Genetic variability in response to clopidogrel therapy and its clinical implications

Liana Yukhanyan; Matthias K. Freynhofer; Jolanta Siller-Matula; Karsten Schrör; Kurt Huber

doi:10.1160/THS10-11-0747

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 2011; 105(S 06): S55-S59
DOI: 10.1160/THS10-11-0747

Thrombosis and Haemostasis Supplement

Schattauer GmbH

Genetic variability in response to clopidogrel therapy and its clinical implications

Autor*innen

Liana Yukhanyan

¹Department of Medicine, Cardiology and Emergency Medicine, Wilhelminenhospital, Vienna, Austria
Matthias K. Freynhofer

¹Department of Medicine, Cardiology and Emergency Medicine, Wilhelminenhospital, Vienna, Austria
Jolanta Siller-Matula

²Department of Cardiology, Medical University of Vienna,Vienna, Austria
Karsten Schrör

³Institute for Pharmacology und Clinical Pharmacology, Heinrich-Heine-Universität, Düsseldorf, Germany
Kurt Huber

¹Department of Medicine, Cardiology and Emergency Medicine, Wilhelminenhospital, Vienna, Austria

Abstract

Summary

This article concentrates on individual genetic differences responsible for variations of action of clopidogrel, which have been found to be partially responsible for increased cardiovascular events in patients with coronary artery disease under dual antiplatelet therapy. According to these results, genotyping for the relevant gene polymorphisms, especially for the CYP2C19 loss-of-function alleles, has been discussed to be an effective method of individualising and optimising clopidogrel treatment. However, due to the facts that 1) there are no prospective studies demonstrating a clinical benefit of personalising antiplatelet therapy based on genotyping; 2) CYP2C19 polymorphisms account for only approximately 12% of variability in clopidogrel platelet response; 3) the positive predictive value of CYP2C19 loss-of-function polymorphisms for cardiovascular events in patients with acute coronary syndrome undergoing percutaneous coronary intervention is only approximately 12% – 20%; 4) it is likely that other clinical factors and risk constellations might be of greater clinical importance; and 5) it is unknown whether a specific genetic polymorphism is capable of influencing outcome for the individual patient; genetic profiling cannot be recommended for routine use at present but will remain of considerable scientific interest.

Keywords

Antiplatelet agents - coronary syndrome - gene mutations - thrombosis

Volltext

Referenzen

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