CAD severity in a Tunisian population.

Methods: We used PCR with restriction fragment length polymorphism analysis to detect the G894T variant of the eNOS gene in 100 patients with CAD and 120 healthy controls. The severity of CAD was expressed by the number of affected vessels. Total plasma homocysteine concentrations were determined by direct chemiluminescence assay.

Results: The frequencies of the eNOS GG, GT, and TT genotypes in the CAD group were significantly different from those in the control group (45%, 44%, and 11% vs 60%, 35.8% and 4.2%, respectively; P = 0.035). There was no association between the eNOS G894T genotype frequencies and the number of stenosed vessels (P = 0.149). In the CAD group, the coexistence of the 894 GT or TT genotypes and hyperhomocysteinemia led to an increased risk of CAD severity.

Conclusion: The G894T polymorphism of the eNOS gene is associated with the presence of CAD, and in conjunction with hyperhomocysteinemia, increased the risk of CAD severity in a Tunisian population.




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