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September 5, 2012

Glucose-Insulin-Potassium for Suspected Acute Myocardial Infarction—Reply

Author Affiliations

Letters Section Editor: Jody W. Zylke, MD, Senior Editor.

Author Affiliations: Institute for Clinical Research and Health Policy Studies, Division of Cardiology, Tufts Medical Center, Boston, Massachusetts (hselker@tuftsmedicalcenter.org).

JAMA. 2012;308(9):859-860. doi:10.1001/jama.2012.9771

In Reply: We agree with the interpretation of Dr Chaudhuri and colleagues about the beneficial effects seen with GIK in the Immediate Myocardial Metabolic Enhancement During Initial Assessment and Treatment in Emergency care (IMMEDIATE) Trial on cardiac arrest, acute mortality, and infarct size. We also agree that there remain undefined associations of hyperglycemia and mortality in the use of GIK. The association between hyperglycemia and mortality seen in previous GIK trials1,2 may just reflect the propensity for hyperglycemia among patients with diabetes, who also have higher mortality rates from AMI, rather than reflecting any influence of GIK. If GIK caused hyperglycemia, which in turn increased mortality, there would be increased mortality among those treated with GIK, especially among those with diabetes, who would have more hyperglycemia—and no such effect was found. The forest plot (eFigure) in our article showed an odds ratio (OR) for cardiac arrest or mortality with the use of GIK of 0.31 (95% CI, 0.10-0.99; P = .05) for patients with diabetes vs an OR of 0.56 (95% CI, 0.29-1.09; P = .09) for patients without diabetes, suggesting a positive, not negative, GIK effect.