ACCEL-LOADING-ACS Study

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.

Inclusion criteria

• at least 18 years of age
• Non-ST-elevation ACS patients undergoing PCI within 48 hours after hospitalization

Exclusion criteria

• ST segment elevation acute myocardial infarction
• NSTE ACS with high-risk features warranting emergency coronary angiography
• Oral anticoagulation therapy with warfarin
• Use of pre-procedural glycoprotein IIb/IIIa inhibitor
• Contraindication to antiplatelet therapy
• AST or ALT ≥ 3 times upper normal
• Left ventricular ejection fraction < 30%
• WBC < 3,000/mm3, platelet < 100,000/mm3
• Creatinine ≥ 3 mg/dl
• stroke within 3 months