EDITORIALS

Metabolic Changes in Myocardial infarction RICHARD J. BING, MD, FACC Pasadena,

California

Efforts to study cardiac metabolism have focused on matters of physiologic and biochemical interest; little attention has been paid to clinical applicability. At the outset, concern was with the nutrition of the heart, as first studied in the perfused cold-blooded animal and finally in the human heart in situ.’ This phase was followed by investigations into the mechanism of coupling between excitation and contraction in heart muscle, processes related to calcium binding and uptake, and studies on the nature of contractile proteins. In addition, changes in biochemical pathways in myocardial infarction were defined and morphologic correlations accompanying the repair of myocardial infarction were described.” During these phases, the clinician’s interest in cardiac metabolism has been peripheral, although the fundamental importance of these studies to the clinical investigator must have been obvious. They concern the nature of disturbances underlying myocardial failure, the morphology and biochemistry of heart muscle exposed to sudden ischemia, and the development and progression and healing of a myocardial infarcti0n.s The knowledge gained has been valuable, but has failed to influence clinical thinking even though evidence has been presented showing that it is possible to increase the rate of healing of a myocardial infarction with growth hormones, catabolic steroids, ascorbic acid or insulin.* From these fundamental bases, Opie, in an article in this issue of the Journal,” has taken a further step in relating fundamental studies on cardiac metabolism to the clinical course of patients with myocardial infarction. From a discussion of the metabolism of free fatty acids and their still doubtful relation to arrhythmias and myocardial infarction, he digresses to a discussion of the interaction between free fatty acids and catecholamines, the cellular effects of free fatty acids and the therapeutic use of glucose in heart

disease. The article would have been more complete had he included observations on the link between protein synthesis, the effect of insulin, growth hormone and the repair of infarcted tissue. He stresses the concepts of Sodi-Pallares, primarily as they pertain to the prevention of cellular potassium loss. As indicated, more subtle effects of glucose-insulin-potassium mixture have been described in relating the action of insulin on protein synthesis in the infarcted area.’ Unfortunately, in man this effect cannot be verified and in animals they necessitate difficult biochemical procedures such as the incorporation of labeled amino acids into proteins. This effect of glucose-insulin-potassium precedes by a considerable time span the other more rapid actions of glucose such as the provision of anaerobic energy to the ischemit tissue, the inhibition of lipolysis, the increase in plasma volume or the effect on the tissue content of glycogen, lactate and high energy phosphate. I believe that the main contribution of Opie’s article lies in an appraisal of the difficulties in applying results obtained “at the bench” to “the bedside.” Opie has given us a scholarly discussion of the physiologic and biochemical mechanisms underlying myocardial infarction, but we must be aware that a valid translation of these results into therapy are still speculative: No Rosetta stone has yet been found. Herein lies the frustration of all of us interested in cardiac metabolism who have labored in the laboratories and have tried to apply our results to the clinic. Only too often has pure clinical judgment at the bedside alone preceded any application of fundamental scientific principles. Yet, we must continue to try to relate our academic data to the clinical situation, and eventually the stones of the mosaic may fall into place and reveal a valid and useful picture. Dr. Opie’s article is a step in this direction.

From the Department of Medicine, University of Southern California and the Department of Intramural Medicine and Experimental Cardiology, Huntington Memorial Hospital, Pasadena, Calif. Address for reprints: Richard J. Bing, MD, Department of Intramural Medicine and Experimental Cardiology, Huntington Memorial Hospital. 100 Congress St., Pasadena, Calif. 91105.

1. Bfng RJ: Cardiac metabolism. Physiol Rev 45171-213, 1965 2. Bin9 RJ: Reparative processes in heart muscle following myocardial infarction. Cardiology 56:314-324, 1971 3. Opie LH: Metabolism of free fatty acids, glucose and catecholamines in acute myocardial infarction. Relation to myocardial ischemia and infarct size. Am J Cardiol 36:938-953, 1975

974

December 1975

The American Journal of CARDIOLOGY

References

Volume 36

Editorial: Metabolic changes in myocardial infarction.

EDITORIALS Metabolic Changes in Myocardial infarction RICHARD J. BING, MD, FACC Pasadena, California Efforts to study cardiac metabolism have focus...
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