Glucose-insulin-potassium therapy in patients with ST-segment elevation myocardial infarction

Rafael Díaz1, Abhinav Goyal, Shamir R Mehta

  • 1Etudios Cardiologica Latin America, Rosario, Argentina.

JAMA
|November 29, 2007
PubMed

Insights

Glucose-insulin-potassium (GIK) infusion showed no benefit for ST-segment elevation myocardial infarction (STEMI) patients and may increase early harm. GIK therapy is not recommended due to potential risks of hyperglycemia, hyperkalemia, and fluid overload.

Area of Science:

  • Cardiology
  • Critical Care Medicine
  • Metabolic Research

Background:

  • The clinical utility of glucose-insulin-potassium (GIK) infusion in ST-segment elevation myocardial infarction (STEMI) remains uncertain, with conflicting results from previous studies.
  • While some smaller trials suggested potential benefits, a large trial (CREATE-ECLA) found no effect on 30-day mortality in over 20,000 STEMI patients.

Purpose of the Study:

  • To investigate the association between GIK infusion therapy and patient outcomes at 30 days and 6 months following STEMI.
  • To analyze pooled data from multiple large-scale randomized controlled trials to provide a comprehensive assessment of GIK therapy in STEMI.

Main Methods:

  • Primary analysis of the OASIS-6 GIK randomized controlled trial (2748 patients) and prespecified analyses combining data from OASIS-6 and CREATE-ECLA (22,943 patients).
  • Subgroup analyses examined the impact of GIK initiation timing on outcomes.
  • Post hoc analyses explored potential early harm associated with GIK, focusing on glucose levels, potassium levels, and net fluid gain.

Main Results:

  • At 6 months in the OASIS-6 trial, GIK infusion showed no significant difference in mortality, heart failure, or the composite of death or heart failure compared to control.
  • Combined analysis of OASIS-6 and CREATE-ECLA revealed a statistically significant increase in 3-day mortality with GIK infusion (HR, 1.13; P = .03), which disappeared by 30 days.
  • GIK therapy increased glucose, potassium, and net fluid gain, all of which were independently associated with increased mortality; adjusting for these factors eliminated the early mortality benefit observed with GIK.

Conclusions:

  • GIK infusion therapy offers no clinical benefit for patients with STEMI and may be associated with early harm.
  • Future research on metabolic modulation in STEMI should consider avoiding or carefully managing infusion-related hyperglycemia, hyperkalemia, and net fluid gain.
Abstract

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