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Effect of cilostazol on platelet aggregation in patients with non-ST elevation acute coronary syndrome
S Pattanaik1, S Malhotra, Y P Sharma
1Department of Pharmacology, Postgraduate Institute of Medical Education and Research, Chandigarh-160 012, India.
Insights
Cilostazol added to aspirin and clopidogrel significantly reduced platelet aggregation in non-ST elevation acute coronary syndrome (NSTEACS) patients. This triple therapy showed potential benefits, though PAI-1 levels and clinical outcomes did not significantly differ from dual therapy.
Area of Science:
- Cardiology
- Pharmacology
- Thrombosis
Background:
- Non-ST elevation acute coronary syndrome (NSTEACS) presents a high risk of ischemic events.
- The optimal antithrombotic regimen for NSTEACS remains undefined.
- Standard antiplatelet therapy may not fully mitigate ischemic risks.
Purpose of the Study:
- To evaluate the effect of cilostazol on platelet aggregation and PAI-1 levels in NSTEACS patients.
- To assess the efficacy and safety of adding cilostazol to standard antiplatelet therapy.
- To determine if cilostazol improves clinical outcomes in NSTEACS.
Main Methods:
- A randomized controlled trial involving 40 NSTEACS patients treated conservatively.
- Patients received either cilostazol (100 mg b.i.d.) or placebo for 7 days, alongside aspirin and clopidogrel.
- Primary endpoints included changes in agonist-induced platelet aggregation and serum PAI-1 levels after 7 days; safety and clinical outcomes were assessed at 7 and 30 days.
Main Results:
- Triple therapy with cilostazol significantly reduced ADP and collagen-induced platelet aggregation compared to dual therapy (p=0.003 and p=0.04, respectively).
- No significant difference was observed in serum PAI-1 levels between the groups (p=0.42).
- The composite endpoint of recurrent ischemia, myocardial infarction, intervention, or death occurred in 4 patients in the cilostazol group versus 7 in the placebo group (p=0.48) at 30 days.
Conclusions:
- Cilostazol demonstrates additional platelet aggregation inhibition when combined with aspirin and clopidogrel in NSTEACS patients.
- While cilostazol enhances antiplatelet effects, its impact on PAI-1 and major adverse cardiovascular events requires further investigation.
- The findings suggest a potential role for cilostazol in managing NSTEACS, warranting larger studies.
Aims:
The optimal antithrombotic regimen for non-ST elevation acute coronary syndrome(NSTEACS) has not yet been defined and the risk of ischemic events remains high in these patients. We aimed to evaluate the effect of cilostazol on agonist induced platelet aggregation and serum plasminogen activator inhibitor-1(PAI-1) in the patients with NSTEACS administered along with the standard antiplatelet regimen.
Patients And Methods:
40 patients of NSTEACS presenting within 72 h of onset of symptoms were randomized to cilostazol or placebo in 1 : 1 ratio, in whom a conservative treatment strategy was adopted. Cilostazol 100 mg b.i.d was administered within 12 h of hospital admission for 7 days along with standard doses of aspirin and clopidogrel. The primary end points were effect on agonist-induced platelet aggregation and serum PAI-1 levels after 7 days of treatment. Safety and clinical outcome assessment were also done at 7 and 30 days.
Results:
Patients in the triple therapy group showed significant decrease in the ADP (25.5 +/- 27.4 vs. 5.6 +/- 8.4; p = 0.003) and collagen (24.9 +/- 25.5 vs. 11.7 +/- 11; p = 0.04) induced percentage platelet aggregation after 7 days of treatment compared to the dual therapy group. There was no significant change in levels of serum PAI-1 (50.30 +/- 10.17 ng/ml vs. 53.47 +/- 14.08 ng/ml; p = 0.42). The composite of recurrent ischemia, myocardial infarction, need for intervention and death occurred in 4 patients in the cilostazol group compared to 7 in the placebo group at the end of 30 days of follow-up (p = 0.48).
Conclusion:
Cilostazol has additional platelet aggregation inhibition action in patients with NSTEACS along with aspirin and clopidogrel.
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