Does Tight Glucose Control Prevent Myocardial Injury and Inflammation?

Abstract

Hyperglycemia has been postulated to be cardiotoxic. We addressed the hypothesis that uncontrolled blood glucose induces myocardial damage in diabetic patients undergoing isolated coronary artery bypass graft surgery receiving continuous insulin infusion in the immediate postoperative period. Our primary aim was to assess the degree of tight glycemic control for each patient and to link the degree of glycemic control to intermediate outcome of myocardial damage. We prospectively enrolled 199 consecutive patients with diabetes undergoing isolated coronary artery bypass graft surgery from October 2003 through August 2005. Preoperative hemoglobin A1c and glucose measures were collected from the surgical admission. We measured biomarkers of myocardial damage (cardiac troponin I) and metabolic dysfunction (blood glucose and hemoglobin A1c) to identify a difference among patients under tight (90–100% of glucose measures ≤150 mg/dL) or loose (<90%) glycemic control. All patients received continuous insulin infusion in the immediate postoperative period. We discovered 45.6% of the patients were in tight control. We found tight glycemic control resulted in no significant difference in troponin I release. Mean cardiac troponin I for tight and loose control was 4.9 and 8.5 (ng/mL), p value .3. We discovered patients varied with their degree of control, even with established protocols to maintain glucose levels within the normal range. We were unable to verify tight glycemic control compared to loose control was significantly associated with decreased cardiac troponin I release. Future studies are needed to evaluate the cardiotoxic mechanisms of hyperglycemia postulated in this study.