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Published on: May 14, 2013
Clopidogrel resistance: implications for coronary stenting
Paul A Gurbel1, Wei C Lau, Kevin P Bliden
1Sinai Center for Thrombosis Research, Baltimore, Maryland 21215, USA. Pgurbel@lifebridgehealth.org
Insights
Clopidogrel resistance and high platelet reactivity increase risks for thrombotic events after stent implantation. Further research is needed to understand the clinical impact and cost-effectiveness of assessing platelet inhibition.
Area of Science:
- Cardiology
- Pharmacology
- Thrombosis Research
Background:
- Clopidogrel with aspirin is standard for preventing thrombosis post-coronary stent implantation.
- Current practice administers clopidogrel without assessing platelet inhibition, despite known response variability and resistance.
- Patients with nonresponsive platelets may face increased thrombotic event risk, though this is under-investigated.
Purpose of the Study:
- To investigate the relationship between clopidogrel resistance, high platelet reactivity, and thrombotic events (stent thrombosis, myocardial infarction, stroke, death).
- To determine if a threshold of platelet reactivity predicts thrombotic risk.
- To assess the cost implications of treating non-responsive patients with clopidogogrel.
Main Methods:
- The study aims to address key questions regarding clopidogrel response and clinical outcomes.
- It emphasizes the need for validated point-of-service devices to facilitate understanding.
- Mechanisms underlying clopidogrel response variability are under investigation.
Main Results:
- Preliminary data suggest a link between clopidogrel nonresponsiveness and thrombotic event risk.
- The magnitude of this clinical effect and specific risk thresholds remain largely unknown.
- The cost-effectiveness of current clopidogrel administration strategies is not fully elucidated.
Conclusions:
- Understanding clopidogrel resistance and high platelet reactivity is crucial for optimizing patient outcomes after stent implantation.
- Further research is required to define clinical relevance, establish risk thresholds, and evaluate cost-effectiveness.
- Investigating the mechanisms of response variability is essential for improving antiplatelet therapy.
Abstract:
Clopidogrel, in combination wih aspirin, is currently the drug of choice to prevent thrombosis after coronary stent implantation. Currently, clopidogrel is administered to the vast majority of patients without any assessment of platelet inhibition. Response variability and resistance, however, definitely occur to clopidogrel treatment. Preliminary data support the hypothesis that patients with reactive or clopidogrel nonresponsive platelets are at risk for thrombotic events. However, the magnitude of the clinical effect remains unknown and relationship between nonresponsiveness and risk of clinical events is under-investigated. Several important questions that must be answered are: A) What is the relation of clopidogrel resistance and high platelet reactivity to the occurrence of stent thrombosis, recurrent myocardial infarction, stroke and death?; B) Is there a threshold of platelet reactivity that correlates with the onset of thrombotic risk?; and C) What is the cost of administering clopidogrel to non-responsive patients? Finally, our understanding of the clinical relevance of drug resistance and high platelet reactivity should be facilitated by the use of validated point-of-service devices. The mechanisms of the response variability to clopidogrel remain incompletely defined. The contribution of intra- and extracellular pathways are under investigation.
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