ST Elevation Myocardial Infarction, STEMI
Conditions
Brief summary
Neuraminidase-1 can cause the removal of terminal sialic acid residues from the cell surface or serum sialyloconjugates. The level of Neu5Ac was positively related to the activity of neuraminidase-1. Elevation of Neu5Ac was observed in myocardial ischemia animal model, as well as patients with coronary artery disease. It is interesting to note that Neu5Ac and its regulatory enzyme neuraminidase-1 seem to play a key role in triggering myocardial ischemic injury. Oseltamivir, a structural mimic of sialic acid, was widely used as anti-influenza drug. It suppressed neuraminidase-1 activity in the heart. Targeting neuraminidase-1 may represent a new therapeutic intervention for coronary artery disease. This project seeks to identify whether neuraminidase inhibitor (Oseltamivir) treatment could decrease the myocardial infarct size in STEMI patients and improve clinical outcomes.
Interventions
Treatment group vs. Control group
Sponsors
Tongji Hospital
Study design
Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
TREATMENT
Masking
NONE
Eligibility
Sex/Gender
ALL
Age
18 Years to 75 Years
Healthy volunteers
No
Inclusion criteria
1. Between the ages of 18 and 75, regardless of gender; 2. STEMI should be diagnosed by two attending physicians or above, including history, clinical symptoms and signs; 3. Participate voluntarily and sign informed consent, and can be followed up for more than one month.
Exclusion criteria
1. Allergic to oseltamivir; 2. Creatinine clearance rate less than 60%; 3. Severe liver insufficiency; 4. Female patients who have or plan to become pregnant; 5. Life expectancy less than one year; 6. Patients refused to comply with the requirements of this study; 7. According to the discretion of investigator, the patient was unable to complete the study or comply with the requirements of the study (for administrative or other reasons).
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Myocardial infarct size at 1 week | 1 week | Myocardial infarct size at 1 week after acute myocardial infarction (quantified by Gadolinium-enhanced MRI). |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Myocardial infarct size based on culprit vessel with TIMI 0-1 blood flow | 1 week | Evaluated by coronary angiography and CMR. |
| The proportion of viable myocardium and ratio of myocardial reperfusion | 1 week | The proportion of viable myocardium and reperfusion was determined by the range of abnormal enhancement of gadolinium. |
| Myocardial infarct size | 1 week | Myocardial infarct size under the curve of creatine kinase-MB (CK-MB) and hypersensitive troponin I. |
| Myocardial infarct size at 3 month | 3 month | Myocardial infarct size at 3 month after acute myocardial infarction (quantified by Gadolinium-enhanced MRI). |
| Composite end point at 6 month | 6 month | Composite end point at 6 month, including all-cause death, reinfarction, heart failure after myocardial infarction, and rehospitalization of unstable angina at 6 month. |
| Composite end point at 1 week | 1 week | A composite end point of cardiogenic shock, cardiac death, malignant arrhythmia, and resuscitated cardiac arrest (including ventricular fibrillation) at 1 week. |
Countries
China
Contacts
Primary ContactLuyun Wang, M.D., Ph.D
Backup ContactJiangang Jiang, M.D., Ph.D
Outcome results
None listed