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The target population of this interventional study was STEMI patients. Primary discussion: Early rhBNP reduces microcirculation obstruction in STEMI patients undergoing primary PCI
Direct percutaneous coronary intervention is the preferred reperfusion strategy for acute ST-segment elevation myocardial infarction. During the opening of infarct-related vessels, 5%-50% of patients showed slow flow or no reflow and other coronary microcirculation dysfunction, which aggravated myocardial injury and increased the incidence and mortality of heart failure. Studies have shown that recombinant human brain natriuretic peptide (rhBNP) can reduce reperfusion injury and reduce myocardial infarction area CMD. Prolonged ischemia leads to rapid depletion of intracellular ATP and tissue metabolic acidosis. Blood flow irrigation during reperfusion leads to decreased levels of ATP precursors, calcium overload in mitochondria, release of a large number of inflammatory factors and oxygen free radicals, which can lead to injury or death of myocardial and endothelial cells. rhBNP can enhance the activity of antioxidant enzymes, reduce the irreversible oxidative damage caused by free radicals to myocardium, reduce the myocardial infarction area during ischemia reperfusion, and may reduce the reperfusion injury and protect the viable myocardium.
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| Label | Type | Description | Intervention Names |
|---|---|---|---|
| Experimental Group 1 | Experimental | The experimental group was given neoptin within 3h after PCI for 72 hours (first at 1.5μg /kg intravenous load, then at 0.015μg /kg/min). |
|
| Control Gruop | No Intervention | The experimental group was given an intravenous infusion of the same amount of normal saline |
| Name | Type | Description | Arm Group Labels | Other Names |
|---|---|---|---|---|
| recombinant human B-type natriuretic peptide | Drug | The recombinant human B-type natriuretic peptide produces physiological effects by imitating endogenous B-type natriuretic peptide |
| Measure | Description | Time Frame |
|---|---|---|
| MVO/LV(%) | Microvascular obstruction assessed by magnetic resonance imaging | 3-14 days after PPCI |
| Measure | Description | Time Frame |
|---|---|---|
| LGE/LV(%) | Cardiac magnetic resonance imaging | 3-14 days and 90±7 days after PPCI |
| IMH | Intramuscular hemorrhageCardiac assessed by magnetic resonance imaging |
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Inclusion Criteria:
Exclusion Criteria:
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| Name | Role | Phone | Extension | |
|---|---|---|---|---|
| Quan Guo | Contact | +8615670510031 | xinyiguoquan@163.com |
| Name | Affiliation | Role |
|---|---|---|
| Muwei Li, MD | Fuwai central China cardiovascular hospotial | Study Chair |
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| ID | Term |
|---|---|
| D000072657 | ST Elevation Myocardial Infarction |
| ID | Term |
|---|---|
| D009203 | Myocardial Infarction |
| D017202 | Myocardial Ischemia |
| D006331 | Heart Diseases |
| D002318 | Cardiovascular Diseases |
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|
| 3-14 days after PPCI |
| MVO/LV(%) | Microvascular obstruction assessed by magnetic resonance imaging | 30±7 days after PPCI |
| LVEDV(ml) | Assessed by magnetic resonance imaging | 3-14 days and 90±7 days after PPCI |
| LVESV(ml) | Assessed by magnetic resonance imaging | 3-14 days and 90±7 days after PPCI |
| Troponin (highest value) | Troponin (highest value) | 3-14 days after PPCI |
| MACCEs | Major Adverse Cardiac and Cerebrovascular event:Death, nonfatal myocardial infarction, heart failure, revascularization, stroke | 7days,30days,3months,6 months |
| D014652 |
| Vascular Diseases |
| D007238 | Infarction |
| D007511 | Ischemia |
| D010335 | Pathologic Processes |
| D013568 | Pathological Conditions, Signs and Symptoms |
| D009336 | Necrosis |