Τίτλος:
Genetics in the clinical decision of antiplatelet treatment
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Background: Coronary artery disease remains the leading cause of death globally. Dual antiplatelet treatment with aspirin and aP2Y12 receptor significantly reduces thrombotic events. However, antiplatelet drug response displays considerable interindividual variability. Methods: Genetic factors account for up to 70% of impaired drug response. A number of genes encoding proteins involved in the pharmacokinetic pathway have been found to alter drug response. Results: According to most studies, CYP2C19 gene is the strongest genetic determinant. The novel antiplatelet agents prasugrel and ticagrelor, seem to overcome genetic restrictions but in expense of increased bleeding rates. Achieving a balance between adequate platelet inhibition and bleeding complications is challenging. Conclusion: Genetic screening may provide valuable guidance towards an efficient antiplatelet treatment. However, the lack of randomized controls trials testing the effect of a genotype-guided therapy, forbids the implementation of genetic testing into clinical practice. © 2017 Bentham Science Publishers.
Συγγραφείς:
Siasos, G.
Zaromitidou, M.
Oikonomou, E.
Vavuranakis, M.
Tsigkou, V.
Papageorgiou, N.
Chaniotis, D.
Vrachatis, D.A.
Stefanadis, C.
Papavassiliou, A.G.
Tousoulis, D.
Περιοδικό:
Current Pharmaceutical Design
Εκδότης:
Bentham Science Publishers B.V.
Λέξεις-κλειδιά:
acetylsalicylic acid; adenosine diphosphate; antithrombocytic agent; aryldialkylphosphatase 1; clopidogrel; cytochrome P450 2C19; multidrug resistance protein 1; prasugrel; purinergic P2Y12 receptor; ticagrelor; antithrombocytic agent, bleeding; blood clotting; body mass; cause of death; clinical decision making; clinical practice; coronary artery disease; drug response; genetic code; genetic polymorphism; genetic screening; genetic variability; genetics; genome-wide association study; genotype; heredity; human; pharmacokinetics; priority journal; Review; single nucleotide polymorphism; thrombocyte activation; thrombocyte aggregation, Clinical Decision-Making; Coronary Artery Disease; Humans; Platelet Aggregation Inhibitors
DOI:
10.2174/1381612822666161226152529
