Hyperglycemia is a frequent condition in patients with
acute coronary syndromes (ACS).
Hyperglycemia during ACS is caused by an inflammatory and
adrenergic response to ischemic stress, when
catecholamines are released and glycogenolysis induced. Although the involved pathophysiological mechanisms have not yet been fully elucidated, it is believed that
hyperglycemia is associated with an increase in free fat
acids (which induce
cardiac arrhythmias),
insulin resistance, chemical inactivation of
nitric oxide and the production of
oxygen reactive species (with consequent microvascular and endothelial dysfunction), a prothrombotic state, and vascular
inflammation. It is also related to myocardial metabolic disorders, leading to
thrombosis, extension of the damaged area, reduced collateral circulation, and ischemic preconditioning. In the last few years, several observational studies demonstrated that
hyperglycemia in ACS is a powerful predictor of survival, increasing the risk of immediate and long-term complications in patients both with and without previously known
diabetes mellitus.
Glucose management strategies in ACS may improve outcomes in patients with
hyperglycemia, perhaps by reducing inflammatory and clotting mediators, by improving endothelial function and fibrinolysis and by reducing
infarct size. Recent clinical trials of
insulin in ACS have resulted in varying levels of benefit, but the clinical benefit of an aggressive treatment with
insulin is yet unproved.