The role of intensive glycemic control in the management of patients who have acute myocardial infarction.
Hyperglycemia is associated with excess mortality in AMI and should be treated aggressively in the intensive care setting. The exact goal of therapy is unclear because different blood glucose targets were used in earlier studies (eg, 215 mg/dL in DIGAMI versus 110 mg/dL in the Belgian study of critically-ill patients). In the setting of AMI, it is prudent to avoid excessive hypoglycemia and, thus, more modest goals for blood glucose may be considered until more definitive data are present. Aggressive therapy with continuous infusion of insulin seems to improve a host of metabolic and physiologic effects that are associated with acute hyperglycemia and improves mortality in the acute setting. Aggressive glycemic control should be coupled with appropriate use of reperfusion therapies, glycoprotein IIb/IIa inhibitors, aspirin, 1-blockers, ACE inhibitors, and antithrombotic agents. The role of intensive chronic glucose control in reducing CV events is less clear but earlier studies were not well-powered; did not achieve aggressive, durable glycemic control; and did not use insulin-sensitizing agents routinely. Given the results of the DIGAMI trial, the goal of therapy postdischarge should include strict glycemic control while future studies help to delineate the role of insulin-sensitizing agents versus insulin-providing agents in reducing recurrent macrovascular events. Careful attention also should be paid to aggressive lifestyle modifications and treatment of hypertension, hyperlipidemia, and left ventricular dysfunction, as well as appropriate use of anti-platelet and antithrombotic agents.
Zarich
Stuart W
SW
Division of Cardiovascular Medicine, Department of Medicine, Bridgeport Hospital, 267 Grant Street, Bridgeport, CT 06610, USA. pszari@bpthosp.org
D003925:Diabetic Angiopathies / Q000097:blood / Q000503:physiopathology; D051275:Glucose Transporter Type 4; D006801:Humans; D006943:Hyperglycemia / Q000517:prevention & control*; D006949:Hyperlipidemias / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology; D009004:Monosaccharide Transport Proteins / Q000502:physiology; D009124:Muscle Proteins / Q000502:physiology; D009203:Myocardial Infarction / Q000097:blood* / Q000503:physiopathology
D051275:Glucose Transporter Type 4; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; C495692:SLC2A4 protein, human