Anna Remková, Milan Remko
Acetylsalicylic acid and clopidogrel are effective in secondary prevention of coronary artery and cerebrovascular events. In combination, they are the mainstay in the prevention of major adverse cardiovascular events (MACE) in patients with acute coronary syndromes. Wide inter-individual variability of response to clopidogrel has been reported. About one-third of treated patients exhibit a suboptimal inhibition of platelet function. Genetic and environmental factors that influence the absorption and/or the extent of metabolism of clopidogrel can account to response variability. Clopidogrel is a prodrug that needs to be metabolized to an active metabolite to exert its pharmacological effect. Polymorphisms of CYP2C19 gene are associated with variable degrees of production of the active metabolite. Tailored treatment based on the results of laboratory tests has been proposed as a solution to this problem. Various in vitro techniques (like the light transmittance aggregometry, the VerifyNow P2Y12, and the vasodilator-stimulated phosphoprotein-phosphorylation - VASP assay) are used to measure the inhibition of platelet function by clopidogrel and to predict the risk of MACE. However, we still need to identify and standardize the laboratory test for this purpose, and answer basic questions on its clinical utility. When possible, the use of alternative drugs with more uniform and predictable bioavailability, and with favourable profiles in terms of risk/benefit ratio should be preferred. The use of the new P2Y12 antagonist prasugrel or ticagrelor instead of clopidogrel would markedly lessen the problem of hyporesponsiveness, because they effectively inhibit platelet function in the vast majority of patients. Their use in all patients, without testing, might prove more effective than personalized treatment.