Recent data shown that the prevalence of DM or impaired glucose tolerance (IGT) may be as high as 70% in patients who have AMI . In 181 consecutive nondiabetics who had AMI, more than two thirds of patients were diagnosed with DM or IGT by oral glucose tolerance testing. Previously undiagnosed DM accounted for one half of all patients who had AMI and an abnormal glucose metabolism. Only one third of subjects met criteria for DM based on fasting blood glucose criteria. Although a random blood glucose at the time of admission for AMI may not be reliable in making the diagnosis of DM, concern that the diagnosis of IGT or DM is erroneous in the acute setting because of "stress hyperglycemia" may be unwarranted; the results of glucose tolerance testing that was performed at the time of AMI were similar to those performed 3 months later. Two recent studies in patients who presented for coronary angiography similarly showed that previously undiagnosed DM or IGT was present in up to two thirds of patients who had angiographi-cally-proven coronary artery disease [20-21].
Acute hyperglycemia is associated with a myriad of adverse metabolic and CV effects that may contribute to a poor outcome in AMI (Box 2). Exaggerated metabolic responses to ischemia may play a crucial role in myocardial oxygen use in AMI. Hyperglycemia is a reflection of relative insulinopenia, which is associated with increased lipolysis and free fatty acid (FFA) generation, diminished myocardial glucose uptake, and a decrease in glycolytic substrate for myocardial energy needs in AMI [22-24]. Although glucose metabolism is a major myocardial energy source, oxidation of FFAs is the primary source of energy in the resting aerobic state. During myocardial ischemia, FFA oxidation rates decrease but remain an important source of energy. During reperfusion, fatty acid oxidation again dominates as a source of energy.
Myocardial ischemia results in an increased rate of glycogen breakdown and glucose uptake by way of translocation of glucose transport receptors (GLUT-4) to the sarcolemma [25,26]. This adaptive mechanism is important because
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