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Detection of clopidogrel resistance using ADP induced aggregometry with specific inhibitor PGE1
Insights
Multiple electrode platelet aggregometry (MEA) with prostaglandin E1 (PGE1) is effective for identifying clopidogrel low-responders in cardiovascular disease patients. This method shows significant correlation, unlike tests without PGE1, aiding personalized antiplatelet therapy.
Area of Science:
- Cardiology
- Pharmacology
- Clinical Laboratory Science
Background:
- Antiplatelet therapy is standard for preventing thrombotic events in cardiovascular diseases (CVD).
- A significant number of patients exhibit high residual platelet aggregation, indicating suboptimal response to therapy.
- Current laboratory methods for detecting clopidogrel resistance include monitoring residual platelet aggregation or vasodilator-stimulated phosphoprotein phosphorylation (VASP).
Purpose of the Study:
- To compare light transmission aggregometry (LTA) and multiple electrode platelet aggregometry (MEA) for monitoring clopidogrel resistance.
- To evaluate the efficacy of ADP induction with and without prostaglandin E1 (PGE1) in these assays.
Main Methods:
- Evaluated 84 cardiovascular disease patients undergoing clopidogrel therapy.
- Compared LTA and MEA using 20 micromol/L ADP, with and without PGE1.
- Analyzed data using Spearman's nonparametric correlation.
Main Results:
- Clopidogrel resistance was identified in 11.9% (MEA) and 10.7% (LTA) of patients when using ADP with PGE1.
- Significant positive correlation (p = 0.003) was observed between LTA and MEA when using PGE1.
- No significant correlation was found between LTA and MEA without PGE1 (p = 0.732).
Conclusions:
- The sensitivity of detecting clopidogrel resistance varies (5%-30%) based on the platelet function assay used.
- The ADP test with PGE1, particularly by MEA, is favored for identifying clopidogrel low-responders.
- Findings support the implementation of specific assays for personalized antiplatelet treatment strategies.
Backround:
Antiaggregation therapy is still the most frequently used approach to prevent thrombotic events in cardiovascular diseases. It has a good clinical effect but increasing evidence shows high residual platelet aggregation activity in a number of patients. Laboratory methods only allow us to detect clopidogrel "non-responders" or "low responders". Recent methods are based on monitoring residual platelet aggregation activity (aggregation methods) or detecting the number of free epitopes for binding a specific monoclonal antibody such as vasodilator-stimulated phosphoprotein phosphorylation (VASP).
Methods:
The aims of our study were comparison light transmission aggregometry (LTA) and multiple electrode platelet aggregometry (MEA) with induction by ADP in concentrations of 20 micromol/L with or without prostaglandin E1 (PGE1) for monitoring clopidogrel resistance.
Results:
In the group of 84 patients with cardiovascular disease (CAD) studied, an impaired individual response to clopidogrel therapy was found 11.9% and 10.7% of the patients using MEA and LTA, respectively, induced by ADP with PGE1. The LTA and MEA methods with induction by ADP with PGE1 and without PGE1 were statistically compared using Spearman's nonparametric correlation analysis. Both methods with using PGE, showed a positive significant correlation (p = 0.003) in contrast with the results without PGE1 with a no significant correlation (p = 0.732).
Conclusions:
The sensitivity for detecting clopidogrel resistance correlates well with other data in the literature suggesting that there are 5%-30% clopidogrel low-responders depending on the type of platelet function assay used and the criteria for defining a low-responder [16-18]. These results favor implementation of the ADP test with PGE1 by MEA specifically for identification of low-responders to clopidogrel.
