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

The effects on haemodynamics and infarct size (measured by total creatine kinase release) of intravenous infusions of normal saline, glucose, or glucose-insulin-potassium were studied in 36 patients with transmural acute myocardial infarction qf less than 12 hours' duration. In 12 patients, 2 ml/kg 50 per cent glucose (5.55 mmol/kg) was given over 10 minutes with 0 4 unit/kg soluble insulin 5 minutes later, followed by an infusion of 1-5 ml/kg per hr of 50 per cent glucose (4.2 mmol/kg per hr) containing 0 3 unit/kg insulin and 0-15 mmol/kg potassium chloride. Similar volumes of 50 per cent 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 individualised figures for the enzyme degradation rate. Saline infusion had no significant effect on card.ovascular haemodynamics. Glucose did not affect heart rate, but increased mean arterial pressure and pulmonary artery diastolic pressure by 18 per cent (P<0-001) and 42 per cent (P<0-001) at 30 minutes and by 14 per cent (P<0 005) and 25 per cent (P<0 005) at 60 minutes after infusion, respectively. Glucose-insulin-potassium 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 minutes but not at 60 minutes. Glucose increased cardiac index 22 per cent (P<0 05) at 60 minutes; glucose-insulin-potassium increased cardiac index by 26 per cent (P1<0 005) at 30 minutes and by 22 per cent (P<0 001) at 60 minutes. There was no effect on systemic vascular resistance, but glucose and glucose-insulinpotassium enhanced left ventricular stroke work index by 17 per cent (P<0 02) and 25 per cent (P<0-02) at 30 minutes and by 27 per cent (P<0-02) and 22 per cent (P<0 005) at 60 minutes, respectively. The degree of improvement in haemodynamic functions induced by glucose and glucose-insulin-potassium were comparable. Though the data are limited, these changes were not associated with afavourable trend in enzyme release. Furthermore, in the glucose-insulin-potassium group, one patient died and another was successfully resuscitatedfrom cardiac arrest; 2 patients died in the glucose group, while no serious complications occurred among patients in the saline group. It was concluded that the improvement in haemodynamic functions produced by glucose and glucoseinsulin-potassium infusions in uncomplicated myocardial infarcts was not associated with an obvious beneficial effect on clinical status and infarct size assessed by enzyme release. Continuation of the trial was, therefore, not ethically justifiable.