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Clopidogrel responsiveness in stroke patients on a chronic aspirin regimen
Zohara Sternberg1, Marilou Ching, Robert N Sawyer
1Stroke Center, Millard Fillmore Hospital, Buffalo, New York 14223, USA. zs2@buffalo.edu
Insights
This study shows that clopidogrel (CPG) effectively inhibits platelet function in acute ischemic stroke patients on aspirin. Correcting for baseline variability ensures consistent antiplatelet response measurements across different instruments.
Area of Science:
- Cardiology
- Pharmacology
- Hematology
Background:
- Acute ischemic stroke patients often receive dual antiplatelet therapy.
- Clopidogrel (CPG) is a P2Y12 inhibitor commonly used in stroke patients.
- Assessing antiplatelet therapy response is crucial for patient outcomes.
Purpose of the Study:
- To evaluate the antiplatelet effects of clopidogrel in acute ischemic stroke patients already on aspirin.
- To compare the performance of three point-of-care platelet function analyzers in monitoring CPG's efficacy.
- To determine if correcting for baseline platelet variability impacts CPG response assessment.
Main Methods:
- Patients with acute ischemic stroke on aspirin received a 300-mg CPG loading dose and 75-mg daily maintenance dose.
- Platelet function was measured using Thrombelastograph, VerifyNow, and Chronolog 570VS systems.
- Measurements were taken at baseline, 26 hours, and 64 hours post-loading dose.
Main Results:
- All three instruments demonstrated significant inhibition of platelet function after CPG administration.
- Variations in antiplatelet response measurements among instruments were observed.
- Correcting for baseline platelet variability eliminated inter-instrument discrepancies.
- The proportion of poor CPG responders varied by instrument and time point.
Conclusions:
- Clopidogrel effectively inhibits platelet function in stroke patients on aspirin.
- Platelet function analyzer choice and baseline variability correction influence response assessment.
- Further research is needed to link ex vivo CPG inhibition to clinical outcomes in stroke patients.
Abstract:
This study evaluated the antiplatelet effects of clopidogrel (CPG) in patients sustaining acute ischemic stroke who were already receiving chronic outpatient aspirin therapy (81-325 mg/day). Platelet function was measured using 3 different "point-of-care" platelet function analyzers: the Thrombelastograph hemostasis system, the Accumetrics VerifyNow system, and the Chronolog 570VS impedance aggregometer. Platelet function was assessed before administration of a 300-mg CPG loading dose and again at 26 hours and 64 hours after this loading dose along with a 75-mg daily maintenance dose. All 3 instruments detected marked inhibition of platelet function at 26 hours and 64 hours after CPG administration. There were significant variations among the 3 instruments in monitoring antiplatelet responses to aspirin and CPG; however, these variations were eliminated when the platelet function results were corrected for baseline platelet variability. The percentage of patients who were poor responders to CPG after switching from aspirin depended on the measurement instrument used, but was higher at 26 hours after CPG administration than at 64 hours after CPG administration. Our findings indicate that poor response to antiplatelet agents in general, and to CPG in particular, is a function of the measuring instrument. The correction for baseline platelet variability results in similar levels of platelet inhibition measured by the 3 platelet function analyzers. Future studies are warranted to examine the association between ex vivo CPG-induced platelet inhibition and clinical outcomes in patients with ischemic stroke.
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