Full Study
http://jama.ama-assn.org/content/early/2012/03/21/jama.2012.426.full
Link to full study.
Mechanisms still not fully understood. Search PubMed for other studies, some of them go over the underlying principles....in the past GIK was shown to decrease levels of C reactive protein (biomarker of inflammation) by 40% in ACS, theorized due to anti-inflammatory effects of insulin. It was researched back in the 90's but kinda pushed aside in favor of PCI/thrombolytic therapy. It seems to be making a resurgence now.
Quoted from the study:
"Experimental and clinical studies have shown intravenous glucose-insulin-potassium (GIK) to have 2 types of benefits in cardiac ischemic syndromes. One is protecting against myocardial injury by providing metabolic support to ischemic myocardium, which should limit progression of unstable angina pectoris to myocardial infarction (MI), lessen infarct size, and thereby preserve left ventricular (LV) function.1,2,3,4,5,6,7,8 The other is preventing arrhythmias and cardiac arrest associated with ischemia-related metabolic derangements thought to be promoted by the elevated free fatty acid (FFA) levels during acute coronary syndromes (ACS).1,9 One or both mechanisms could be expected to reduce short- and long-term mortality."
On a side note, it seems the EMSWorld article is alot more encouraging than the actually study data is...
Quoted:
"In conclusion, among patients with suspected ACS, out-of-hospital administration of intravenous GIK by paramedics, compared with administration of glucose placebo, did not reduce progression to MI. Compared with placebo, GIK administration was not associated with improvement in 30-day survival but was associated with lower rates of the composite outcome of cardiac arrest or in-hospital mortality. Further studies are needed to assess the out-of-hospital use of GIK as therapy for patients with ACS."