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Ann Thorac Surg 2002;73:1251-1252
© 2002 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, Boston University School of Medicine, Boston Medical Center, 88 Newton St, Suite B404, Boston, MA 02118 USA
e-mail: harold.lazar{at}bmc.org
In their study, the authors concluded that the infusion of glucose-insulin-potassium (GIK) causes insulin resistent hyperglycemia in elective off-pump coronary artery bypass (OPCAB) patients with no demonstrable benefit. However, these results reflect major flaws in the design of the study and the manner in which GIK was delivered.
The overall incidence of myocardial necrosis was especially high in this group of patients. The release of tropinin was 27 to 100 times higher than reported by Ascione and Bonatti and the infarct rate was 8 and 20 times higher than described by Bouchard [6] and Ascione [5]. New Q-waves developed in 8 patients, however there was no correlation between the appearance of new Q-waves and isoenzyme release. In fact, cardiac index actually improved as troponin release increased; yet, mixed venous oxygen saturation (SVO2) decreased. The authors explain this by stating that inotropic support compensated for regional dysfunction and that the increased incidence of Q-waves reflects different postoperative lead placement. I would conclude that the measurements of ischemic injury were inaccurate and the degree of ischemia present was very minimal. How else can we explain the fact that most patients were discharged by the fifth or sixth postoperative day? If the amount of ischemic damage was negligible, should we expect to see any improvement in the GIK treated patients? The authors are remiss in not using two-dimensional echocardiography to determine the clinical significance of the observed ECG and enzyme changes.
A major flaw in the study design was the inclusion of five non-GIK patients who received elective preoperative, intraaortic balloon pumps (IABP) because of low ejection fraction. I strongly suspect that if these patients had not received an IABP, the need for inotropic support and the incidence of infarcts may have been increased; thereby, influencing the results of the study.
I am very concerned about how the GIK was administered and its indiscriminate use in diabetic patients. The authors elected to infuse GIK at 1.5 mL · kg-1 · h-1 based on an overview of randomized, placebo-controlled trials in patients with acute infarctions who were not undergoing coronary artery bypass graft (CABG) surgery. In our study in patients undergoing CABG for unstable angina, we delivered a similar GIK solution at 1 mL · kg-1 · h-1 and currently use 0.75 mL · kg-1 · h-1 [1]. The decreased volume is more conductive to surgical patients and makes it easier to control serum glucose. In our study, GIK was discontinued if serum glucose exceeded 325 mg/dL and was strictly avoided in all diabetic patients. We were concerned that diabetics undergoing surgical stress could not handle the increased glucose load and that persistent hyperglycemia could be detrimental to this group of patients. It is disconcerting that the authors would include 6 diabetic patients (28%) in their GIK group and not describe in their manuscript whether the persistent hyperglycemia and the two sternal wound infections did indeed occur in diabetic patients. Using a modified GIK solution (500 mL D5W + 80 U regular insulin + 40 mEq KCL) with rates adjusted to achieve glucose levels between 140 to 200 mg/dL, we found that GIK improved hemodynamics and decreased the incidence of inotropic support and atrial fibrillation in diabetic CABG patients [2]. As our study population has increased, we have noted a significant decrease in all wound infections in diabetic, GIK treated, CABG patients. I strongly suspect that the resistant hyperglycemia seen in this study was due to the administration of unmodified GIK to diabetic patients.
Despite my criticisms, I wish to congratulate the authors in attempting to use GIK to minimize ischemic damage during OPCABG procedures. I would urge them to redesign the study, properly randomize patients requiring elective preop IABP support, decrease the volume of the D25 GIK solution, and use our diabetic GIK solution for all diabetic patients. I am optimistic that by instituting these changes, they will find that GIK will indeed diminish ischemic injury in all their patients.
References
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