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Identification of low responders to a 300-mg clopidogrel loading dose in patients undergoing coronary stenting
Dominick J Angiolillo1, Antonio Fernandez-Ortiz, Esther Bernardo
1Division of Cardiology, University of Florida, Shands Jacksonville, 655 West 8th Street, Jacksonville, FL 32209, USA. dominick.angiolillo@jax.ufl.edu
Insights
Many patients show a poor response to clopidogrel after coronary stenting. Early assessment of glycoprotein IIb/IIIa activation can identify these individuals for intensified antiplatelet therapy.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Hematology
Background:
- Coronary stenting patients receive dual antiplatelet therapy to prevent stent thrombosis.
- Suboptimal clopidogrel response (low responders) is linked to increased stent thrombosis risk.
- Identifying low clopidogrel responders is crucial for optimizing treatment.
Purpose of the Study:
- To assess platelet function profiles in patients undergoing coronary stenting.
- To identify patients with a suboptimal response to a standard 300-mg clopidogrel loading dose.
- To compare platelet function between normal and low clopidogrel responders.
Main Methods:
- Light transmittance aggregometry and whole blood flow cytometry were used to assess platelet aggregation and activation.
- Platelet function was measured at baseline, and at 10 minutes, 4 hours, and 24 hours post-clopidogrel loading.
- Low responders were defined as having <40% platelet aggregation inhibition 24 hours after clopidogrel administration.
Main Results:
- 44% of patients were identified as low clopidogrel responders.
- Low responders exhibited higher baseline glycoprotein (GP) IIb/IIIa activation compared to normal responders.
- Elevated GP IIb/IIIa activation persisted in low responders at 24 hours post-clopidogrel.
Conclusions:
- A significant proportion of patients exhibit an early suboptimal response to a 300-mg clopidogrel loading dose.
- Increased pre-intervention GP IIb/IIIa activation may predict low clopidogrel response.
- These findings suggest considering more aggressive antithrombotic strategies for identified high-risk patients.
Background:
Although patients undergoing coronary stenting routinely receive dual antiplatelet treatment to reduce the risk of stent thrombosis, this undesired event still occurs. A suboptimal response to clopidogrel treatment (low responders) has been suggested to contribute to stent thrombosis. In the present study, platelet function profiles were assessed in patients undergoing coronary stenting receiving a standard 300-mg clopidogrel loading dose with the aim to identify low clopidogrel responders.
Materials And Methods:
Platelet aggregation was assessed by light transmittance aggregometry following 6 microM ADP stimuli in 48 patients before and 10 min, 4 and 24 h after receiving clopidogrel front-loading. Patients having > or =40% inhibition of platelet aggregation 24 h after clopidogrel administration were defined as normal responders, whereas those having <40% inhibition were low responders. Glycoprotein (GP) IIb/IIIa activation and P-selectin expression were assessed by whole blood flow cytometry following 2 microM ADP stimuli at the same time points. Platelet function profiles were compared between normal and low clopidogrel responders.
Results:
Twenty-seven patients (56%) were normal responders and 21 (44%) low responders. Baseline GP IIb/IIIa activation was higher in low responders (74.6+/-16.6% vs. 58.2+/-24.5%, p=0.03). Although GP IIb/IIIa activation reduced following clopidogrel front-loading in both groups, it remained increased among low responders at 24 h (58.6+/-21.3% vs. 40.2+/-28.7%, p=0.05) and during the overall study time course (p=0.02). There were no differences in P-selectin expression.
Conclusions:
A considerable proportion of patients have an early suboptimal response to a 300-mg clopidogrel loading dose. An increased GP IIb/IIIa activation before intervention may identify this group of patients suggesting the use of a more aggressive antithrombotic treatment in these individuals.
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