Open-label Study of Neuraminidase Inhibitor Treatment in STEMI Patients

Tongji Hospital382 enrolled

Overview

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.

Study Type

INTERVENTIONAL

Allocation

RANDOMIZED

Purpose

TREATMENT

Masking

NONE

Enrollment

382

Conditions

ST Elevation Myocardial Infarction STEMI

Interventions

Eligibility

Sex: ALLMin age: 18 YearsMax age: 75 Years

Medical Language ↔ Plain English

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).

Outcomes

Primary Outcomes

Myocardial infarct size at 1 week

Myocardial infarct size at 1 week after acute myocardial infarction (quantified by Gadolinium-enhanced MRI).

Time frame: 1 week

Secondary Outcomes

Myocardial infarct size

Myocardial infarct size under the curve of creatine kinase-MB (CK-MB) and hypersensitive troponin I.

Time frame: 1 week

Myocardial infarct size based on culprit vessel with TIMI 0-1 blood flow

Evaluated by coronary angiography and CMR.

Time frame: 1 week

The proportion of viable myocardium and ratio of myocardial reperfusion

The proportion of viable myocardium and reperfusion was determined by the range of abnormal enhancement of gadolinium.

Time frame: 1 week

Composite end point at 1 week

A composite end point of cardiogenic shock, cardiac death, malignant arrhythmia, and resuscitated cardiac arrest (including ventricular fibrillation) at 1 week.

Time frame: 1 week

Myocardial infarct size at 3 month

Myocardial infarct size at 3 month after acute myocardial infarction (quantified by Gadolinium-enhanced MRI).

Time frame: 3 month

Composite end point at 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.

Time frame: 6 month

Open-label Study of Neuraminidase Inhibitor Treatment in STEMI Patients

Overview

Conditions

Interventions

Eligibility

Locations (1)

Outcomes

Primary Outcomes

Secondary Outcomes

Central Contacts