The investigators planned to evaluate the effects of liraglutide on no-reflow in patients with acute ST-segment elevation myocardial infarction (STEMI).
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.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
DOUBLE
Enrollment
190
Liraglutide were taken 30 min before PCI.
Placebo were taken 30 min before PCI.
PLA General Hospital
Beijing, Beijing Municipality, China
RECRUITINGa change in the prevalence of no-reflow
The primary efficacy variable was the prevalence of no-reflow assessed immediately post procedure.
Time frame: immediately after PCI
a change in troponin T
Secondary efficacy variable was troponin T level.
Time frame: immediately after PCI, at 1,3,5 days after PCI
a change in high-sensitivity C-reactive protein (hsCRP)
Secondary efficacy variable was high-sensitivity C-reactive protein level.
Time frame: immediately after PCI, at 1,3,5 days after PCI
a change in superoxide dismutase (SOD)
Secondary efficacy variable was superoxide dismutase level.
Time frame: immediately after PCI, at 1,3,5 days after PCI
This platform is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional.