Thromb Haemost 2011; 105(S 06): S60-S66
DOI: 10.1160/THS11-01-0025
Thrombosis and Haemostasis Supplement
Schattauer GmbH

Platelet function variability and non-genetic causes

Ioannis Tentzeris*
1   3rd Medical Department with Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria
,
Jolanta Siller-Matula*
2   Department of Cardiology, Medical University of Vienna, Vienna, Austria
,
Serdar Farhan
1   3rd Medical Department with Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria
,
Rudolf Jarai
1   3rd Medical Department with Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria
,
Johann Wojta
2   Department of Cardiology, Medical University of Vienna, Vienna, Austria
,
Kurt Huber
1   3rd Medical Department with Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria
› Author Affiliations
Financial support: This work was supported by the Association for the Promotion of Scientific Research in Atherosclerosis, Thrombosis and Vascular Biology (ATVB), Vienna, Austria. Received: January 17, 2011 Accepted after major revision: March 25, 2011 Prepublished online: April 14, 2011
Further Information

Publication History

Received: 17 January 2011

Accepted after major revision: 25 March 2011

Publication Date:
06 December 2017 (online)

Summary

Dual antiplatelet therapy (DAPT) has been established for the treatment of coronary artery disease, especially in and after acute coronary syndromes, and after coronary interventions. Data suggest that a significant percentage of individuals treated with clopidogrel do not receive the expected therapeutic benefit because of a decreased responsiveness of their platelets, which is caused by several extrinsic and intrinsic mechanisms. The clinical consequence of clopidogrel non-responsiveness is severe cardiovascular complications. Besides genetic variability in response to antiplatelet therapy, non-genetic causes such as drug interactions (proton-pump inhibitors, statins, calcium-channel blockers, coumarine derivates, antibiotics, antimycotics) and co-morbidities (diabetes mellitus, renal failure, obesity) are responsible for this phenomenon. Large clinical trials with standardised laboratory methods and hard clinical endpoints are needed to identify these interactions with clopidogrel and predictors for its non-responsiveness.

* Ioannis Tentzeris and Jolanta Siller-Matula contributed to the same extent as first authors in the writing of this paper.


 
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