Comparison of Platelet Inhibition With Adjunctive Cilostazol Versus High Maintenance-Dose Clopidogrel According to Hepatic Cytochrome 2C19 Allele (CYP2C19) Polymorphism (ACCEL2C19)
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT00891670|
Recruitment Status : Unknown
Verified April 2009 by Gyeongsang National University Hospital.
Recruitment status was: Not yet recruiting
First Posted : May 1, 2009
Last Update Posted : May 1, 2009
|Condition or disease||Intervention/treatment||Phase|
|Coronary Artery Stenosis Maximal Platelet Aggregation Late Platelet Aggregation High Post-Treatment Platelet Reactivity||Drug: cilostazol Drug: clopidogrel Drug: aspirin||Phase 3|
The additional platelet inhibition with clopidogrel, a thienopyridine inhibitor of the platelet P2Y12 adenosine diphosphate (ADP) receptor, has reduced the risk of ischemic events after coronary stent implantation. Because of inter-individual variability in platelet response to clopidogrel, a significant proportion of suboptimal platelet inhibition has been reported. In addition, persistent residual platelet reactivity measured with platelet function testing has shown the association with the cardiovascular outcomes after percutaneous coronary intervention(PCI).
Various clinical factors and genetic polymorphisms have been studied to predict the degree of antiplatelet response to clopidogrel. Interestingly, recent studies found that carriers of the loss-of-function hepatic cytochrome (CYP) 2C19 allele had significantly lower levels of the active metabolite of clopidogrel, diminished platelet inhibition, and a higher rate of major adverse cardiovascular events than did non-carriers, in the setting of PCI and acute coronary syndrome(ACS). These findings raise the need of solutions to overcome enhanced post-clopidogrel platelet reactivity by the influence of the loss-of-function CYP2C19 allele. Increasing the dose of clopidogrel and new potent P2Y12 antagonists(such as prasugrel) may be alternative antiplatelet regimens in patients with the loss-of-function CYP variant.
Cilostazol reversibly induces platelet inhibition via its blockade of phosphodiesterase (PDE) type 3 and is catalysed mainly by CYP3A. A recent study demonstrated that adjunctive cilostazol to dual antiplatelet therapy (triple antiplatelet therapy) intensified platelet inhibition as compared with a high maintenance-dose (MD) of 150 mg/day. Therefore, triple antiplatelet therapy could also be an alternative antiplatelet therapy to improve platelet inhibition and clinical outcomes in carriers of CYP2C19 mutant allele.
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||80 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||None (Open Label)|
|Official Title:||Validation of Adjunctive Cilostazol According to CYP2C19 Polymorphism: Prospective, Randomized, Single-Center Trial:|
|Study Start Date :||May 2009|
|Estimated Primary Completion Date :||June 2009|
|Estimated Study Completion Date :||July 2009|
Active Comparator: triple group
received cilostazol 100 mg twice daily in addition to aspirin 100mg and clopidogrel 75mg once daily
100mg twice daily for at least 1 month
Other Name: pletaalDrug: aspirin
Active Comparator: high maintenance dose group
received clopidogrel 150 mg/day with aspirin 100mg once daily
75mg once daily (triple group arm)
150mg once daily (high maintenance dose group arm)
Other Name: plavixDrug: aspirin
- Reduction of maximal platelet aggregation [ Time Frame: 30 days ]
- Rate of high post-clopidogrel platelet reactivity [ Time Frame: 30 days ]
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00891670
|Contact: Young-Hoon Jeong, MD, phDfirstname.lastname@example.org|
|Korea, Republic of|
|Gyeong-Sang National University Hospital||Not yet recruiting|
|Jinju, Gyeong-Nam, Korea, Republic of, 660-702|
|Principal Investigator: Young-Hoon Jeong, MD, PHD|
|Principal Investigator:||Young-Hoon Jeong, MD, phD||Gyeong-Sang Natinal University Hospital|