Platelet function variability and non-genetic causes

Ioannis Tentzeris; Jolanta Siller-Matula; Serdar Farhan; Rudolf Jarai; Johann Wojta; Kurt Huber

doi:10.1160/THS11-01-0025

Thrombosis and Haemostasis, Inhaltsverzeichnis

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^*

¹3^rd Medical Department with Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria

,

Jolanta Siller-Matula^*

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

,

Serdar Farhan

¹3^rd Medical Department with Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria

,

Rudolf Jarai

¹3^rd Medical Department with Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria

,

Johann Wojta

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

,

Kurt Huber

¹3^rd Medical Department with Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria

› Institutsangaben

Abstract

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.

Keywords

ADP receptors - antiplatelet agents - platelet pharmacology

Volltext

Referenzen

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