Insulin vs. strict blood glucose control to achieve a survival benefit after AMI?

Abstract

This editorial refers to ‘Intense metabolic control by means of insulin in patients with diabetes mellitus and acute myocardial infarction (DIGAMI 2): effects on morbidity and mortality’† by K. Malmberg et al. , on page 650 Patients with diabetes mellitus have a 1.5–2 times higher risk of death after myocardial infarction than do non-diabetic patients. In diabetic myocardium, the consumption of fatty acid as metabolic fuel is thought to be increased, whereas glycolysis is impaired both in ischaemic and non-ischaemic areas. As the consumption of fatty acids instead of glucose requires more oxygen, such a shift may be deleterious particularly when oxygen supply is limited. More than four decades ago, the concept of infusing glucose together with insulin and potassium (GIK) to protect the ischaemic myocardium was introduced.1 Early clinical studies on the effect of such a ‘metabolic cocktail’ yielded promising results suggesting that GIK might be a way to reduce morbidity and early mortality in patients with an acute myocardial infarction (AMI). As the possible mechanism behind a cardioprotective effect of GIK, Opie2 proposed the promotion of glycolysis in cardiomyocytes and the diversion of fatty acids to adipocytes thereby reducing oxygen consumption in the heart. With the advent of aggressive and acute revascularization strategies (thrombolysis and percutaneous transluminal coronary angioplasty), the potential of metabolic supportive therapy with GIK was not further pursued. In 1995, the Diabetes and Insulin-Glucose infusion in AMI (DIGAMI) study was the first to randomize diabetic patients with an AMI to either ‘intensive insulin therapy’ or standard treatment.3 Intensive insulin therapy comprised intravenous infusion of GIK as soon as possible after the AMI and continued for 48 h. Thereafter, patients in the intensive insulin therapy group were submitted to a ‘stricter’ blood glucose control regimen with subcutaneous insulin continued for ∼3 months after discharge. … *Corresponding author. Tel: +32 16 34 4021; fax: +32 16 34 4015. E-mail address : greta.vandenberghe{at}uz.kuleuven.ac.be