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Individual variations of platelet inhibition after loading doses of clopidogrel
P Järemo1, T L Lindahl, S G Fransson
1Department of Cardiology, Linköping University Hospital, Linköping, Sweden. peter.jaremo@beta.telenordia.se
Insights
Clopidogrel loading doses show significant individual differences in platelet inhibition. A flow cytometry method can identify patients with abnormal responses to clopidogrel therapy.
Area of Science:
- Cardiology
- Pharmacology
- Biomedical Engineering
Background:
- Clopidogrel is a widely used antiplatelet medication.
- Individual responses to clopidogrel can vary significantly.
- Assessing platelet inhibition is crucial for optimizing therapy.
Purpose of the Study:
- To evaluate the variability in platelet inhibition following clopidogrel loading doses.
- To assess the efficacy of a flow cytometry technique in measuring platelet reactivity.
Main Methods:
- 18 patients with stable angina undergoing percutaneous coronary interventions (PCI) received clopidogrel loading doses.
- Platelet reactivity was measured using flow cytometry with adenosine diphosphate (ADP) stimulation.
- Soluble P-selectin was used as a marker for platelet activity.
Main Results:
- Significant individual heterogeneity in platelet inhibition was observed.
- Four patients showed strong platelet inhibition (<10% reactivity), while five showed weak inhibition (>60% reactivity).
- Clopidogrel did not consistently suppress platelet activity as measured by soluble P-selectin.
Conclusions:
- Clopidogrel's antiplatelet effect demonstrates considerable inter-individual variability.
- The flow cytometry method is effective in identifying patients with atypical responses to clopidogrel.
- This technique may aid in personalizing antiplatelet therapy.
Objective:
To investigate individual variations of platelet inhibition after clopidogrel-loading doses.
Setting:
Department of Cardiology, Linköping University Hospital, Linköping, Sweden.
Subjects:
Individuals with stable angina pectoris (n = 18) subject to percutaneous coronary interventions (PCI) and subsequent stenting were investigated. METHODS AND EXPERIMENTAL PROTOCOL: A 300-mg clopidogrel loading dose was administrated immediately after stenting (day 1) followed by an additional 75 mg clopidogrel after 24 h (day 2). The ADP-evoked platelet fibrinogen binding was analysed to estimate platelet reactivity immediately before angiography and on day 2. A flow cytometry technique was used with two ADP solutions (final concentrations 0.6 and 1.7 micromol L-1) employed as platelet activating agents. Soluble P-selectin was used as a marker of platelet activity.
Results:
When using 1.7 micromol L-1 ADP to activate platelets four individuals had a strong inhibition (i.e. platelet reactivity <10% of the day 1-value day 2). In contrast, five patients demonstrated a weak inhibition (i.e. platelet reactivity >60% of the day 1-value day 2). Similar results were obtained when using 0.6 micromol L-1 ADP as a platelet-activating agent. Clopidogrel, however, fails to suppress platelet activity as estimated from soluble P-selectin.
Conclusions:
Clopidogrel evoked platelet inhibition exhibits a considerable individual heterogeneity. Some individuals only had weak responses whereas others displayed strong platelet inhibition. The present flow cytometry technique appears suitable for identifying patients with abnormal reactions after clopidogrel exposure.