Acute ST-segment Elevation Myocardial Infarction
Conditions
Brief summary
The investigators planned to evaluate the effects of liraglutide on no-reflow in patients with acute ST-segment elevation myocardial infarction (STEMI).
Detailed description
Acute myocardial infarction (AMI) is a major cause of mortality and morbidity. Primary percutaneous coronary intervention (PCI) is currently the most effective treatment strategy for AMI. Brisk thrombolysis in myocardial infarction (TIMI) grade 3 flow immediately after PCI in patients with AMI is associated with improved clinical outcomes compared with lower flow grades. However, myocardial reperfusion is suboptimal in many patients, mostly because of the 'no-reflow' phenomenon. No-reflow is defined as suboptimal myocardial reperfusion in part of the coronary circulation without angiographic evidence of mechanical vessel obstruction. To date, however, very few drugs have been shown to reverse established no-reflow. Glucagon-like peptide-1 (GLP-1) is an incretin hormone that regulates plasma glucose, and GLP-1 analogues were recently introduced for the treatment of acute myocardial infarction. GLP-1 has antioxidant and anti-inflammatory properties, and may protect endothelial function. Experimental studies have also revealed that GLP-1 or its analogues protect against reperfusion injury in pigs. Exenatide, a GLP-1 analogue, was reported to reduce reperfusion injury in patients with ST-segment elevation myocardial infarction. Similarly, liraglutide was reported to reduce cardiac rupture and infarct size and improve cardiac output in normal and diabetic mice. To date, however, there is no clinical evidence for the effects of liraglutide on no-reflow in patients with AMI. Therefore, the aim of this study was to evaluate the effects of liraglutide pretreatment on myocardial no-reflow of prime PCI in patients with AMI.
Interventions
Liraglutide were taken 30 min before PCI.
Placebo were taken 30 min before PCI.
Sponsors
Study design
Eligibility
Inclusion criteria
Patients with ST-segment elevation myocardial infarction were eligible for the study.
Exclusion criteria
Patients were excluded for the following reasons: unconscious at presentation; had cardiogenic shock, hypoglycaemia, or diabetic ketoacidosis; had a history of myocardial infarction, stent thrombosis, or renal insufficiency; or had previously undergone coronary artery bypass surgery.
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| a change in the prevalence of no-reflow | immediately after PCI | The primary efficacy variable was the prevalence of no-reflow assessed immediately post procedure. |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| a change in troponin T | immediately after PCI, at 1,3,5 days after PCI | Secondary efficacy variable was troponin T level. |
| a change in high-sensitivity C-reactive protein (hsCRP) | immediately after PCI, at 1,3,5 days after PCI | Secondary efficacy variable was high-sensitivity C-reactive protein level. |
| a change in superoxide dismutase (SOD) | immediately after PCI, at 1,3,5 days after PCI | Secondary efficacy variable was superoxide dismutase level. |
Other
| Measure | Time frame | Description |
|---|---|---|
| differences in the incidences of treatment-emergent adverse events | immediately after PCI, at 1,3,5 days after PCI | Treatment-emergent adverse events (TEAEs): hypoglycaemia, pancreatitis, thyroid cancer |
Countries
China