Abstract
In patients admitted to intensive care units with an acute myocardial infarction (AMI), the concomitant occurrence of hyperglycemia enhances the risk of morbidity and mortality, whether or not the patient has a prior diagnosis of diabetes. Stress hyperglycemia shares many properties with hyperglycemia associated with type 2 diabetes, including increased oxidative stress, inflammation, and activation of stress-responsive kinases. Infarcts are usually larger in patients with stress or diabetes-related hyperglycemia, and animals with type 2 diabetes sustain dramatically larger infarcts following experimental ischemia-reperfusion than do nondiabetic controls. Increased sensitivity to ischemia-reperfusion injury and more severe infarction is one reason for the poor prognosis of AMI patients with stress hyperglycemia. Evidence from clinical and preclinical studies suggests that insulin resistance and glucose homeostasis play key roles by predisposing hyperglycemic myocardial tissue to injury during ischemia and reperfusion.
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