@article{3148073,
    title = "The Role of the Cytochrome P450 Polymorphisms in Clopidogrel Efficacy
and Clinical Utility",
    author = "Tousoulis, D. and Siasos, G. and Zaromytidou, M. and Papageorgiou, N. and and Stefanadi, E. and Oikonomou, E. and Stefanadis, C.",
    journal = "Current Medicinal Chemistry",
    year = "2011",
    volume = "18",
    number = "3",
    pages = "427-438",
    publisher = "BENTHAM SCIENCE PUBL LTD",
    issn = "0929-8673",
    doi = "10.2174/092986711794839151",
    keywords = "Clopidogrel resistance; cytochrome P450; gene polymorphisms; platelets",
    abstract = "Clopidogrel, an antiplatelet agent, prevents platelet aggregation by
inhibiting the adenosine disphosphate (ADP) P2Y12 receptor, which is
located on the platelet surface. Although dual antiplatelet therapy
appears to be efficient, a considerable number of patients continue to
experience adverse cardiovascular events, such as stent thrombosis. The
percentage of low response to antiplatelet therapy varies from 4% to
30% of patients depending on the cut-off values. In addition, several
factors such as poor absorption, drug-to-drug interactions, inadequate
dosing, elevated body mass index, insulin resistance and the nature of
acute coronary syndromes have been implicated in low clopidogrel
response. Recently, studies have focused on the role of genetic
polymorphisms encoding enzymes that participate in clopidogrel hepatic
metabolism or receptors involved in intestinal absorption and ADP
induced platelet aggregation, which may affect the percentage of
platelet inhibition after clopidogrel administration.
The management of clopidogrel resistance remains a controversial issue
and additional studies are required to evaluate the safety and efficacy
of increased loading of clopidogrel or replacement with other new
antiplatelet agents such as prasugrel."
}