The purpose of this study is to determine whether adjunctive cilostazol loading/maintenance to standard treatment (aspirin, clopidogrel, and statin) is effective in reduction of major adverse cardiovascular events, platelet activation, inflammation and myonecrosis in patients with non-ST-elevation acute coronary syndrome (ACS)undergoing percutaneous coronary intervention (PCI).
In ACS patients, platelet activation, inflammation, and ischemia-reperfusion injury can be closely associated with the risk of post-PCI myonecrosis and ischemic events occurrence. In the ACCEL-AMI (Adjunctive Cilostazol versus high maintenance-dose ClopidogrEL in patients with Acute Myocardial Infarction)study, adjunctive cilostazol increased platelet inhibition compared with double-dose clopidogrel. Meanwhile, statins can reduce the extent of myonecrosis via limiting inflammation and myocardial infarct size by activating phosphatidylinositol-3-kinase (PI3K), ecto-5'-nucleotidase, Akt/endothelial nitric oxide synthase (eNOS), and the downstream effectors inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Inhibition of PI3K, adenosine receptors, eNOS, iNOS, or COX-2 abrogates the protective effects of statins. In animal study, the combination of low-dose statin with cilostazol synergistically limits infarct size. Multiple studies have shown that cilostazol can influence inflammation and RISK pathway using the similar pathway with statin. This study will be performed to evaluate the role of adjunctive cilostazol in platelet inhibition, inflammation, and myonecrosis compared with standard treatment.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Enrollment
220
* Loading: aspirin 300mg + clopidogrel 600mg * Maintenance: aspirin 200mg/d + clopidogrel 75mg/d for 1 month
* Loading: cilostazol 200mg + aspirin 300mg + clopidogrel 600mg * Maintenance: cilostazol 100mg bid+ aspirin 200mg/d+ clopidogrel 75mg/d for 1 month
Gyeonsang National University Hospital
Jinju, Gyeonsangnam-do, South Korea
Major adverse cardiovascular events (MACE)
Composite of cardiac death, MI and ischemia-driven target lesion revascularization (TLR)
Time frame: 1 month
P2Y12 reaction unit levels in the 2 arms
Time frame: 1 month
MACE incidence according to P2Y12 reaction unit
Time frame: 1 month
any post-procedural increase of markers of myocardial injury above ULN
Time frame: 1 month
post-procedural variations from baseline of hs-CRP levels in the 2 arms
Time frame: 1 month
ACUITY major/minor bleeding rate
Time frame: 1 month
24hr post-procedural variations from baseline of inflammation markers (IL-6, TNF-alpha, cell adhesion molecules (VCAM, ICAM, E-selectin)
Time frame: 1 month
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