- Email: [email protected]
Provision of carbohydrate in acute MI
Letters
Provision
to the Editor
of carbohydrate
in acute
MI
To the Editor: The article by Warren and associates (AM. HEART J. 95:130, 1978) about diet in the Coronary Care Unit, touches on an important practical point. He agrees that there should be no restriction of carbohydrate, because of the possibility that glucose is the beneficial fuel for the acutely ischemic myocardium, but he does not refer to our study,’ showing that provision of carbohydrate in the diet can bring down free fatty acids in patients with acute myocardial infarction. Our more recent work’ has suggested that such effects of carbohydrate feeding are more likely to be evident in those patients less acutely ill. Whether such reductions of free fatty acid are beneficial to the patient still requires proof, but experimental data suggest that provision of carbohydrate and decreased circulating free fatty acid concentrations should be beneficial rather than harmful. Lionel H. Opie, M.D. MRC Ischaemic Heart Disease Research Unit Department of Medicine University of Cape Town and Groote Schuur Hospital Cape Town, South Africa REFERENCES
1.
2.
Opie, L. H., Bruyneel, K. J. J., and Kennelly, B. M.: Effects of early oral feeding on plasma free fatty acid concentrations in patients in a coronary care unit, Br. Heart J. 37:760, 1978. Tansey, M. J. B., Opie, L. H., and Kennelly, B. M.: The effects of oral sucrose and of estimated infarct size on plasma free fatty acids, plasma glucose and serum insulin in the early stages of acute myocardial infarction, Europ. J. Clin. Invest. (In press, 1979)
ciates” have themselves positively related infarct size to peak serum free fatty acid levels in 20 patients with acute myocardial infarction. A matter of less clarity, however, is the interaction between serum glucose, insulin, free fatty acids, and catecholamines, and its therapeutic implications. Generally, levels of all these substances are elevated in acute myocardial infarction.” Patients in shock (precisely those who have the lowest circulating insulin levels),‘” also have increased catecholamine release” with presumably secondary increases in free fatty acids.” The relative contributions of glucose underutilization, free-fatty-acid myocardial depression, or increased myocardial contractility and work secondary to catecholamine release cannot be judged at present. Thus, exactly how dietary carbohydrate “brings down” fatty acids is not known, but it is possible that increased myocardial performance might improve tissue perfusion, decrease catecholamine levels, and thereby inhibit lipolysis. Therapeutically, one is left with the options of (1) blocking catecholamine release or action pharmacologically, (2) blocking release of free fatty acids by such agents as nicotinic acid, or (3) supplying ischemic myocardium with a ready source of energy (glucose) which will be preferentially utilized and not depress performance. Until more elaborate maneuvers are proven to be of value, I shall opt for the latter. S. E. Warren, M.D. LT, MC, USNR Cardiology Branch Department of Internal Medicine Naval Regional Medical Center San Diego, Cal+ 92134 REFERENCES
1.
Reply To the Editor: In his letter Dr. Opie emphasizes two points: the favorable effects of glucose upon acutely ischemic myocardium, and the deleterious influence of free fatty acids-two phenomena which I heartily accept on experimental grounds. With myocardial cell hypoxia there occurs increased glucose transport into myocardium, increased glycogenolysis, and rapid myocardial glucose depletion as anaerobic heat is produced.’ The fact that the arteriovenous difference of glucose across ischemic myocardium reportedly is increased while that of free fatty acids is unchanged* also suggests preferential utilization of glucose as energy substrate. In the laboratory, increased provision of glucose is associated with enhanced myocardial performance during hyposia.3 The work of Nixon and colleagues’, 5 suggests further that patients with cardiogenic shock may respond to glucose infusions by increasing cardiac function. Conversely, free fatty acids in high concentration depress cardiac function in animals,” and their levels were shown to correlate positively with arrhythmias and mortality in patients with acute myocardial infarction.’ Opie and asso-
268
2.
3.
4.
5.
6.
7.
Schlant, R. C.: Metabolism of the Heart, in The Heart, ed. by J. W. Hurst et al., 3rd edition, New York, 1974, McGraw-Hill Book Company, Inc., pp. 115-128. Christakis, G., and Winston, M.: Nutritional therapy in acute myocardial infarction, J. Am. Diet. Assoc. 63:233. 1973. Weissler, A. M., Kruger, F. A., Baba, N., Scarpelli, D. G., Leighton, R. F.. and Gallimore. J. K.: Role of anaerobic metabolism in the preservation of functional capacity and structure of anoxic myocardium, J. Clin. Invest, 47:403, 1968. Nixon, P. G. F., Ikram, H., and Morton, S.: Cardiogenic shock treated with infusion of dextrose solution, AM. HEART J. 73:843, 1967. Nixon, P. G. F., Taylor, D. J. E., and Morton, S. D.: Left ventricular diastolic pressure in cardiogenic shock treated by dextrose infusion and adrenaline, Lancet 1:1230, 1968. Henderson, A. H., Craig, R. J., Gorlin, R., and Sonnenblick, E. H.: Free fatty acids and myocardial function in perfused rat hearts, Cardiovasc. Res. 4:466, 1970. Oliver, M. F., Kurien, V. A., and Greenwood, T. W.: Relation between serum free fatty acids and arrhythmias and death after acute myocardial infarction, Lancet 1:710,
8.
1968.
Opie, L. H., Tansey, M., and Kennelly, metabolic vicious circle in patients with
February,
1979,
B. M.: Proposed large myocardial
Vol.
97, No.
2
Provision
to the Editor
of carbohydrate
in acute
MI
To the Editor: The article by Warren and associates (AM. HEART J. 95:130, 1978) about diet in the Coronary Care Unit, touches on an important practical point. He agrees that there should be no restriction of carbohydrate, because of the possibility that glucose is the beneficial fuel for the acutely ischemic myocardium, but he does not refer to our study,’ showing that provision of carbohydrate in the diet can bring down free fatty acids in patients with acute myocardial infarction. Our more recent work’ has suggested that such effects of carbohydrate feeding are more likely to be evident in those patients less acutely ill. Whether such reductions of free fatty acid are beneficial to the patient still requires proof, but experimental data suggest that provision of carbohydrate and decreased circulating free fatty acid concentrations should be beneficial rather than harmful. Lionel H. Opie, M.D. MRC Ischaemic Heart Disease Research Unit Department of Medicine University of Cape Town and Groote Schuur Hospital Cape Town, South Africa REFERENCES
1.
2.
Opie, L. H., Bruyneel, K. J. J., and Kennelly, B. M.: Effects of early oral feeding on plasma free fatty acid concentrations in patients in a coronary care unit, Br. Heart J. 37:760, 1978. Tansey, M. J. B., Opie, L. H., and Kennelly, B. M.: The effects of oral sucrose and of estimated infarct size on plasma free fatty acids, plasma glucose and serum insulin in the early stages of acute myocardial infarction, Europ. J. Clin. Invest. (In press, 1979)
ciates” have themselves positively related infarct size to peak serum free fatty acid levels in 20 patients with acute myocardial infarction. A matter of less clarity, however, is the interaction between serum glucose, insulin, free fatty acids, and catecholamines, and its therapeutic implications. Generally, levels of all these substances are elevated in acute myocardial infarction.” Patients in shock (precisely those who have the lowest circulating insulin levels),‘” also have increased catecholamine release” with presumably secondary increases in free fatty acids.” The relative contributions of glucose underutilization, free-fatty-acid myocardial depression, or increased myocardial contractility and work secondary to catecholamine release cannot be judged at present. Thus, exactly how dietary carbohydrate “brings down” fatty acids is not known, but it is possible that increased myocardial performance might improve tissue perfusion, decrease catecholamine levels, and thereby inhibit lipolysis. Therapeutically, one is left with the options of (1) blocking catecholamine release or action pharmacologically, (2) blocking release of free fatty acids by such agents as nicotinic acid, or (3) supplying ischemic myocardium with a ready source of energy (glucose) which will be preferentially utilized and not depress performance. Until more elaborate maneuvers are proven to be of value, I shall opt for the latter. S. E. Warren, M.D. LT, MC, USNR Cardiology Branch Department of Internal Medicine Naval Regional Medical Center San Diego, Cal+ 92134 REFERENCES
1.
Reply To the Editor: In his letter Dr. Opie emphasizes two points: the favorable effects of glucose upon acutely ischemic myocardium, and the deleterious influence of free fatty acids-two phenomena which I heartily accept on experimental grounds. With myocardial cell hypoxia there occurs increased glucose transport into myocardium, increased glycogenolysis, and rapid myocardial glucose depletion as anaerobic heat is produced.’ The fact that the arteriovenous difference of glucose across ischemic myocardium reportedly is increased while that of free fatty acids is unchanged* also suggests preferential utilization of glucose as energy substrate. In the laboratory, increased provision of glucose is associated with enhanced myocardial performance during hyposia.3 The work of Nixon and colleagues’, 5 suggests further that patients with cardiogenic shock may respond to glucose infusions by increasing cardiac function. Conversely, free fatty acids in high concentration depress cardiac function in animals,” and their levels were shown to correlate positively with arrhythmias and mortality in patients with acute myocardial infarction.’ Opie and asso-
268
2.
3.
4.
5.
6.
7.
Schlant, R. C.: Metabolism of the Heart, in The Heart, ed. by J. W. Hurst et al., 3rd edition, New York, 1974, McGraw-Hill Book Company, Inc., pp. 115-128. Christakis, G., and Winston, M.: Nutritional therapy in acute myocardial infarction, J. Am. Diet. Assoc. 63:233. 1973. Weissler, A. M., Kruger, F. A., Baba, N., Scarpelli, D. G., Leighton, R. F.. and Gallimore. J. K.: Role of anaerobic metabolism in the preservation of functional capacity and structure of anoxic myocardium, J. Clin. Invest, 47:403, 1968. Nixon, P. G. F., Ikram, H., and Morton, S.: Cardiogenic shock treated with infusion of dextrose solution, AM. HEART J. 73:843, 1967. Nixon, P. G. F., Taylor, D. J. E., and Morton, S. D.: Left ventricular diastolic pressure in cardiogenic shock treated by dextrose infusion and adrenaline, Lancet 1:1230, 1968. Henderson, A. H., Craig, R. J., Gorlin, R., and Sonnenblick, E. H.: Free fatty acids and myocardial function in perfused rat hearts, Cardiovasc. Res. 4:466, 1970. Oliver, M. F., Kurien, V. A., and Greenwood, T. W.: Relation between serum free fatty acids and arrhythmias and death after acute myocardial infarction, Lancet 1:710,
8.
1968.
Opie, L. H., Tansey, M., and Kennelly, metabolic vicious circle in patients with
February,
1979,
B. M.: Proposed large myocardial
Vol.
97, No.
2