Thromb Haemost 2011; 106(02): 211-218
DOI: 10.1160/TH11-03-0137
Theme Issue Article
Schattauer GmbH

Clinical, genetic and confounding factors determine the dynamics of the in vitro response/non response to clopidogrel

Thomas Gremmel
1  Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria
Simon Panzer
2  Clinical Department for Blood Group Serology and Transfusion Medicine, Medical University of Vienna, Vienna, Austria
› Author Affiliations
Further Information

Publication History

Received: 01 March 2011

Accepted after major revision: 29 April 2011

Publication Date:
25 November 2017 (online)


Platelet inhibition by clopidogrel varies from one individual to the next. Further, in vitro high on-treatment residual adenosine-diphosphate inducible platelet reactivity (HRPR) is associated with an increased risk for major adverse cardiovascular events after percutaneous coronary intervention (PCI) with stent implantation. Recent studies identified numerous influencing factors for the antiplatelet effect of clopidogrel. Besides genetic predispositions, diverse clinical conditions as well as pharmacological interactions were shown to significantly impair clopidogrel-mediated platelet inhibition. Consequently, these influencing factors may affect clinical outcome after PCI and it is therefore desirable to identify cofounders of HRPR by platelet reactivity testing. It is apparent, that not all assays are sensitive to the same variables, and only cofounders of HRPR that are repeatedly identified by more than one test system may be clinically meaningful. However, treatment adjustment based on platelet function testing has not been associated with improved patients’ outcome. This summary shall provide an overview over current knowledge on influencing factors for clopidogrel-mediated platelet inhibition and aid guidance for critical interpretation of in vitro obtained data on HRPR.