Table of Contents Author Guidelines
Genetics Research International
Volume 2017, Article ID 9532471, 7 pages
Research Article

Does i-T744C P2Y12 Polymorphism Modulate Clopidogrel Response among Moroccan Acute Coronary Syndromes Patients?

1Laboratory of Genetics and Molecular Pathology, Medical School, University Hassan II, Casablanca, Morocco
2Department of Cardiology, University Hospital Center Hassan II, Fes, Morocco
3Department of Cardiology, University Hospital Center Ibn Rochd, Casablanca, Morocco

Correspondence should be addressed to Hind Hassani Idrissi; rf.liamtoh@dnih-issirdi-inassah

Received 17 October 2016; Revised 3 January 2017; Accepted 12 January 2017; Published 5 February 2017

Academic Editor: Norman A. Doggett

Copyright © 2017 Hind Hassani Idrissi 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.


Background. An interindividual variability in response to Clopidogrel has been widely described in patients with acute coronary syndromes (ACS). The contribution of genetics on modulating this response was widely discussed. The objective of our study was to investigate the potential effect of i-T744C P2Y12 polymorphism on Clopidogrel response in a sample of Moroccan ACS patients. We tried also to determine the frequency of this polymorphism among Moroccan ACS compared to healthy subjects. Methods and Results. 77 ACS patients versus 101 healthy controls were recruited. DNA samples were genotyped by PCR-RFLP method. The VerifyNow assay was used to evaluate platelet function among ACS patients. Our results show that the mutant allele C was more frequent among ACS ST (+) than ST (−) patients (39% versus 19.8%, resp.), when the wild-type allele was more represented in the ACS ST (−) group (80.2%). The C allele frequency was higher among resistant than nonresistant patients (30% versus 20.8%, resp.). Comparison of ACS patients and healthy controls shows higher frequency of mutant C allele among cases compared to controls (22.73% versus 19.31%, resp.); there was a statistically significant association of the recessive and additive transmission models with the ACS development risk (OR [95% CI] = 1.78 [1.58–5.05], and OR [95% CI] = 1.23 [0.74–2.03], , resp.), increasing thus the association of this polymorphism with the pathology. Conclusion. Our results suggest that this polymorphism may have a potential effect on Clopidogrel response among our Moroccan ACS patients and also on ACS development.