Impact of acute hyperglycemia on myocardial infarct size, area at risk and salvage in patients with ST elevation myocardial infarction and the association with exenatide treatment – results from a randomized study

  1. Thomas Engstrøm, MD, PhD, DMSc*
  1. *Department of Cardiology, Rigshospitalet, Copenhagen University Hospital, Denmark
  2. Department of Cardiology, Skejby, Aarhus University Hospital, Denmark
  3. Department of Biomedical Sciences and The Danish National Foundation Research Centre for Heart Arrhythmia, Copenhagen University, Denmark
  1. Address for correspondence: Jacob Thomsen Lønborg, E-mail: Jacoblonborg{at}


Hyperglycemia upon admission in ST-segment elevation myocardial infarction (STEMI) patients occurs frequently and is associated with adverse outcome. It is however unsettled whether elevated blood glucose is the cause or consequence of increased myocardial damage. In addition, whether the cardioprotective effect of exenatide, a glucose-lowering drug, is dependent on hyperglycemia remains unknown. The objectives of this sub-study were to evaluate the association between hyperglycemia and infarct size, myocardial salvage and area-at-risk, and to assess the interaction between exenatide and hyperglycemia. A total of 210 STEMI patients were randomized to receive intravenous exenatide or placebo before percutaneous coronary intervention. Hyperglycemia was associated with larger area-at-risk and infarct size compared to patients with normoglycemia, but the salvage index and infarct size adjusting for area-at-risk did not differ between the groups. Treatment with exenatide resulted in increased salvage index both among patients with normoglycemia and hyperglycemia. Thus, we conclude that the association between hyperglycemia upon admission and infarct size in STEMI patients is a consequence of a larger myocardial area-at-risk but not on a reduction in myocardial salvage. Also, cardioprotection by exenatide treatment is independent of admission glucose levels. Thus, hyperglycemia does not influence the effect of the reperfusion treatment but rather represents a surrogate marker for the severity of myocardium at risk and injury.

  • Received December 5, 2013.
  • Accepted February 26, 2014.

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