Pharmacological Postconditioning to Reduce Infarct Size Following Primary PCI

• Status: Completed
• Trial end date: 2015-05-01
• Target enrollment: 0
• Participant gender: All

Summary

Both pre- and postconditioning seem to protect cardiomyocytes during reperfusion therapy. Investigations both ex vivo and in vivo suggest that a gut derived hormone, Glucagon-Like-Peptide-1 (GLP-1), is able to reduce reperfusioninjury after myocardial ischemia. Results from our own laboratory have shown a marked reduction in infarct size when rat hearts in a Langendorf preparation were exposed to the GLP-1 analogue, exendin-4. The investigators want to investigate to what extent this effect can be translated to humans in the setting of acute STEMI treated with primary PCI when evalutaed by cardiac magnetic resonance imaging.

• Phase: Phase 4
• Accepts Healthy Volunteers?: No

Details

• Lead Sponsor: Rigshospitalet, Denmark
• Collaborator: University Hospital, Gentofte, Copenhagen
• Treatments: Exenatide; Polystyrene sulfonic acid

Criteria

Inclusion Criteria:

• More than 18 years of age.

• STEMI less than 12 hours from onset of pain. STEMI defined as as ST-segment elevation in 2 contiguous electrocardiographic leads of >0.1 mV in V4 - V6 or limb leads II, III and aVF, or >0.2 mV in lead V1 - V3.

• TIMI 0-1 in infarct related artery.

• Oral and written informed consent.

Exclusion Criteria:

• Multivessel disease defined by one or more stenoses >70% in diameter in the non infarct related artery.

• Previous myocardial infarction.

• Stent trombosis.

• Previous CABG.

• Less than TIMI 2 following wiring and predilatation of the infarct related artery but prior to postconditioning or placebo treatment.

• Renal insufficiency (creatinin >200).

• Pregnancy or lactation.

• Diabetic ketoacidose eller hypoglycemia (plasma glukose < 2.5 mmol/l).

• Pancreatitis.