Cardiac Metabolic and Hemodynamic Effects of Insulin in Patients With Coronary Artery Disease

  1. Per Henningsen
  1. Department of Cardiology Skejby Sygehus, North Århus, Denmark
  1. Address correspondence and reprint requests to Dr. Anne Thomassen, Department of Cardiology, Skejby Sygehus, 8200 Århus N, Denmark.

Abstract

To assess the effects of insulin in stable coronary artery disease (CAD), 2 U i.v. insulin was given to 9 control and 10 CAD patients during coronary sinus catheterization. Hemodynamic and metabolic data were obtained before and for 90 min after insulin injection. Insulin induced no changes in heart rate, mean aortic pressure, rate-pressure product, coronary sinus flow, or coronary resistance. Metabolic changes were similar in both groups and included 1) 30% decrease of arterial glucose (P < .001) and 3-fold increase of myocardial glucose uptake (P < .001), 2) 1.5- to 2.5-fold elevation of arterial lactate (P < .001) and myocardial lactate usage (P < .001), respectively, 3) 50–70% suppression of arterial levels (P < .001) and myocardial uptake of free fatty acids (P < .01), and 4) 10% reduction of myocardial net oxygen consumption (P < .05). Myocardial citrate efflux increased in the CAD patients (P < .05), whereas alanine release rose only in control patients (P < .01), suggesting that glucose enters glycogen production in the CAD patients and pyruvate production in the control patients to a high degree. Myocardial glutamate uptake remained unchanged. In conclusion, insulin sensitivity was not altered in CAD. The insulin-induced shift from myocardial free fatty acid to carbohydrate usage may be beneficial to the ischemie heart by increasing glycogen stores, saving oxygen, and inhibiting an excess free-fatty acid concentration, which may be toxic during ischemia.

  • Received October 10, 1988.
  • Revision received May 3, 1989.
  • Accepted May 3, 1989.
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