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Diabetes and CABG
Abstract & Commentary
Synopsis: Tight glycemic control during surgery and 12 hours after CABG in diabetic patients improves perioperative outcomes and survival, and decreases wound infections and episodes of recurrent ischemia.
Source: Lazar HL, et al. Circulation. 2004;109: 1497-1502.
Diabetics who undergo coronary artery bypass graft (CABG) surgery have increased perioperative and long-term morbidity and mortality. Although originally thought to be inevitable, there is now evidence that tighter glycemic control may improve outcomes in diabetics. Thus, Lazar and colleagues from Boston University sought to test the hypothesis that tighter glycemic control during CABG in diabetics would improve outcomes. They prospectively randomized 141 diabetic patients undergoing CABG to tight glycemic control (serum glucose 125-200 mg/dL) or standard therapy (glucose < 250). The tight control group received D5W with regular insulin and potassium IV just before surgery and up to the start of cardiopulmonary bypass. It was then restarted after the aorta was unclamped and continued for 12 hours. Then the patients resumed their preoperative diabetic regimens. The tight control group had a lower serum glucose (138 vs 260 mg/dL; P < .001); a lower incidence of atrial fibrillation (17% vs 42%; P < .002), and a shorter length of stay (6.5 vs 9.2 d; P = .003). Tight control patients had an increased survival over 2 years (P = .04), decreased episodes of recurrent ischemia (5 vs 19%; P = .01), and developed fewer wound infections (1% vs 10%; P = .03). Perioperative mortality was zero in both groups. Lazar et al concluded that tight glycemic control during surgery and 12 hours after CABG in diabetic patients improves perioperative outcomes and survival, and decreases wound infections and episodes of recurrent ischemia.
Comment by Michael H. Crawford, MD
A glucose insulin and potassium (GIK) infusion has been shown in experimental myocardial infarct animal models to reduce ischemic injury. Although more difficult to control for confounders, human studies supported these findings. However, GIK never caught on in the treatment of acute myocardial infarction because of the overwhelmingly positive effect of reperfusion. Perhaps in the coronary surgical setting in diabetic patients it will find a role. This setting is almost like an animal model since blood flow to the heart is interrupted for a defined period of time and medications can be given before the major ischemic insult. Although even in this setting, it is unclear if GIK is necessary since other studies have shown benefit with insulin infusions alone. The important factor here may be glycemic control, which was achieved with GIK. Other studies in patients with acute ischemic syndromes have shown the deleterious effects of high blood glucose levels and the Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) study showed reduced mortality after acute MI in diabetics whose glucose was kept below 200 mg/dL. The exact mechanism of the benefit of lower blood sugar is unknown, but experimental studies suggest that high glucose levels may impair endothelial function, enhance inflammation, and augment thrombogenicity. It now seems clear that tight glucose control is important in acute ischemic syndromes and CABG. Several questions remain: Is the glucose and potassium necessary or is insulin enough? What is the ideal blood sugar level? Expect to see more studies in this important area.
Michael H. Crawford, MD, Professor of Medicine, Associate Chief of Cardiology for Clinical Programs, University of California San Francisco, is Editor of Clinical Cardiology Alert.