Effects of glucose and glucose-insulin-potassium on haemodynamics and enzyme release after acute myocardial infarction.

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Abstract
The effects on hemodynamics and infarct size (measured by total creatine kinase release) of i.v. infusions of normal saline, glucose, or glucose-insulin-K were studied in 36 patients with transmural acute myocardial infarction of less than 12 h duration. In 12 patients, 2 ml/kg 50% glucose (5.55 mmol/kg) was given over 10 min with 0.4 unit/kg soluble insulin 5 min later, followed by an infusion of 1.5 ml/kg per h of 50% glucose (4.2 mmol/kg per h) containing 0.3 unit/kg insulin and 0.15 mmol/kg KCL. Similar volumes of 50% glucose alone or normal saline alone were administered to 9 and 15 patients, respectively. Cardiac output and right heart pressures were measured in 28 patients by Swann-Ganz thermodilution catheter, and arterial pressure by an indwelling plastic cannula. Calculation of total enzyme release from serial creatine kinase measurements was made using individualized figures for the enzyme degradation rate. Saline infusion had no significant effect on cardiovascular hemodynamics. Glucose did not affect heart rate, but increased mean arterial pressure and pulmonary artery diastolic pressure by 18% (P < 0.001) and 42% (P < 0.001) at 30 min and by 14% (P < 0.005) and 25% (P < 0.005) at 60 min after infusion, respectively. Glucose-insulin-K increased heart rate (+ 13%; P < 0.05), mean arterial pressure (+ 15%; P < 0.01), and pulmonary artery diastolic pressure (+ 27%; P < 0.005) at 30 min but not at 60 min. Glucose increased cardiac index 22% (P < 0.05) at 60 min; glucose-insulin-K increased cardiac index by 26% (P < 0.005) at 30 min and by 22% (P < 0.001) at 60 min. There was no effect on systemic vascular resistance, but glucose and glucose-insulin-K enhanced left ventricular stroke work index by 17% (P < 0.02) and 25% (P < 0.02) at 30 min and by 27% (P < 0.02) and 22% (P < 0.005) at 60 min, respectively. The degree of improvement in hemodynamic functions induced by glucose and glucose-insulin-K were comparable. Though the data are limited, these changes were not associated with a favorable trend in enzyme release. In the glucose-insulin-K group, 1 patient died and another was successfully resuscitated from cardiac arrest; 2 patients died in the glucose group, while no serious complications occurred among patients in the saline group. The improvement in hemodynamic functions produced by glucose and glucose-insulin-K infusions in uncomplicated myocardial infarcts appeared not to be associated with an obvious beneficial effect on clinical status and infarct size assessed by enzyme release. Continuation of the trial was not ethically justifiable.