Metabolic Response during Impending Myocardial Infarction

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Abstract
Both glucose and free fatty acids (FFA) are major fuels for the normally oxygenated heart with the dominant contribution being derived from glucose in the resting, fed state and FFA in the resting, fasted state. In anoxia, all energy must be produced anaerobically from glycogen or glucose. Anoxia by itself accelerates glycolysis, but further increases may follow an increased circulating glucose concentration and the addition of insulin. Even maximal rates of anaerobic glycolysis, achieved at high coronary flow rates, can only sustain the energy needs of the K+-arrested heart but not of the working heart. FFA cannot be utilized for energy in anoxia and may accumulate intracellularly as triglyceride or FFA. From these and other animal data have grown the concepts that glucose is "good" for the survival of the ischemic heart, and that FFA is "bad." However, glucose-fatty acid interaction has not been well studied in the infarcting, ischemic myocardium. While a "toxic" effect of FFA has been shown in many experimental models, there are other reports of increased FFA concentrations having no harmful effect or even a beneficial effect on the infarcting myocardium. The possible benefits of administration of glucose (with insulin) to patients with acute myocardial infarction could only be assessed by a controlled therapeutic trial.