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Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
Published on: March 15, 2022
Inter-individual variability in response to clopidogrel in patients with coronary artery disease
Artur Dziewierz1, Dariusz Dudek, Grzegorz Heba
12nd Department of Cardiology, Institute of Cardiology, Jagiellonian University College of Medicine, Cracow, Poland.
Insights
Clopidogrel resistance can be identified early, within six hours of treatment initiation, using platelet function tests. This rapid assessment helps identify non-responders to clopidogrel, improving patient management.
Area of Science:
- Pharmacology
- Cardiovascular Medicine
- Clinical Chemistry
Background:
- Clopidogrel, often combined with aspirin, is vital for reducing ischemic events in coronary artery disease (CAD).
- Limited data exist on inter-individual variability in clopidogrel response.
Purpose of the Study:
- To determine the incidence of clopidogrel resistance.
- To evaluate early identification of non-responders using platelet function assessment.
Main Methods:
- Assessed platelet aggregation inhibition (DPAI) in 31 stable angina patients treated with aspirin.
- Measured DPAI at baseline and 3, 6, 12, and 24 hours post-clopidogrel loading dose (300 mg).
Main Results:
- 22.6% of patients were non-responders (DPAI ≤10%) at 24 hours.
- Early non-responders at 6 hours (87.5%) remained resistant at 24 hours.
- No significant differences in ischemic or bleeding complications were observed between groups.
Conclusions:
- Platelet aggregation inhibition assessment enables early identification of clopidogrel resistance within six hours.
- Rapid whole blood platelet function assessment is clinically feasible for routine practice.
Background:
Clopidogrel, especially when combined with aspirin, reduces the rate of ischaemic events in patients with coronary artery disease (CAD). There are scare data in literature on the inter-individual variability in response to clopidogrel.
Aim:
To assess the incidence of clopidogrel resistance using rapid whole blood platelet function assessment, and to examine the possibility of early identification of non-responders.
Methods:
In 31 consecutive patients with stable angina treated with aspirin, the degree of platelet aggregation inhibition (DPAI) in the whole blood was assessed at baseline and 3, 6, 12 as well as 24 hours after administration of loading dose of clopidogrel (300 mg). Response to clopidogrel was measured by calculating the absolute difference between the baseline DPAI and DPAI obtained at the investigated time-points (DPAI).
Results:
After 24 hours from clopidogrel administration, seven (22.6%) patients were identified as non-responders (DPAI < or =10%). Demographic and clinical variables as well as baseline DPAI were similar in responders and non-responders (DPAI: 5.8+/-3.7% vs 7.1+/-5.3%, p=NS). Out of the patients who were found to be resistant to clopidogrel at the six-hour time-point, 87.5% remained resistant to this agent 24 hours after drug administration. DPAI calculated at the 24-hour time-point highly correlated with the six-hour DPAI (r=0.74). No differences in the rate of ischaemic or bleeding complications between responders and non-responders were noted.
Conclusions:
The assessment of the degree of platelet aggregation inhibition allows early (six hours from the initiation of treatment) identification of patients who are resistant to clopidogrel. The method of the rapid whole blood platelet function assessment is feasible in every-day clinical practice.
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