Targeting Glucose in Acute Myocardial Infarction

Abstract

Proinflammatory mechanisms may contribute to hyperglycemia-associated adverse outcomes in acute myocardial infarction (AMI) (1–3). Insulin exerts anti-inflammatory effects in ST elevation myocardial infarction and coronary artery bypass graft patients (4–6). Inflammation plays an important role in the pathogenesis of atherosclerosis and thrombosis (7,8). Thus, insulin infusion in AMI should be beneficial. However, glucose, insulin, and potassium (GIK) infusion was neutral in its benefit in the Clinical Trial of Metabolic Modulation in Acute Myocardial Infarction Treatment Evaluation–Estudios Cardiologicos Latinoamerica (CREATE-ECLA) study (9). The GIK regimen (fixed combination of 1 l of 25% dextrose with 50 units regular insulin and 80 meq/l potassium) used in CREATE-ECLA is known to lower serum free fatty acid concentrations (10) and to reduce mortality by 18% in AMI, as previously reviewed (11). However, the infusion of 30 g/h glucose without titration of glucose or insulin in CREATE-ECLA led to a significant increase in blood glucose concentrations. Mehta et al. suggested that the adverse effect of GIK-induced hyperglycemia may have neutralized any potential benefit of insulin in the GIK regimen. However, Mehta et al. did not comment on the magnitude of the potential contribution of hyperglycemia to neutralize benefits of GIK. Since admission hyperglycemia was predictive of mortality in AMI in CREATE-ECLA, we have estimated the potential effects of GIK-induced hyperglycemia on mortality in this study. Based on the admission blood …