title: Enhanced preservation of acutely ischemic myocardium and improved clinical outcomes using glucose-insulin-potassium (GIK) solutions.
abstract: Although the primary energy source for normal myocardium is free fatty acids, glucose appears to be a more favorable energy substrate for the myocardium during ischemia and reperfusion. Glucose-insulin-potassium (GIK) solutions have been shown to limit ischemic damage in experimental models of ischemia. This review summarizes our experimental and clinical studies involving GIK solutions during urgent surgical revascularization of ischemic myocardium. A pig model was used to simulate the conditions of urgent coronary artery bypass graft (CABG) surgery. The second and third diagonal vessels were occluded with snares for 90 minutes followed by 30 minutes of cardioplegic arrest and 180 minutes of reperfusion. Animals receiving GIK during the periods of coronary occlusion and reperfusion had significantly less tissue acidosis, better recovery of wall motion scores, and smaller infarct size. In a prospective, randomized, clinical study involving patients undergoing CABG surgery for unstable angina, GIK therapy resulted in higher cardiac indices, less weight gain, earlier extubation, lower incidence of atrial arrhythmia, and shorter ICU and hospital stays. In conclusion, GIK enhances myocardial performance during ischemia and results in faster recovery after CABG surgery for unstable angina.
authors.affiliation: Department of Cardiothoracic Surgery, Boston University Medical Center, Massachusetts 02118, USA.
authors.forename: H L
authors.initials: HL
authors.lastname: Lazar
mesh_terms: D000208:Acute Disease; D000255:Adenosine Triphosphate / Q000378:metabolism; D015906:Angioplasty, Balloon, Coronary; D000818:Animals; D002314:Cardioplegic Solutions / Q000627:therapeutic use*; D002986:Clinical Trials as Topic; D001026:Coronary Artery Bypass; D004195:Disease Models, Animal; D005227:Fatty Acids / Q000097:blood; D005947:Glucose / Q000627:therapeutic use; D006019:Glycolysis; D006801:Humans; D007328:Insulin / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D017202:Myocardial Ischemia / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D011188:Potassium / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D002314:Cardioplegic Solutions; D005227:Fatty Acids; D007328:Insulin; C030396:glucose-insulin-potassium cardioplegic solution; D000255:Adenosine Triphosphate; D005947:Glucose; D011188:Potassium