What is the clinical evidence from this study?

Study design: RCT. Population: ST-segment-elevation myocardial infarction (n=58). Intervention: Exenatide vs. Placebo (saline). Primary outcome: Absolute mass of delayed hyperenhancement on cardiac magnetic resonance at 1 month (p=<0.01).

July 19, 2013Open Access

Cardioprotective Effects of Exenatide in Patients With ST-Segment–Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Q: What are the key findings of this study?

Adjunctive exenatide significantly reduced infarct size on CMR at 1 month compared with placebo in STEMI patients undergoing primary PCI (12.8±11.7 vs 26.4±11.6 g; P<0.01).

Key Result

Adjunctive exenatide significantly reduced infarct size on CMR at 1 month compared with placebo in STEMI patients undergoing primary PCI (12.8±11.7 vs 26.4±11.6 g; P<0.01).

Study Design

Type

RCT (n=58)

Randomization

Randomly assigned

Structured PICO

Does exenatide reduce infarct size in patients with ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention?

Population

58 patients with ST-segment-elevation myocardial infarction and TIMI flow 0 undergoing primary percutaneous coronary intervention, followed for 6 months.

Intervention

Exenatide administered subcutaneously at the time of primary percutaneous coronary intervention.

Comparator

Placebo (saline) administered subcutaneously.

Outcome

Infarct size assessed by measuring the release of creatine kinase-MB and troponin I during 72 hours and by performing cardiac magnetic resonance imaging (absolute mass of delayed hyperenhancement) at 1 month after infarction.surrogate

Adjunctive subcutaneous exenatide administered at the time of primary PCI significantly reduces infarct size and improves subclinical left ventricular function in patients with STEMI.

Main Result

Absolute Event Rate: 12.8% vs 26.4%

p-value: p=<0.01

Abstract

OBJECTIVE: Experimental evidence suggests that exenatide, a glucagon-like peptide 1 receptor analogue, has significant cardiovascular protective effects in various conditions. We examined whether routine use of exenatide at the time of primary percutaneous coronary intervention would reduce infarct size in patients with ST-segment-elevation myocardial infarction. APPROACH AND RESULTS: Fifty-eight patients with ST-segment-elevation myocardial infarction and thrombolysis in myocardial infarction flow 0 were enrolled in the study and randomly assigned to receive either exenatide or placebo (saline) subcutaneously. Infarct size was assessed by measuring the release of creatine kinase-MB and troponin I during 72 hours and by performing cardiac magnetic resonance imaging at 1 month after infarction. Routine and speckle tracking echocardiography was performed at initial presentation and at 3 days and 6 months after primary percutaneous coronary intervention. The exenatide and control groups had similar results with respect to ischemia time, demographic characteristics, and ejection fraction before primary percutaneous coronary intervention. The releases of creatine kinase-MB and troponin I were significantly reduced in the exenatide group. In 58 patients evaluated with cardiac magnetic resonance, the absolute mass of delayed hyperenhancement was significantly reduced in the exenatide group as compared with the control group (12.8±11.7 versus 26.4±11.6 g; P<0.01). At 6 months, the exenatide group showed a significantly lower value of E/E' with improved strain parameters. No significant adverse effects of exenatide administration were detected. CONCLUSIONS: In patients with ST-segment-elevation myocardial infarction, adjunctive exenatide therapy with primary percutaneous coronary intervention was associated with reduction of infarct size and improvement of subclinical left ventricular function.