title: [Insulin in acute coronary syndromes].
abstract: There is a state of major stress during acute coronary syndromes with insulin resistance which results in cardiac cellular metabolism becoming almost completely dependant on fatty acids. This increases cellular oxygen demand with consequent cellular necrosis and apoptosis. Under normal conditions, the metabolism in type 2 diabetes is almost exclusively based on fatty acids. During ischaemia, these phenomena are accentuated which partially explains the higher morbid-mortality after myocardial infarction. It has been demonstrated that insulin administration (GIK) creates conditions for an "optimal milieu" protecting the myocardium during the ischaemic and reperfusion phases by the effects of glucose, the anti-inflammatory action of insulin and its action on NO synthesis. Its efficacy in reduction in post-infarction mortality has been demonstrated in type 2 diabetes in the DIGAMI trial and also in all coronary patients and after cardiac surgery, especially in the ECLA, DUTCH, Texas Heart Institute trials. The results were convergent with respect to insulin dosage, blood sugar levels and volumes of solute, also in the context of cardiac failure. However, in type 2 diabetes, the GIK protocol remains underused in our acute cardiac units and insulin therapy is often prescribed in conditions which do not provide a real benefit. Very few centres use the GIK protocol in non-diabetics in acute coronary syndromes with a risk of loss of benefit for these patients. Therapeutic protocols which can be used by paramedical personnel should be developed.
authors.affiliation: CHU de Grenoble, département urologie, néphrologie, endocrinologie, UF diabétologie. shalimi@chu-grenoble.fr
authors.forename: S
authors.initials: S
authors.lastname: Halimi
mesh_terms: D000208:Acute Disease; D000789:Angina, Unstable / Q000188:drug therapy* / Q000378:metabolism; D002986:Clinical Trials as Topic; D003925:Diabetic Angiopathies / Q000188:drug therapy* / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000627:therapeutic use*; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000378:metabolism; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000378:metabolism; D013577:Syndrome
chemical_list: D007328:Insulin