This paper investigates the metabolic changes, including increased catabolism, that occur following acute myocardial infarction in the absence of shock.
Highlights post-MI catabolism without shock; leaves open whether targeted interventions alter outcomes.
IT IS well known that a disturbance of carbohydrate metabolism characterized by hyperglycemia and, at times, glycosuria may occur after myocardial infarction. Less generally recognized is the appearance of creatinuria in patients with the latter disorder.1These phenomena suggest the occurrence of changes in metabolism after myocardial infarction which resemble those described in other conditions of stress or damage, such as trauma,2burns,3exposure to cold4and infection.5Indeed, a recent study by Davidson and others5brecords the occurrence of striking changes in intermediary metabolism in a patient in shock after myocardial infarction. The last-named authors5bstressed the role of shock as the factor responsible for the changes observed, but in view of the fact that similar changes have been described in patients not in shock with infection or after trauma,6it seemed important to study patients with myocardial infarction who were not in a state
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M. D. Altschule (1947) studied this question.
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