Abstract
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.Keywords: Antiplatelets, atherosclerosis, clopidogrel, coronary artery disease, genetics, polymorphisms.
Current Pharmaceutical Design
Title:Genetics in the Clinical Decision of Antiplatelet Treatment
Volume: 23 Issue: 9
Author(s): Gerasimos Siasos*, Marina Zaromitidou, Evangelos Oikonomou, Manolis Vavuranakis, Vicky Tsigkou, Nikolaos Papageorgiou, Dimitrios Chaniotis, Dimitrios A. Vrachatis, Christodoulos Stefanadis, Athanasios G. Papavassiliou and Dimitrios Tousoulis
Affiliation:
- Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School and Harvard-MIT Biomedical Engineering Center, Massachusetts Institute of Technology, Boston, MA,United States
Keywords: Antiplatelets, atherosclerosis, clopidogrel, coronary artery disease, genetics, polymorphisms.
Abstract: 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.Export Options
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Cite this article as:
Siasos Gerasimos *, Zaromitidou Marina , Oikonomou Evangelos , Vavuranakis Manolis , Tsigkou Vicky , Papageorgiou Nikolaos , Chaniotis Dimitrios , Vrachatis A. Dimitrios , Stefanadis Christodoulos , Papavassiliou G. Athanasios and Tousoulis Dimitrios , Genetics in the Clinical Decision of Antiplatelet Treatment, Current Pharmaceutical Design 2017; 23 (9) . https://dx.doi.org/10.2174/1381612822666161226152529
DOI https://dx.doi.org/10.2174/1381612822666161226152529 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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