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(Circulation. 2004;110:e505.)
© 2004 American Heart Association, Inc.
Correspondence |
Department of Anesthesia, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada
To the Editor:
We read with great interest the study by Lazar et al1 reporting improved outcomes in patients with diabetes after CABG by tight perioperative glycemic control via glucose-insulin-potassium (GIK). Some aspects of this work deserve further comment.
The authors statement that patients in the no-GIK group received standard therapy is misleading. Withholding insulin treatment until the patients blood glucose exceeds 250 mg/dL and administering insulin subcutaneously during cardiac procedures does not constitute standard care. Furthermore, challenging patients with diabetes with intravenous glucose during cardiac surgery (a time of pronounced insulin resistance even in subjects without diabetes) without the metabolic support of insulin may be questioned.
The authors do not disclose whether they used medications that often are diluted in glucose-containing solutions such as antibiotics, vasopressors, and nitroglycerin, although this is crucial for interpreting studies on perioperative glucose control. It also remains unclear whether, when, and how many blood products (which contain high levels of glucose) were used. In addition, important details about the studys fluid replacement strategy/algorithm are missing. Interestingly, patients in the no-GIK group postoperatively gained
3 kg more than did patients in the GIK group, a gain that presumably resulted from excess fluid administration, but the authors give no explanation for this major discrepancy. One could, therefore, argue that excess fluid administration per se was responsible for or at least contributed to the increased incidence of atrial fibrillation and time on ventilators in the no-GIK group.
The authors compare their results to findings previously reported by the Diabetes Mellitus Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) study, which administered a similar GIK regimen in patients with diabetes and acute myocardial infarction.2 Unlike the present study, the DIGAMI trial continued insulin therapy for an obligatory 3 months. In the group of patients that received GIK, 72% were still taking insulin 1 year later as compared with 49% in the control group. Lazar and colleagues do not provide information about the postoperative long-term care of their patients, making it difficult to appreciate the GIK groups 2-year survival advantage. Thus, it would be interesting to know whether more patients in the GIK group continued taking insulin after CABG than in the no-GIK group.
References
Boston University School of Medicine, Boston, Mass
We thank Drs Carvalho and Schricker for their comments on our study. Both groups received the same doses of antibiotics, vasopressors, and nitroglycerin. No difference occurred in the use of blood products between the groups. The difference in postoperative weight gain did not result from excess fluid administration in the non-GIK patients because fluid management strategies were identical for both groups. In fact, the amount of fluid administered to both groups did not differ. We hypothesize that the decreased weight gain that was observed in the GIK patients was caused by better renal protection and improved systemic endothelial function. This improvement resulted in less capillary leakage, which accounts for the increased fluid accumulation seen in patients with diabetes who underwent CABG.
All patients were examined by our endocrine service, and their glucose management was optimized before they were discharged. No difference in the incidence of insulin use was noted between the 2 groups at discharge. Patients were observed subsequently by their own internists and endocrinologists.
Carvalho and Schricker contend that withholding insulin treatment until blood glucose exceeds 250 mg/dL does not constitute the standard of care, and we agree. They must realize, however, that this was the standard of care for cardiac surgery patients in most centers in the early 1990s, when our study was initiated. It is only recently that both cardiologists and cardiac surgeons, based on studies such as this1 and the DIGAMI trial,2 have begun to understand the importance of glycemic control during acute coronary syndromes and myocardial revascularization. In fact, one might argue that the non-GIK group did well because no difference in the 30-day mortality or the incidence of myocardial infarctions was found between the groups. GIK was beneficial during the immediate postoperative period in reducing weight gain, improving myocardial performance, and decreasing arrhythmias. These benefits were reflected in the improved long-term survival of the GIK group, which is similar to that seen in both the DIGAMI trial2 and a meta-analysis of trials with GIK during acute myocardial infarctions.3 We suspect that the enhanced long-term survival seen in patients who received perioperative GIK resulted from improved endothelial preservation in vein grafts in areas of ischemic myocardium, thus preventing further deterioration of myocardial function.
References
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