Platelet function variability and non-genetic causes

Journal: Thrombosis and Haemostasis
ISSN: 0340-6245

Contemporary issues in atherothrombosis

Issue: 2011: 105/Supplement 1
Pages: S60-S66

Platelet function variability and non-genetic causes

I. Tentzeris (1), J. Siller-Matula (2), S. Farhan (1), R. Jarai (1), J. Wojta (2), K. Huber (1)

(1) 3rd Medical Department with Cardiology and Emergency Medicine, Wilhelminen Hospital, Vienna, Austria; (2) Department of Cardiology, Medical University of Vienna, Vienna, Austria


platelet pharmacology, Antiplatelet agents, ADP receptors


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.

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