OBJECTIVE: Reperfusion treatment modalities used in the routine treatment protocols of acute myocardial infarction (AMI) were found to be ineffective in establishing the nutritional cellular reperfusion in the microvascular environment even they succeed to open the infarct related artery. Glucose-insulin-potassium (GIK) solution, which is presumed to stimulate the glycolytic pathway, is experimentally proven to be the most efficacious substrate for the preservation of energy production and therefore the myocardial viability, in the setting of acute ischemia. METHODS: We compared, 54 patients who suffered AMI and receivedGIK solution (300 g glucose+50 IU crystallized insulin+80 mEq potassium chloride in one liter solution) in addition to conventional treatment (GIK group) with 27 patients who were traditionally treated (control group) for in-hospital and early-term (1 month) cardiac morbidity. We also compared the two groups in terms of heart rate variability (HRV). RESULTS: Eight patients in the control group developed new-onset symptomatic congestive heart failure whereas only 5 patients in GIK group were found to have such a cardiac morbidity (p=0.01). Reduced HRV (<50 ms) was found in 3 patients of control group whereas no patient in GIK group had abnormal HRV (p=0.01). CONCLUSION: The GIK solution decreased the incidence of new-onset symptomatic congestive heart failure and low HRV after myocardial infarction. Larger multicenter trials need to resolve the questions on the efficiency of metabolic intervention with GIK solution in acute myocardial infarction.
RCT Entities:
OBJECTIVE: Reperfusion treatment modalities used in the routine treatment protocols of acute myocardial infarction (AMI) were found to be ineffective in establishing the nutritional cellular reperfusion in the microvascular environment even they succeed to open the infarct related artery. Glucose-insulin-potassium (GIK) solution, which is presumed to stimulate the glycolytic pathway, is experimentally proven to be the most efficacious substrate for the preservation of energy production and therefore the myocardial viability, in the setting of acute ischemia. METHODS: We compared, 54 patients who suffered AMI and received GIK solution (300 g glucose+50 IU crystallized insulin+80 mEq potassium chloride in one liter solution) in addition to conventional treatment (GIK group) with 27 patients who were traditionally treated (control group) for in-hospital and early-term (1 month) cardiac morbidity. We also compared the two groups in terms of heart rate variability (HRV). RESULTS: Eight patients in the control group developed new-onset symptomatic congestive heart failure whereas only 5 patients in GIK group were found to have such a cardiac morbidity (p=0.01). Reduced HRV (<50 ms) was found in 3 patients of control group whereas no patient in GIK group had abnormal HRV (p=0.01). CONCLUSION: The GIK solution decreased the incidence of new-onset symptomatic congestive heart failure and low HRV after myocardial infarction. Larger multicenter trials need to resolve the questions on the efficiency of metabolic intervention with GIK solution in acute myocardial infarction.