Optimal dosage of insulin and glucose in glucose-insulin-potassium treatment of acute myocardial infarction remains to Be established

Glucose-Insulin-Potassium Treatment of Acute Myocardial Infarction Remains to Be Established To the Editor: The dosage of insulin and glucose plays an important role for the efficacy of GIK (glucose-insulin-potassium) treatment. Until the ECLA study, only 4 trials in acute myocardial infarction (AMI) had used the GIK therapy required to achieve adequate suppression of plasma free fatty acids (FFAs).1 Pooled data from these trials demonstrated a 48% reduction in mortality. In the ECLA study, a significant survival advantage relative to the control group was only found in the “high-dose GIK group.”2 In spite of these encouraging results, we do not yet know the optimal dosage of insulin and glucose in AMI. To establish appropriate metabolic interventions, these should preferably be evaluated in the relevant clinical settings. Surprisingly little is known about the metabolic consequences of myocardial infarction in humans or the impact of metabolic interventions in this setting. In stable coronary artery disease, an infusion of 30 g of glucose, 50 IU of regular insulin, and 80 mmol of KCl per liter at 1.5 mL/kg body weight reduced myocardial FFA uptake and myocardial oxygen demand, whereas the uptake of glucose and lactate increased.3 In AMI, it was demonstrated that this regimen reduced the level of plasma FFAs substantially.4 However, its impact on myocardial metabolism in this setting remains obscure. The neuroendocrine stress response, for instance, may be expected to influence myocardial metabolism and attenuate the effect of GIK due to insulin resistance. In coronary surgery, where systematic studies on GIK and its effects on systemic and myocardial metabolism have been done by Dr Rolf Ekroth and colleagues at Sahlgrenska University Hospital in Göteborg, Sweden, it has been shown that insulin resistance can be severe early after the operation. Furthermore, substantially higher doses of insulin are required to achieve full metabolic effects than to achieve suppression of plasma FFAs.5 Hence, before large-scale prospective, randomized studies on GIK in AMI are undertaken, further studies of myocardial metabolism in AMI and the impact of different GIK regimens may be advisable.