To evaluate whether nicorandil as an adjunctive therapy for AMI reduces myocardial infarct size and improves regional wall motion
The benefits of percutaneous coronary intervention (PCI) in acute myocardial infarction (AMI) are limited by reperfusion injury. In animal models, nicorandil, a hybrid of an ATP-sensitive K+ (KATP) channel opener and nitrates, reduces infarct size, so the Japan-Working groups of acute myocardial Infarction for the reduction of Necrotic Damage by a K-ATP channel opener (J-WIND-KATP) designed a prospective, randomized, multicenter study to evaluate whether nicorandil reduces myocardial infarct size and improves regional wall motion when used as an adjunctive therapy for AMI. Twenty-six hospitals in Japan are participating in the J-WIND-KATP study. Patients with AMI who are candidates for PCI are randomly allocated to receive either intravenous nicorandil or placebo. The primary end-points are (1) estimated infarct size and (2) left ventricular function. Single nucleotide polymorphisms (SNPs) that may be associated with the function of KATP-channel and the susceptibility of AMI to the drug will be examined. Furthermore, a data mining method will be used to design the optimal combined therapy for post-myocardial infarction (MI) patients. It is intended that J-WIND-KATP will provide important data on the effects of nicorandil as an adjunct to PCI for AMI and that the SNPs information that will open the field of tailor-made therapy. The optimal therapeutic drug combination will also be determined for post-MI patients.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Enrollment
600
(0∙067 mg/kg as a bolus, followed by 1∙67 μg/kg per min as a 24-h continuous intravenous infusion
Control
National Cardiovascular Center
Suita, Osaka, Japan
estimated infarct size
Time frame: 72hrs
left ventricular function (left ventricular ejection fraction and end-diastolic volume) and regional wall motion
Time frame: 2-8weeks and 6-12months
survival rate
Time frame: 2.7years (median follow-up)
cardiovascular events (ie, cardiac death, nonfatal re-infarction, re-hospitalization because of cardiac disease, revascularization)
Time frame: 2.7years (median follow-up)
reperfusion injury (ie, malignant ventricular arrhythmia during reperfusion periods, re-elevation of ST-segment, worsening of chest pain)
Time frame: 24hrs
the association of SNPs of ANP-related genes with response to ANP treatment
Time frame: 2.7years (median follow-up)
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