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Updated: Jun 10, 2026

A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Lack of clopidogrel-statin interaction in patients undergoing coronary stent implantation
Carlos Vicente Serrano Júnior1, Alexandre de Matos Soeiro, Leila Fernandes Araújo
1Hospital das Clínicas, Instituto do Coração, Universidade de São Paulo, Brazil.
Insights
Clopidogrel effectively reduces platelet activation. Combining clopidogrel with statins like atorvastatin or simvastatin does not diminish its antiplatelet effects in patients with stable angina.
Area of Science:
- Cardiology
- Pharmacology
- Hematology
Background:
- Previous studies suggested statins might reduce clopidogrel's effectiveness.
- Platelet activation and adherence are key factors in cardiovascular events.
Purpose of the Study:
- To evaluate clopidogrel's impact on platelet activation and aggregation.
- To determine if statins (atorvastatin, simvastatin) alter clopidogrel's antiplatelet action.
Main Methods:
- Prospective study of 68 stable angina patients undergoing percutaneous coronary intervention (PCI).
- Patients were grouped based on prior statin use (atorvastatin, simvastatin, or none).
- Platelet activation markers (P-selectin, glycoprotein IIb/IIIa) were measured via flow cytometry before and after PCI and clopidogrel administration.
Main Results:
- Clopidogrel administration led to a significant reduction in platelet activity.
- No significant differences in platelet activation markers were observed between patients taking clopidogrel with or without statins.
- P-selectin and glycoprotein IIb/IIIa levels showed no reduction in clopidogrel's antiplatelet efficacy when co-administered with atorvastatin or simvastatin.
Conclusions:
- Clopidogrel effectively decreases platelet activation.
- The antiplatelet effects of clopidogrel are not reduced when used concurrently with atorvastatin or simvastatin.
Background:
Some studies have suggested reduced activity of clopidogrel on platelet activation and adherence in patients using statins.
Objective:
To assess whether platelet activation and aggregation decrease with clopidogrel, and whether there is a reduction of the action of clopidogrel when associated with atorvastatin or simvastatin.
Methods:
This prospective study included 68 patients with stable angina with previous use of simvastatin, atorvastatin, or no statin (control group), with previous elective indication of percutaneous coronary intervention (PCI). Platelet activation was analyzed by means of platelet count, levels of P-selectin and glycoprotein IIb/IIIa (with and without ADP stimulation) by flow cytometry. The findings were analyzed before and after percutaneous coronary intervention and the administration of clopidogrel.
Results:
We observed reduction in platelet activity with use of clopidogrel. Furthermore, no differences were found between the variables analyzed to prove reduced activity of clopidogrel when combined with statins. We observed levels of p-selectin (pre-angioplasty: 14.23 ± 7.52 x 8.83 x 11.45 ± 7.65 ± 7.09; after angioplasty: 21.49 ± 23.82 x 4 37 ± 2.71 x 4.82 ± 4.47, ρ < 0.01) and glycoprotein IIb/IIIa (pre-angioplasty: 98.97 ± 0.43 ± 1.25 x 98.79 x 99.21 ± 0.40 after angioplasty: 99.37 ± 0.29 ± 1.47 x 98.50 x 98.92 ± 0.88, ρ = 0.52), respectively, in the control, atorvastatin and simvastatin groups.
Conclusion:
We concluded that platelet activation decreases with administration of clopidogrel, and clopidogrel has no antiplatelet effect reduced in the presence of simvastatin or atorvastatin.
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