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Monitoring of clopidogrel action: comparison of methods
Jörg Geiger1, Lino Teichmann, Ralf Grossmann
1Institut für Klinische Biochemie und Pathobiochemie und Zentrallabor, Universität Würzburg, Würzburg, Germany. Geiger@klin-biochem.uni-wuerzburg.de
Insights
Assessing clopidogrel effectiveness is crucial due to variable patient response. The vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay reliably quantifies clopidogrel
Area of Science:
- Cardiovascular pharmacology
- Platelet biology
- Clinical diagnostics
Background:
- Clopidogrel is vital for preventing adverse events post-coronary intervention.
- A significant patient subset exhibits inadequate response to clopidogrel.
- Failure in antiplatelet therapy carries severe clinical implications, necessitating reliable monitoring.
Purpose of the Study:
- To evaluate the reliability of various assays in quantifying clopidogrel's antiplatelet effects.
- To identify a specific assay that accurately reflects clopidogrel's impact on platelet function.
Main Methods:
- Healthy volunteers received clopidogrel or placebo.
- Platelet function was assessed using aggregometry, flow cytometry (P-selectin), PFA-100, and VASP phosphorylation assays.
- Monitoring occurred at baseline, during treatment (days 1-5), and post-treatment (day 9).
Main Results:
- Clopidogrel intake led to a loss of platelet response to ADP within 12 hours.
- VASP phosphorylation status strongly correlated with the inhibition of platelet aggregation.
- P-selectin expression and PFA-100 closure time did not clearly indicate clopidogrel's effects.
Conclusions:
- VASP phosphorylation assays provide a reliable method for quantifying clopidogrel's therapeutic effectiveness.
- The VASP assay's direct measurement of P2Y12 receptor function ensures specificity for clopidogrel.
- This assay distinguishes clopidogrel's impact from other commonly used antiplatelet agents.
Background:
Clopidogrel is a potent drug for prevention of adverse effects during and after coronary intervention. Increasing experience indicates that a significant proportion of patients do not respond adequately to clopidogrel. Because failure of antiplatelet therapy can have severe consequences, there is need for a reliable assay to quantify the effectiveness of clopidogrel treatment.
Methods:
Of 24 healthy volunteers admitted to the study, 18 were treated for 1 week with clopidogrel (300-mg loading dose and 75-mg maintenance dose), and 6 with placebo. Platelet function was monitored by 2 assays, based on flow cytometry and enzyme immunoassay, that measure the phosphorylation status of vasodilator-stimulated phosphoprotein (VASP) and by aggregometry, flow cytometry of P-selectin, and the platelet function analyzer at baseline, on days 1-5, and on day 9 of treatment.
Results:
Aggregometry and VASP phosphorylation revealed a loss of platelet response to ADP within 12 h after clopidogrel intake. The phosphorylation status of VASP correlated with the inhibition of platelet aggregation. In contrast, neither P-selectin expression nor PFA-100 closure time was a clear indicator of clopidogrel effects on platelets.
Conclusions:
VASP phosphorylation assays are reliable for quantifying clopidogrel effects. Because the VASP assay directly measures the function of the clopidogrel target, the P2Y12 receptor, the assay is selective for clopidogrel effects rather than effects of other platelet inhibitors commonly in use.
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