What is the clinical evidence from this study?

Study design: Other. Population: Cerebral infarction (n=35). Intervention: Cilostazol vs. Pre-therapy baseline. Primary outcome: Platelet aggregation assessed by VerifyNow IIb/IIIa test in the presence of 10 nM PGE1 (69% inhibition, p=<0.05).

What does this research mean for the field?

The VerifyNow IIb/IIIa test, when used in the presence of 10 nM prostaglandin E1, is the most suitable whole blood assay for monitoring the platelet-inhibitory efficacy of cilostazol. Novelty: ClaimNovelty.METHODOLOGICAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

This research aims to evaluate a monitoring assay for cilostazol using whole blood samples to assess its effect on platelet function.

June 2, 2026Open Access

Assessment of cilostazol inhibition using whole blood samples : comparison of three platelet function tests

Q: What are the key findings of this study?

Cilostazol significantly inhibited platelet aggregation by 69% compared to pre-therapy baseline in patients with cerebral infarction when assessed using the VerifyNow IIb/IIIa test with 10 nM PGE1.

Q: What does this research mean for the field?

The VerifyNow IIb/IIIa test, when used in the presence of 10 nM prostaglandin E1, is the most suitable whole blood assay for monitoring the platelet-inhibitory efficacy of cilostazol. Novelty: ClaimNovelty.METHODOLOGICAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

This research aims to evaluate a monitoring assay for cilostazol using whole blood samples to assess its effect on platelet function.

Key Result

Cilostazol significantly inhibited platelet aggregation by 69% compared to pre-therapy baseline in patients with cerebral infarction when assessed using the VerifyNow IIb/IIIa test with 10 nM PGE1.

Key Points

This research aims to evaluate a monitoring assay for cilostazol using whole blood samples to assess its effect on platelet function.
Measured platelet aggregation with VerifyNow, Multiplate, and T-TAS in healthy volunteers and cerebral infarction patients.
Tested aggregation in the presence and absence of prostaglandin E1 (PGE1) at various concentrations.
Compared pre-therapy and post-cilostazol uptake platelet aggregation results.
Cilostazol decreased platelet aggregation by 46% in the IIb/IIIa test and 24% in the P2Y12 test post-oral uptake.
With 10 nM of PGE1, there was a 69% inhibition of platelet aggregation compared to pre-treatment levels.
VerifyNow IIb/IIIa tests were effective in monitoring cilostazol efficacy.

Structured PICO

Which whole blood platelet function test is most suitable for monitoring the antiplatelet efficacy of cilostazol?

Population

In vitro blood samples, healthy volunteers, and patients with cerebral infarction

Intervention

Cilostazol (in vitro addition, single oral dose, or clinical therapy) assessed with VerifyNow, Multiplate, and Total Thrombus-formation Analysis System (T-TAS) in the presence of prostaglandin E1 (PGE1)

Comparator

Pre-therapy blood samples or absence of cilostazol

Outcome

Platelet aggregationsurrogate

The VerifyNow IIb/IIIa test with added PGE1 is a suitable and effective tool for monitoring the antiplatelet efficacy of cilostazol in clinical settings.

Main Result

Effect estimate: 69% inhibition

p-value: p=<0.05

Limitations

Discrepancies between in vitro and ex vivo studies with the aspirin and P2Y12 tests without a reasonable explanation.
Lack of a method to measure the intracellular concentration of cilostazol.
Small sample size.

Abstract

Introduction: Cilostazol inhibits phosphodiesterase, with resultant increase in intracellular cyclic AMP, leading to platelet inhibition, particularly in the presence of prostaglandin E1 (PGE1). This study aimed to establish a cilostazol monitoring assay, using whole blood samples. Methods: Platelet aggregation in the presence or absence of indicated concentrations of PGE1 were assessed using VerifyNowR, MultiplateR and Total Thrombus-formation Analysis System (T-TASR). Results: In the presence of added PGE1, cilostazol inhibited in vitro platelet aggregation of VerifyNow, with the aspirin test by 19% and the IIb/IIIa test by 44%, respectively. After a single oral uptake of cilostazol in healthy volunteers, cilostazol decreased platelet aggregation, with the IIb/IIIa test by 46% and with the P2Y12 test by 24%, respectively. Multiplate or T-TAS failed to detect cilostazol effi cacy both in vitro and ex vivo. VerifyNow IIb/IIIa tests were used to monitor cilostazol effi cacy on cerebral infarction patients. Compared with pre-therapy blood samples, those after cilostazol uptake showed signifi cant inhibition of platelet aggregation in the presence of 3 nM (37%) and 10 nM PGE1 (69%). Conclusion: The IIb/IIIa tests of VerifyNow in the presence of 10 nM PGE1 is the most suitable tool for monitoring assessing cilostazol.

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