Related Experiment Video
Updated: Jul 9, 2026
Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
Published on: March 15, 2022
Cilostazol could ameliorate platelet responsiveness to clopidogrel in patients undergoing primary percutaneous
Jang-Young Kim1, Kyounghoon Lee, Myungsang Shin
1Institute for Lifelong Health, Yonsei University, Wonju, Korea.
Insights
Adding cilostazol to aspirin and clopidogrel therapy enhances antiplatelet effects, specifically inhibiting adenosine diphosphate (ADP)-induced platelet aggregation. However, it did not improve aspirin
Area of Science:
- Cardiology
- Pharmacology
- Hematology
Background:
- Cilostazol may influence clopidogrel's antiplatelet activity by increasing cyclic adenosine monophosphate levels.
- Patients undergoing primary percutaneous coronary intervention (PCI) often receive dual antiplatelet therapy (aspirin and clopidogrel).
- Assessing enhanced antiplatelet effects and markers of platelet activation is crucial in high-risk cardiovascular patients.
Purpose of the Study:
- To investigate the additional effect of cilostazol on platelet aggregation in patients receiving aspirin and clopidogrel.
- To evaluate the impact of cilostazol on soluble CD40 ligand (sCD40L) levels as a marker of platelet activation.
- To determine if cilostazol improves response to clopidogrel therapy in primary PCI patients.
Main Methods:
- A randomized study involving 60 patients undergoing primary PCI.
- Patients were assigned to dual (aspirin and clopidogrel) or triple (dual plus cilostazol) therapy.
- Platelet aggregation was measured using VerifyNow assays for arachidonic acid and adenosine diphosphate (ADP) and plasma sCD40L levels were measured by ELISA.
Main Results:
- Triple therapy showed significantly lower P2Y12 reaction units and higher % inhibition of ADP-induced platelet aggregation compared to dual therapy.
- Arachidonic acid-induced platelet aggregation was similar between groups.
- Cilostazol was identified as a negative predictor for low responders to clopidogrel; sCD40L levels did not differ significantly between groups.
Conclusions:
- Adding cilostazol to aspirin and clopidogrel significantly enhances inhibition of ADP-induced platelet aggregation.
- Cilostazol did not show an additive effect on aspirin-induced antiplatelet activity.
- The addition of cilostazol did not lead to a significant reduction in sCD40L levels.
Background:
Cilostazol increases the cyclic adenosine monophosphate levels in platelets and might ameliorate the antiplatelet activity of clopidogrel. This study investigated the additional effect of cilostazol on platelet aggregation measured by a VerifyNow analyzer and soluble CD40 ligand (sCD40L) as a marker of activated platelet in patients undergoing primary percutaneous coronary intervention (PCI).
Methods And Results:
Sixty cases of primary PCI were randomly assigned to dual (aspirin and clopidogrel) or triple (dual plus cilostazol) therapy. The antiplatelet effects of aspirin and clopidogrel were evaluated by VerifyNow tests. The plasma sCD40L levels at admission, 24 h and 21 days were measured by the ELISA method. The arachidonic acid induced platelet aggregation was similar in both groups. However, the triple group had a significantly lower P2Y12 reaction unit (dual 208.8+/-69.0 vs triple 168.2+/-79.2, p=0.041) and higher % inhibition of adenosine diphosphate (ADP)-induced platelet aggregation (dual 23.8+/-21.4% vs triple 40.5+/-21.0%, p=0.004). In the multivariate analysis, cilostazol was a negative predictor for low responders to clopidogrel (95% confidence interval 0.067-0.711). The plasma sCD40L levels were not significantly different between the 2 groups at the same point of time.
Conclusions:
The addition of cilostazol to the combination of aspirin plus clopidogrel significantly increases the inhibition of ADP-induced platelet aggregation. However, there was no additive effect on aspirin-induced antiplatelet activity or lowering of sCD40L.
Related Concept Videos
01:20Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
01:27Peripheral Artery Disease III: Interprofessional Care
01:23Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
01:27Coronary Artery Disease V: Interprofessional Care
01:25Antianginal Drugs: Calcium Channel Blockers and Ranolazine
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
01:22Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...