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Circulation. 1998;97:2278-2279

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(Circulation. 1998;97:2278-2279.)
© 1998 American Heart Association, Inc.


Correspondence

Glucose-Insulin-Potassium Therapy for Treatment of Acute Myocardial Infarction

Pertti Ebeling, MD; ; Veikko A. Koivisto, MD

Department of Medicine, Helsinki University Hospital, Helsinki, Finland

To the Editor:

The meta-analysis of Fath-Ordoubadi and Beatt1 suggests a beneficial role for glucose-insulin-potassium therapy for treatment of acute myocardial infarction in nondiabetic patients, a result in accordance with the recently reported beneficial effect in diabetic patients.2

Although the exact mechanisms behind the improvement of prognosis are unclear, we would like to stress the importance of reducing free fatty acids (FAs) as a myocardial fuel by insulin administration. Normally, FA oxidation and cardiac work are closely associated. In ischemic hearts, the proportion of energy produced from FAs increases. Kudo and coworkers3 induced global ischemia of 30 minutes followed by aerobic reperfusion of 60 minutes in isolated working rat hearts. Although cardiac work after reperfusion was reduced to only 16% of aerobic values, palmitate oxidation increased to 136%. The reduced cardiac efficiency in ischemia may depend on the excessive entrance of FAs into mitochondria, leading to uncoupling of mechanical function from FA oxidation. The same phenomenon is seen with medium-chain FAs with free entrance into mitochondria.4 Normally, the access of long-chain FAs, the great majority of FAs, into mitochondria is inhibited by malonyl-CoA through carnitine palmitoyl transferase I. In the work of Kudo et al,3 acetyl-CoA, substrate for malonyl-CoA, and malonyl-CoA levels were reduced in concert after ischemia. However, malonyl-CoA levels were much further reduced during aerobic reperfusion, although acetyl-CoA levels did not decrease further. The level of malonyl-CoA after reperfusion was only {approx}1% of aerobic level. Thus, FAs probably had almost uncontrolled access into mitochondria. The activity of acetyl . . . [Full Text of this Article]

Farzin Fath-Ordoubadi, BSc MB BCh MRCP; ; Kevin J. Beatt, PhD, FESC, FACC

Hammersmith Hospital, London, UK