Doubling the clopidogrel dose in patients with reduced responsiveness to the standard dose is associated with a limited effectiveness as evaluated by impedance aggregometry.

Autor: Stellbaum C; Department of Internal Medicine/Cardiology, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin, Germany., Ayral Y, Morguet A, Schultheiss HP, Rauch U
Jazyk: angličtina
Zdroj: Cardiovascular revascularization medicine : including molecular interventions [Cardiovasc Revasc Med] 2012 May-Jun; Vol. 13 (3), pp. 159-66. Date of Electronic Publication: 2012 Apr 14.
DOI: 10.1016/j.carrev.2012.02.009
Abstrakt: Background: Different methods are available for quantifying platelet function inhibition. Measuring vasodilator-stimulated phosphoprotein (VASP) phosphorylation is currently the most specific method for assessing the clopidogrel effect. The aim of our study was to compare different tests in view of a clinically applicable bedside test. Further, we examined whether doubling the clopidogrel dose to 150mg/d in clopidogrel low-responder would lead to a reduction in platelet reactivity.
Methods and Results: ADP-, ADP Hs-, and TRAP-induced platelet aggregation were measured by impedance aggregometry in 100 patients with CAD and 18 healthy controls. Moreover, platelet aggregation was assessed by flow cytometrical detection of VASP-phosphorylation and surface P-selectin in a subgroup of 34 patients and in healthy controls. Another 10 patients with CAD, identified as low-responder, were treated with a clopidogrel dose of 150mg/d. Thereafter, ADP-induced platelet aggregation was assessed by impedance aggregometry. Significant correlations were observed between ADP-induced platelet aggregation assessed by VASP-phosphorylation and by impedance aggregometry. Doubling the dose of clopidogrel to 150mg/d was associated with a reduction of ADP-induced platelet aggregation in only 60% of the patients.
Conclusions: Impedance aggregometry is a valuable bedside test to assess platelet function inhibition. Doubling the clopidogrel dose is not effective to reduce high on-treatment platelet reactivity in almost half of these patients, pointing to the need of a more powerful platelet inhibitor.
(Copyright © 2012 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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