Glucose-insulin-potassium (GIK) therapy addresses the metabolic changes of ischaemia secondary to acute myocardial infarction. These changes include elevated plasma free fatty acid concentration and glucose intolerance. A meta-analysis of trials from the pre-thrombolysis era showed a significant reduction in the number of deaths in the GIK group in comparison to placebo (16.1% vs. 21% respectively, p=0.004). High-dose GIK therapy was found to be of particular benefit.
Three randomised trials in the post-thrombolysis era have been published, with variable results. The DIGAMI study (in diabetics) and the ECLA pilot trial had positive results: in the latter there was a 60% reduction in in-hospital mortality in patients who received GIK therapy plus reperfusion. By contrast, the Pol-GIK trial was negative.
Outstanding questions include the usefulness of GIK therapy and beta blockade in the presence of thrombolysis or primary angioplasty. GIK therapy and beta blockade might act in complementary fashion to antagonise the metabolic changes of ischaemia while thrombolysis or angioplasty improve early reperfusion and limit infarct size. Patients with acute coronary syndrome might benefit more from GIK therapy since they have some coronary flow.
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