Open AccessASSOCIATION BETWEEN SMOKING AND THE ANTIPLATELET EFFECT OF CLOPIDOGREL
Author(s) -
K. Yu. Lukianets,
М. Л. Лындина
Publication year - 2020
Publication title -
juvenis scientia
Language(s) - English
Resource type - Journals
eISSN - 2414-3790
pISSN - 2414-3782
DOI - 10.32415/jscientia_2020_6_5_14-24
Subject(s) - clopidogrel , medicine , p2y12 , antiplatelet drug , pharmacodynamics , coronary artery disease , ticagrelor , cyp2c19 , clinical significance , myocardial infarction , pharmacogenetics , cardiology , platelet aggregation inhibitor , drug , pharmacokinetics , intensive care medicine , pharmacology , aspirin , genotype , biochemistry , chemistry , cytochrome p450 , metabolism , gene
Clopidogrel is the most widely used P2Y12 inhibitor, which is administered for secondary prevention of atherothrombotic events in patients with cardiovascular disease after myocardial infarction and coronary stenting. Given the complexity of the clopidogrel metabolism and variety of potential drug-drug interactions, the issue of individual variability of its antiplatelet effects is of paramount concern. Another issue of clinical relevance is related to so-called “smoker’s paradox”. This phenomenon implies that in some patients smoking is associated with increased antiplatelet potency of clopidogrel. In this review, we analyze recent international data on the features of pharmacokinetics and pharmacodynamics of clopidogrel, plausible mechanisms of the “smoker’s paradox” and its clinical significance in patients with coronary artery disease. Comparative efficacy of available P2Y12 inhibitors and possible implications of smoking are considered. Pharmacogenetic aspects and the issues of personalized antiplatelet therapy are discussed.