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Journal of Biomedicine and Biotechnology
Volume 2007 (2007), Article ID 80687, 9 pages
Research Article

Thermolabile Methylenetetrahydrofolate Reductase C677T Polymorphism and Homocysteine Are Risk Factors for Coronary Artery Disease in Moroccan Population

1National League of Cardiology, Biochemistry and Molecular Biology Laboratory, Ibn-Sina Hospital, PB 1326, Rabat 10000, Morocco
2UFR of Biology and Healthy, Laboratory of Biochemistry and Molecular Biology, Faculty of Sciences, Hassan II University, Ain Chock, PB 5366, Maarif 20100, Casablanca, Morocco
3UFR of Cellular and Molecular Biology, Faculty of Sciences, Abdelmalek Es-saadi University, P.O. Box 2121, Tetuan 93000, Morocco
4Cardiology A Department, National League of Cardiology, Ibn-Sina Hospital, PB 1326, Rabat 10000, Morocco

Received 21 September 2006; Revised 20 December 2006; Accepted 9 January 2007

Academic Editor: Mohamed Boutjdir

Copyright © 2007 Nawal Bennouar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Increased plasma total homocysteine (tHcy) levels have been shown to be a risk factor for coronary artery disease (CAD). The common methylenetetrahydrofolate reductase C677T (MTHFR C677T) polymorphism has been reported to be a strong predictor of mild hyperhomocysteinaemia (HHcy). We assessed whether this mutation was associated with increased risk of CAD and plasma levels of tHcy. We also evaluated interactions between this polymorphism, mild elevated tHcy levels and conventional risk factors of CAD. Method. Using PCR-RFLP analysis, we studied the frequency of the C677T genotypes and its effect on CAD and on tHcy concentrations in 400 subjects without and with CAD angiographically confirmed. There were 210 subjects with CAD and 190 subjects without CAD. Results. The frequencies of the C677T genotypes were 53% (59.5% in controls versus 48.1% in cases), 34.8% (32.1 in controls versus 37.1 in cases), and 11.8% (8.4% in controls versus 14.8% in cases), respectively, for 677CC, 677CT, and 677TT. The genotype frequencies were significantly different between case and control groups (P<.05). The 677T allele enhances the risk of CAD associated to HHcy (P<.01). In multivariate analysis models, MTHFR C677T polymorphism effect on CAD was masked by other risk factors. HHcy was only and independently influenced by MTHFR polymorphism and smoking habits, and it is a strong predictor of CAD independently of conventional risk factors. Conclusion. Our data suggest that HHcy is strongly and independently associated to CAD risk increase; and MTHFR C677T polymorphism and smoking habits were the main predictors of tHcy levels. The CAD risk increase is mainly associated with mild HHcy in 677TT, whereas in 677CT and 677CC it is mainly associated with the conventional risk factors.