Metabolic Response during Impending Myocardial Infarction

The immediate local metabolic response of the myocardium to acute regional ischemia is determined by an interaction of various influences. These include: (1) the extent of and the variability in reduction of blood flow; (2) the degree and persistence of hypoxia; and (3) the effects of local release of catecholamines, particularly in relation to loss of intracellular potassium. The subsequent metabolic response of the myocardium is partly dependent on the degree of impairment locally of normal myocardial metabolism and partly on the systemic reaction to increased catecholamine activity and hence on: (1) adipose tissue lipolysis; (2) hepatic and muscle glycogenolysis; (3) insulin suppression; and (4) growth hormone and cortisol activity. These determine the extent of the uptake from blood of FFA and glucose by the ischemic myocardium. There is increasing evidence that high arterial concentrations of FFA can depress myocardial performance by leading to ventricular arrhythmias and decreased contractility. This effect probably depends on a critical interaction between the local concentration of FFA, catecholamines, and hypoxia. Metabolic intervention in the management of heart attacks should accordingly be directed toward reducing mobilization of adipose tissue FFA and increasing myocardial glycolytic activity.