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Acute myocardial infarction (AMI) is an acute metabolic stress, as has been recognized for at least 40 years.1,2 Its components include a rapid rise in plasma catecholamines, plasma free fatty acids, and blood glucose within the first 1 to 2 hours of onset of symptoms.3 Recent attention has focused on the possible adverse effects of hyperglycemia,4 now thought to have adverse effects in its own right, such as formation of oxygen free radicals5 and consequent adverse inflammatory response.6,7 Therefore, the level A recommendation of the American Heart Association (AHA) Diabetes Committee is that glucose levels should be measured in all patients with suspected or confirmed acute coronary syndromes (ACS). There follows, perhaps with a little less conviction (level of evidence B), the proposal that intensive glucose control may be considered if plasma glucose is >180 mg/dL (10 mmol/L) or even if the degree of hyperglycemia is less (level C). The recommendation to use intravenous insulin is based on extrapolation from other patient populations in acute intensive care,8,9 and a wise call is made for further studies to define the best approach to glucose control in patients with ACS.See Circulation. 2008:117:1610–1619 These recommendations raise several challenges, each of which merits closer examination. This Editorial will argue the case for a broader view of the relationship between glucose metabolism and ACS, with particular analysis of the proposal that it is the high adrenergic mediated levels of free fatty acids (FFAs or nonesterified fatty acids [NEFAs]) that may be the major lethality of the general metabolic reaction of which glycemia is but a marker. Thus, there could be 2 apparently discordant metabolically based therapeutic strategies: (1) rectification of hyperglycemia, versus (2) amelioration of adverse effects of excessive circulating FFAs on the ischemic tissue as it undergoes …

Metabolic Management of Acute Myocardial Infarction Comes to the Fore and Extends Beyond Control of Hyperglycemia