Glucose, insulin and myocardial ischaemia

Purpose of review The importance of glucose metabolism and insulin therapy during myocardial ischaemia is increasingly being investigated. Insulin is used to achieve a tight glucose control or as part of glucose-insulin-potassium therapy. We have reviewed (1) the physiological and physiopathological consequences of hyperglycaemia focusing on potential machanisms of myocardial ischaemia, (2) the effects of insulin on vascular tone, on the release of free fatty acids, on inflammatory pathways, on the switch of energy source and on apoptosis, and (3) clinical data reporting the effects of intensive insulin therapy and glucose-insulin-potassium solutions during myocardial ischaemia and ischaemic heart failure. Recent findings In addition to its known toxic cellular effects, hyperglycaemia increases the activity of inducible nitric oxide synthase and promotes inflammation. Conversely insulin exerts anti-inflammatory and anti-apoptotic effects. Glucose-insulin-potassium solutions could improve survival after acute myocardial infarction or after surgery, according to recent meta-analyses, but confirmation of these data is eagerly awaited. Summary Hyperglycaemia is toxic, while insulin is beneficial during acute myocardial ischaemia. Some recent evidence confirms a substantial benefit of insulin administered either alone to achieve a tight glucose control or as a component of glucose-insulin-potassium therapy. Further research is needed to confirm that tendency and to define the threshold of tight glucose control.