Since clopidogrel is a prodrug its antiplatelet effect is highly depended on cytochrome P450 isoenzymes. The aim of the study was to analyze several clinical trials and to determine the importance of genetic polymorphism of cytochrome P450 isoenzyme CYP2C19 in clopidogrel effectiveness in patients with acute coronary syndrome and/or percutaneous coronary intervention. Materials and methods: articles refering to the interrelation between clopidogrel and CYP2C19 genetic polymorphism were selected from PubMed database and 7 completed clinical trials from U.S. National Institute of Health database with published results that have studied this interrelation were analized. Results: Clinical trials confirmed the involvement of CYP2C19 polymorphism in the clopidogrel efficiency. Within European population the loss-of-function allele (CYP2C19*2) is found in ~15-25% of cases. Studies suggest that poor metabolizers need another antiplated agent, while intermediate metabolizers are candidates to increased dose regimen to achieve the desired clinical effect. Conclusions: CYP2C19 genetic polymorphism substantially influences clopidogrel pharmacokinetics and pharmacodynamics and in some patients with acute coronary syndrome and/or percutaneous coronary intervention is reasonable to genetically guide the antiplated therapy. CYP2C19 genotyping is available in Republic of Moldova and is especially recommended in patient with high risk of major adverse cardiac events. In intermediate metabolizers the increase of clopidogrel dosage could be an option, while in poor metabolizers is necessary to switch to other antiplatelet agents such as prasugrel or ticagrelor.