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Ann Thorac Surg 2002;73:1246-1251
© 2002 The Society of Thoracic Surgeons

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Original article: cardiovascular

Glucose-insulin-potassium infusion for myocardial protection during off-pump coronary artery surgery

^a Departments of Anesthesiology St, Birmingham, AL, USA
^b Surgery, The University of Alabama at Birmingham St, Birmingham, AL, USA
^c Kemp Carraway Heart Institute, Birmingham, Alabama, USA

Accepted for publication December 16, 2001.

* Address reprint requests to Dr Lell, Department of Anesthesiology, The University of Alabama at Birmingham, 619 South 19th St, Birmingham, AL 35249-6810 USA
e-mail: william.lell{at}ccc.uab.edu

	Abstract

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Background. The purpose of this randomized, double-blind, placebo-controlled pilot study was to determine the effectiveness of an intravenous glucose-insulin-potassium (GIK) infusion in preventing myocardial damage and maintaining cardiac performance in patients undergoing "off-pump" myocardial revascularization.

Methods. Forty-six adult patients undergoing elective off-pump coronary artery bypass received either normal saline or a GIK infusion immediately after the induction of anesthesia through the first 12 hours of intensive care unit convalescence. Measurements of blood glucose, circulating creatine kinase MB and troponin I concentrations, as well as cardiac index (CI) and mixed venous oxygen saturation (S_VO₂), were obtained immediately before starting the infusion (baseline) and at 6,12, and 24 hours post–initial coronary artery occlusion.

Results. Five patients (8%) requiring cardiopulmonary bypass were excluded from data analysis. Twenty patients received saline. Twenty-one received GIK. Blood glucose was significantly higher in the GIK group. The concentration of circulating creatine kinase MB and troponin I significantly increased over time after off-pump coronary artery bypass, with no significant intergroup differences. Cardiac index and S_VO₂ did not differ significantly between groups.

Conclusions. A GIK infusion protocol commonly used as an adjunct to reperfusion therapy for acute myocardial infarction causes insulin-resistant hyperglycemia in elective off-pump coronary artery bypass patients with no demonstrable benefit. The finding of significant release of cardio-specific enzymes in individual patients implies an ongoing need to develop more effective strategies for myocardial protection during off-pump coronary artery bypass.

	Introduction

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Technologic advances and reports of fewer complications and reduced costs have catalyzed renewed interest in myocardial revascularization without cardiopulmonary bypass (off-pump coronary artery bypass [OPCAB]) [1, 2]. Ironically, myocardial damage continues to complicate an operation designed ultimately to prevent myocardial infarction. Previous studies [3–6] document overall low levels of heart-specific enzyme release with OPCAB. However, individual patients, no matter what their risk, remain vulnerable to unpredictable ischemic-reperfusion damage and impaired cardiac performance. This implies an ongoing need to develop strategies for myocardial protection during OPCAB. Experience with glucose-insulin-potassium (GIK) as an adjunct to reperfusion therapy for acute myocardial infarction [7] and during myocardial revascularization with cardiopulmonary bypass [8] suggests this inexpensive intervention might also prove useful in the setting of OPCAB. Therefore, the purpose of this randomized, double-blind, placebo-controlled study was to determine the effectiveness of a continuous, intravenous GIK infusion in reducing myocardial damage and maintaining cardiac performance in patients undergoing OPCAB.

	Material and methods

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Adult patients, scheduled for elective, primary myocardial revascularization without cardiopulmonary bypass, by two surgeons, were screened for this internal review board–approved study. Patients were excluded for any of the following: (1) inability to obtain informed consent; (2) documented myocardial infarction with elevated cardiac enzymes (troponin I > 0.3 ng/mL CK-MB > 5 ng/mL) and or new Q waves within 5 days of operation; (3) renal dialysis or preop creatinine more than 2 mg/dL; or (4) preoperative fasting glucose more than 350 mg/dL. Previously prescribed cardiovascular medications and antiplatelet agents were continued until the time of operation. Standardized anesthetic and surgical management protocols were used in all patients and no interventions were withheld during the study period, including the use of cardiopulmonary bypass if deemed necessary. Intraaortic balloon pumps were electively placed before incision for a preoperative ejection fraction less than 20%. Major goals of hemodynamic management were to maintain cardiac index greater than 2.0 L/min¹/m² and mixed venous oxygen saturation (S_VO₂) greater than 60%. No pharmacologic agents were administered prophylactically. However, interventions were made at the discretion of the managing clinicians to treat adverse hemodynamic events unresponsive to repositioning the heart and or use of the Trendelenberg and right tilt position. These included the use of nitroglycerine, beta adrenergic blockers, inotropic agents, vasopressors, and antiarrythmics. Warmed Normosol-R and packed cells were used to replace fluid losses and maintain hemoglobin at 8 to 10 gm/dL. Hyperglycemia (> 350 mg/dL) was managed with intermittent doses and continuous infusions of regular human insulin.

Patients were randomized by the central pharmacy into two groups to receive in a blinded fashion a freshly prepared solution of either normal saline (SAL) or GIK (25% glucose, 50 IU insulin, 80 mmol KCL/L). The infusion began immediately after anesthesia induction and continued, at a rate of 1.5 mL/kg¹/h¹, through a dedicated port of a pulmonary artery catheter for an additional 12 hours after the start of the first distal coronary anastamosis. The composition and rate of GIK administration are based on the work of Stanley and associates [9]. The infusion protocol is commonly used as an adjunct to reperfusion therapy for acute myocardial infarction. Study infusions were terminated if blood glucose exceeded 350 mg/dL despite supplemental insulin.

A median sternotomy was performed and the pericardium opened. The left internal mammary artery was then taken down concurrent with saphenous vein or radial artery harvest. Heparin was administered to achieve and maintain an activated clotting time (ACT) between 300 and 400 seconds. Proximal anastomoses were then performed using a partial occlusion clamp and continuous 5-0 Prolene suture. The usual order of performance of distal anastomoses was left anterior descending coronary artery, right coronary artery, followed by circumflex marginal branches. Access to the marginal branches of the circumflex was enhanced by using a deep Trendelenburg position with the patient rolled to the right side and retracting up on the pericardium on the left side using a gauze sling sutured to the pericardium just anterior to the left pulmonary veins. Each artery was stabilized in turn using the Medtronic Octopus II Tissue Stabilization System (Medtronic, Inc, Minneapolis, MN). After the arteriotomy, an appropriately sized Flo-Thru intraluminal shunt (Biovascular Incorporated, St. Paul, MN) was inserted. Circumferential snares were avoided to minimize injury to the target vessel. The distal anastomosis was then performed with 7-0 Prolene with shunt removal just before tying the suture. Visualization was enhanced by the use of a carbon dioxide gas blower-humidifier during the distil anastomosis. After revascularization, protamine was administered to achieve an ACT of 150 to 200 seconds. All patients were transferred to the cardiac intensive care unit intubated. Forced-air heating blankets were used to facilitate rewarming.

Measurements to evaluate myocardial injury included cardiac enzyme profiles for CK-MB, and troponin I (microparticle enzyme immunoassay technique, Abbot AXSYM system; Abbot Laboratories, Chicago, IL) after induction of anesthesia (base line) and 4, 6, 12, and 24 hours post–initial distal coronary occlusion; as well as 12-lead electrocardiograms (ECGs) in the preoperative period and 12 and 24 hours after initiation of the first distal coronary anastamosis. A cardiologist, blinded to patient identity, read the ECGs. A perioperative myocardial infarction was defined as a peak troponin I and or CK-MB concentration greater than the 75th percentile for the entire population.

Cardiac performance was assessed using continuous cardiac output and S_VO₂ as well as heart rate, systemic, and pulmonary artery pressures. Secondary outcome measurements included the following: (1) in-hospital mortality, (2) incidence of hyperglycemia (glucose > 350 mg/dL), (3) requirements for vasoactive, inotropic, antiarryhthmic, and other adjuvant agents, (4) use of intraaortic balloon pump, and (5) duration of intubation, intensive care unit (ICU), and hospital stay.

Operating room and ICU hemodynamic, respiratory, and other physiologic data were recorded continuously in real time using CompuRecord AIS (Pittsburgh, PA) and Hewitt Packard Careview (Atlanta, GA) electronic acquisition devices.

All serially measured parametric data were analyzed with analysis of variance (ANOVA) with repeated measures. Two-tailed student t tests were utilized in post hoc analysis. Due to the variability in the CK-MB and troponin I data, these results were analyzed with Friedman repeated-measures ANOVA. Demographic and other nominal data were analyzed with ² or Fisher’s exact tests as appropriate. All parametric variables are expressed as mean ± SD and nonparametric variables as median and first and third quartiles. An alpha error of less than 0.05 was considered significant.

	Results

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Forty-six patients of 52 screened patients undergoing primary OPCAB during the period from August 1999 to July 2000 were enrolled in the study. Five patients (3 SAL, 2 GIK, 11% total) were excluded from further analysis due to persistent hemodynamic instability requiring CPB during exposure of the circumflex marginal artery. Of the remaining patients, 20 received saline and 21 received GIK. Preoperative patient characteristics for the two groups were similar, with the exception of a significantly lower ejection fraction in the saline group (Table 1). There were no significant intergroup differences with regard to preoperative medication (Table 2). The total number of grafts per patient (2.4 ± 0.9 SAL versus 2.5 ± 0.7 GIK) and the mean total distal anastamotic time per patient (SAL 31.4 ± 14 minutes, GIK 33.7 ± 13 minutes.) were not significantly different between groups. The study infusion was discontinued in 2 GIK patients after 3 and 8 hours, respectively, due to persistent blood glucose greater than 350 mg/dL unresponsive to supplemental insulin.

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

Pioneering work by Rackley and associates [10] in the 1970s demonstrated that a continuous intravenous infusion of GIK provides metabolic support for the heart during acute myocardial infarction, resulting in improved ventricular performance and a reduction in cardiac arrhythmias and mortality. These investigators defined the dose and suggested possible mechanisms of actions in terms of altered myocardial metabolism. Despite reports of beneficial effects in cardiac surgical patients by Gradinak [11] and Lazar [8], interest in GIK waxed and waned until 1998, when a randomized, prospective trial from the ECLA collaborative group confirmed the efficacy of GIK together with reperfusion in reducing mortality from acute myocardial infarction with no important side effects [12]. Based on this information, we hypothesized that a GIK infusion during OPCAB would protect the heart from ischemic-reperfusion damage resulting in improved cardiac performance.

Recognizing the limitations of enzyme and ECG analysis to precisely document perioperative injury [13–15], our study documents important myocardial damage can occur even in elective patients. Overall, 19% of the patients had new Q waves on the 24-hour ECG. Twenty-two percent had isoenzyme levels exceeding the predefined cutoff value defining perioperative myocardial infarction. The high incidence of new Q waves is difficult to interpret because there was no correlation of ECG changes with heart-specific enzyme release. We suspect that different lead placement postoperatively relative to the preoperative baseline ECGs may have influenced the results. Nevertheless, the extent of injury in our study is clearly higher than previously reported. Different patient populations, enzyme assay methods, and the fact that the study was conducted early in our OPCAB experience may explain the higher levels. Certainly, not all our patients were "good risk." Ten percent had ejection fractions less than 20%. Twenty-four percent had base line CIs less than 2. Whatever the reasons, the more extensive damage documented in our study should make it easier to demonstrate a cardio-protective effect of GIK. However, we found no significant intergroup differences in the markers of myovardial injury.

We were also unable to show a beneficial effect of GIK on cardiac performance using the clinical measurements of cardiac index, SVO2, and inotropic requirements. These global measurements no doubt lack the sensitivity and specificity necessary to differentiate subtle changes in regional ventricular performance. Unfortunately, state-of-the-art nuclear medicine methods are expensive and not readily applicable during the intra- and early postoperative period. Although echo images are frequently used clinically to monitor ischemic changes, retraction and repositioning of the heart during OPCAB confounds interpretation. Recognizing the limitations of the methods used, we find no evidence that GIK improves cardiac performance during OPCAB. Improving global hemodynamics, in the face of progressive enzyme release, probably reflects the ability of inotropic support to compensate for regional dysfunction secondary to localized myocardial injury. Analysis of secondary outcomes also revealed no benefit from prophylactic GIK administration.

Why were we unable to document a benefit from GIK? Excluding patients with recent or evolving myocardial infarctions (MIs) at screening in order not to confound interpretation of the enzyme data may have eliminated the patients most likely to benefit from GIK. Can the negative findings be explained in terms of the method of drug infusion? During administration, was the insulin component of the GIK solution bound to the plastic surfaces of bags and intravenous tubing? Our methodology met criteria for insuring 100% insulin delivery [16]. Assuming adequate insulin delivery to the patient, does the GIK solution reach jeopardized myocardium distal to the anastamotic site? We can only speculate that the use of shunts together with native collateral flow and the absence of occlusive snares result in drug delivery to the targeted site of action.

We recognize this study lacks sufficient power to eliminate a type II statistical error. The finding of persistent hyperglycemia, despite the use of supplemental insulin, led us to suspend patient enrollment after 1 year and conduct an interim analysis of unblinded data. A power analysis revealed a minimum of 120 additional subjects in each group would be required to reject the null hypothesis (alpha of 0.05, power of 0.8) for many of the outcome variables. We decided not to continue the study in an attempt to establish statistical significance because of concerns that insulin-resistant hyperglycemia might increase the risk of the following hyperglycemic related complications: (1) Myocardial injury. The mean glucose at 4 hours in the 9 patients with perioperative MI was 403 ± 193 mg/dL versus 271 ± 122 mg/dL for those without MI (p = 0.02). There is increasing evidence that hyperglycemia is an independent predictor of cardiovascular risk in humans. Gerstein demonstrated that an increase in postprandial blood glucose of 21 mg/dL is independently associated with an increased risk of MI in nondiabetic patients [17]. Kersten and associates recently documented that hyperglycemia abolishes the benefits of ischemic preconditioning preceding coronary occlusion. They showed the extent of myocardial injury was directly related to blood glucose concentration in both diabetic and acutely hyperglycemic dogs, independent of serum osmolarity, insulin concentration, coronary collateral blood flow, or hemodynamics [18]. (2) Neurologic dysfunction. Although we observed no permanent neurologic deficits in either group, 1 patient in the SAL group versus 6 in the GIK group were disoriented as to time, place, or person for a period greater than 24 hours (p = 0.09). Griffin and associates documented better cognitive function in normoglycemic versus hyperglycemic patients after CABG with bypass [19]. (3) Wound infection. In our study, the incidence of deep sternal wound infection was SAL, 1; GIK, 2. Furnary documented a decreased risk of deep sternal wound infection when blood glucose was maintained below 200 mg/dL in diabetic patients after cardiac surgery [20].

Although all our patients demonstrated characteristic increases in blood glucose known to occur as a result of perioperative hormonal changes [21, 22], hyperglycemia was particularly difficult to manage in GIK patients. A reduced GIK infusion rate, used by Lazar in coronary artyery bypass graft patients, may simplify glucose control [8].

In conclusion, we document that a GIK infusion protocol commonly used as an adjunct to reperfusion therapy for acute myocardial infarction causes insulin-resistant hyperglycemia in elective OPCAB patients with no demonstrable benefit. The finding of significant release of cardio-specific enzymes in individual patients implies an ongoing need to develop more effective strategies for myocardial protection during OPCAB.

	Acknowledgments

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
This study was supported in part by the Benjamin Carraway Endowed Chair of Anesthesiology and the Department of Anesthesiology. We thank Diana Wilhite, RN, CCRC, and Margaret Jones, RN, MS, for assistance in data collection.

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): David C. McGiffin Frank E. Schmidt, Jr James K. Kirklin Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lell, W. A. Articles by Stanley, A. W. Search for Related Content PubMed PubMed Citation Articles by Lell, W. A. Articles by Stanley, A. W., Jr Related Collections Myocardial protection Related Article