Effects of liraglutide on no-reflow in patients with acute ST-segment elevation myocardial infarction.

BACKGROUND: The 'no-reflow' phenomenon after a percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI) is a strong predictor of both short- and long-term mortality. Glucagon-like peptide-1 (GLP-1) exerts a cardioprotective effect during ischemia reperfusion injury. We planned to evaluate the effects of liraglutide on myocardial no-reflow after PCI for STEMI. METHODS: A total of 284 patients with STEMI undergoing PCI were enrolled in this study between September 2013 and March 2015. Of these, 210 patients were randomized 1:1 to receive either liraglutide or placebo 30 min before PCI (1.8 mg). RESULTS: The primary end point, the prevalence of no-reflow, was significantly lower in the liraglutide group than in the control group (5% vs. 15%, P=0.01). Administration of liraglutide was consistently identified as a significant determinant for no-reflow ratio. There was a significant decrease in serum high-sensitivity C-reactive protein levels at 6-hour reperfusion in the liraglutide group compared to the control group (0.87 ± 0.09 mg/dL vs. 0.96 ± 0.10mg/dL, P<0.001). During a 3-month follow-up period, no difference was observed in the incidence of major adverse cardiovascular event. CONCLUSIONS: Liraglutide may be associated with less no-reflow in STEMI, which should be confirmed by larger-scale trials.

Effects of liraglutide on left ventricular function in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

BACKGROUND: Several studies have shown that exenatide protects against ischemia-reperfusion injury and improves cardiac function in patients with acute ST-segment elevation myocardial infarction (STEMI). The effects of liraglutide, a glucagon-like peptide-1 analogue, on STEMI patients remain unclear. We planned to evaluate the effects of liraglutide on left ventricular function after primary percutaneous coronary intervention for STEMI. METHODS: A total of 92 patients were randomized 1:1 to receive either liraglutide or placebo for 7 days. Study treatment was commenced 30 minutes before intervention (1.8 mg) and maintained for 7 days after the procedure (0.6 mg for 2 days, 1.2 mg for 2 days, followed by 1.8 mg for 3 days). Eighty-five patients completed the trial. Transthoracic echocardiography was used to assess left ventricular function. RESULTS: At 3 months, the primary end point, a difference in change of left ventricular ejection fraction between the two groups was +4.1% (95% CI +1.1% to +6.9%) (P < .001). There was a tendency for a lower rate of no-reflow in liraglutide group that did not reach statistical significance (7% vs control group 15%, P = .20). Liraglutide could significantly improve stress hyperglycemia (P < .05). In addition, liraglutide elicited favorable changes in markers of inflammation and endothelial function. CONCLUSION: A short 7-day course of liraglutide in STEMI patients treated with primary percutaneous coronary intervention is associated with mild improvement in left ventricular ejection fraction at 3 months.