| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J Thorac Cardiovasc Surg 2005;130:1144
© 2005 The American Association for Thoracic Surgery
Cardiopulmonary Support and Physiology |
a Division of Cardiovascular Surgery, Toronto General Hospital and University of Toronto, Toronto, Ontario, Canada
b Department of Anesthesia, Toronto General Hospital and University of Toronto, Toronto, Ontario, Canada
c Department of Cardiovascular Surgery, University of Freiburg, Freiburg, Germany.
Received for publication May 17, 2004; revisions received May 18, 2005; accepted for publication May 25, 2005. * Address for reprints: Michael Borger, MD, Division of Cardiovascular Surgery, Toronto General Hospital, 200 Elizabeth St, 4N-451, Toronto, Ontario M5G 2C4, Canada (Email: michael.borger{at}uhn.on.ca).
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionAppendix E1References |
|---|
METHODS: We performed a multivariate logistic regression analysis on all diabetic (n = 1579) and nondiabetic (n = 4701) patients undergoing cardiac surgery at the Toronto General Hospital between 1999 and 2001. Boluses of insulin were given during cardiopulmonary bypass when the glucose level exceeded 15 mmol/L, when the serum potassium level exceeded 6.0 mmol/L, or both.
RESULTS: Overall mortality was 1.8% (n = 115). A high glucose level during cardiopulmonary bypass was an independent predictor of mortality in both diabetic (odds ratio, 1.20; confidence interval, 1.08-1.32) and nondiabetic (odds ratio, 1.12; confidence interval, 1.06-1.19; per millimole per liter increase in glucose) patients. A high glucose level during cardiopulmonary bypass was also an independent predictor of all major adverse events in both patient groups (odds ratio, 1.06; confidence interval, 1.03-1.09). A high glucose level was not closely related to cardiopulmonary bypass (r = 0.3) or aortic crossclamp times (r = 0.4).
CONCLUSIONS: A high peak serum glucose level during cardiopulmonary bypass is an independent risk factor for death and morbidity in diabetic patients and unexpectedly also in nondiabetic patients.
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix E1References |
|---|
|
Hyperglycemia is common during and after cardiac surgery in both diabetic and nondiabetic patients. Its treatment requires increased dosages of insulin, and even extremely high dosages might sometimes not be successful in establishing euglycemia.
1,2
To date, perioperative hyperglycemia has not been treated aggressively, mainly because it has been considered harmless, and some evidence has even suggested beneficial effects.
1,3
However, recent investigations suggest that postoperative hyperglycemia is directly related to mortality in patients with diabetes mellitus (DM).
4,5
In addition, avoiding postoperative hyperglycemia improves outcomes in patients with prolonged intensive care unit (ICU) stays
6
and in patients with DM.
5
Conclusions from previous studies regarding the effect of hyperglycemia on outcome after cardiac surgery have to be drawn with caution for 3 reasons. First, the degree of postoperative hyperglycemia in diabetic patients might be a reflection of the severity of the patients' DM, which might be a marker for increased comorbidities and greater insulin resistance.
7
Second, patients with a complicated postoperative course are more likely to receive glucogenic drugs (eg, epinephrine) than those with an uncomplicated course. Third, insulin, which was used to treat hyperglycemia in these studies, might have a direct effect on outcome independent of its effects on serum glucose levels.
1,8
It is therefore still unclear whether perioperative hyperglycemia has a direct effect on adverse events and mortality in cardiac surgery, particularly in nondiabetic patients.
The purpose of this study was to determine the influence of peak hyperglycemia (ie, highest measured glucose level during cardiopulmonary bypass [CPB]) on perioperative morbidity and mortality in patients undergoing cardiac surgery. In addition, we attempted to determine whether this relationship is the same in both diabetic and nondiabetic patients. We chose the highest glucose level during CPB as our independent variable because it likely reflects a degree of perioperative insulin resistance and is not influenced by the administration of post-CPB glucogenic drugs.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix E1References |
|---|
Patients were divided into 2 groups: those with an established diagnosis of DM (diabetic subjects, n = 1579) and those without evidence of DM (nondiabetic subjects, n = 4701). The diabetic group included patients with type 1 and type 2 DM, and patients with type 2 diabetes were included regardless of whether they were being treated with diet, oral hypoglycemics, and/or insulin. All patients were assessed preoperatively by their general practitioner and by a cardiologist. Several serum glucose measurements were performed in this process. The likelihood of missing the diagnosis of DM was therefore small.
Perioperative management was the same for all patients. CPB flow rates were maintained at between 2.0 and 2.5 L · min–1 · m–2, and mean arterial pressure was kept at greater than 70 mm Hg at all times. Hematocrit was kept at greater than 20%, and mild hypothermia (34°C) was used during CPB. The CPB priming circuit was free of glucose. Cardioplegia consisted of oxygenated blood mixed with crystalloid in an 8:1 ratio and was administered cold and antegrade in the vast majority of patients, as described previously.
9
Glucose levels were determined on pump on average every 15 minutes. Boluses of insulin were administered during CPB when the glucose level exceeded 15 mmol/L (270 mg/dL), when the serum potassium level exceeded 6.0 mmol/L, or both. In all diabetic patients the usual insulin and oral hypoglycemic medications were held the morning of the operation. In their place, patients received an intravenous solution of glucose (D5W) and insulin that was adjusted according to subsequent glucose levels. The infusion was continued through the perioperative period and was discontinued when the patients were able to ingest adequate amounts of food, usually 2 to 3 days postoperatively.
Data Source
Data were gathered on all patients, including preoperative, intraoperative, and postoperative variables, and were entered into our computerized database by a full-time database manager. We have maintained our institutional database for approximately 15 years, and quality assurance checks have consistently revealed a missing data rate of less than 2% and an error rate of less than 2%. Patients who were missing serum glucose levels (n = 135) were excluded from the analysis. All adverse outcomes were recorded by our database manager, using clinical criteria that have been previously described.
9
Adverse cardiac events were defined as a composite end point of low output syndrome and acute myocardial infarction. All adverse events were defined as a composite end point of death, stroke, deep sternal wound infection, low output syndrome, and acute myocardial infarction. All deaths were recorded as in-hospital deaths. Serum glucose levels were measured with a Rapidpoint 400 (Bayer Healthcare, Philadelphia, Pa), and the highest and lowest levels during CPB were entered into our database. For values of 25 mmol/L or greater, the analyzer displayed a value of 25 mmol/L (450 mg/dL).
Analysis
Categoric data are expressed as percentages, and continuous data are expressed as means ± standard deviations throughout the article. SAS version 8.2 software (SAS Institute, Cary, NC) was used for all statistical analyses. Categoric data were analyzed univariately by means of 
2 or Fisher exact tests, and continuous data were analyzed by using Student unpaired t tests or Wilcoxon rank sum tests where appropriate. Stepwise multivariate logistic regression analysis was used to calculate risk-adjusted odds ratios (ORs) and to determine the independent predictors of each outcome of interest. For a complete list of variables assessed in the logistic regression models, please see the Appendix E1. All variables suggested by the univariate analysis (P < .25) or those judged to be clinically important were entered into the logistic regression models. Model discrimination was evaluated by using the area under the receiver operating characteristic curve, and model precision was evaluated by using the Hosmer-Lemeshow goodness-of-fit statistic, as previously described.
9
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix E1References |
|---|
show the prevalence of risk factors in nondiabetic (Table 1) and diabetic (Table 2) patients included in this study. The tables distinguish between those patients with peak serum glucose levels during CPB of less than and greater than 20 mmol/L (360 mg/dL). The value of 20 mmol/L was chosen on the basis of the inflection point in the relationship between peak serum glucose level during CPB and mortality (Figure 1). Among nondiabetic patients (Table 1), those with severe hyperglycemia had significantly more preoperative risk factors than patients with peak glucose levels of less than 20 mmol/L. The percentages of hypertension, preoperative myocardial infarction, triple-vessel disease, and peripheral vascular disease, as well as low ejection fraction, were higher in the diabetic than in the nondiabetic patients (compare Tables 1 and 2, all P < .05). In contrast, the risk profiles of diabetic patients with peak glucose levels of greater than or less than 20 mmol/L (360 mg/dL) were not different (Table 1). Inotropes were required to be weaned from CPB in 15.4% of diabetic and 12.5% of nondiabetic patients. The peak glucose levels of these patients were not different from those of patients coming off CPB without inotropes (diabetic/nondiabetic: without inotropes, 16.0 ± 3.82/13.8 ± 3.61 mmol/L; with inotropes, 16.3 ± 4.25/14.9 ± 4.16 mmol/L).
|
|
|
Tables 3 and 4
show the ORs for peak serum glucose level as an independent predictor of adverse outcomes in nondiabetic (Table 3) and diabetic (Table 4) patients. In both patient populations, peak glucose level was an independent predictor of death and all adverse events. For adverse cardiac events, the ORs reached significance in nondiabetic patients only. It is interesting to note that the ORs of high glucose level were higher for mortality than for any other adverse event. Other predictors of mortality in nondiabetic patients were (OR and 95% confidence intervals in parentheses): age (1.03 per year; 1.01-1.05), female sex (1.96; 1.18-3.23), congestive heart failure (2.71; 1.54-4.75), previous coronary bypass (12.57; 1.15-5.74), peripheral vascular disease (2.32; 1.26-4.28), and emergency operation (5.42; 2.89-10.20). For diabetic patients, other predictors of mortality were congestive heart failure (3.45; 1.44-8.25), renal failure (4.37; 1.73-11.1), and emergency operation (8.92; 3.23-24.6). Cardiogenic shock, poor left ventricular function, and redo operations (except redo coronary bypass in nondiabetic patients) were not significant risk factors for mortality.
|
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix E1References |
|---|
Perioperative hyperglycemia in the absence of excessive glucose infusion might be caused by either impaired insulin signaling at the target organs (ie, insulin resistance) or inhibition of pancreatic insulin secretion. Although we cannot provide information on insulin secretion for the patients in this study, we demonstrated before that the plasma C-peptide levels (reflecting endogenous insulin secretion) for patients undergoing cardiac surgery with the use of CPB and cardioplegic arrest remained unaltered throughout the surgical procedures.
1
These results strongly suggest that insulin secretion is not impaired during cardiac surgery. In addition, the inability of the insulin bolus infusions given to patients with serum glucose levels of greater than 15 mmol/L to avoid peak glucose levels of greater than 20 mmol/L suggests an impairment of the insulin signaling cascades in target organs. Finally, some patients required inotropes to be weaned from CPB, which might have affected glucose levels. However, comparison of the peak glucose levels of patients coming off bypass with inotropes versus without inotropes revealed no difference. We therefore suggest that hyperglycemia during CPB reflects a state of insulin resistance that develops during surgical intervention and that might contribute to poor outcome.
Currently, the adverse effects of hyperglycemia are most convincingly demonstrated in patients having a stroke.
10,11
Similar adverse relationships begin to emerge for patients with acute myocardial infarction and those undergoing cardiac surgery.
12-14
Furnary and colleagues
4
demonstrated a direct relationship between postoperative glucose levels and mortality in patients with DM. Although the results of these studies are intriguing, 2 potentially confounding factors make their interpretation difficult. First, postoperative serum glucose levels in diabetic patients might be a reflection of the severity of their disease, which might be an indicator for more comorbidities and greater insulin resistance.
7
Second, patients with poor outcome are more likely to receive more glucogenic drugs (eg, epinephrine) than patients with an uncomplicated course and will therefore have higher postoperative glucose levels. The latter argument might be less applicable to the study by Furnary and colleagues
4
because hyperglycemia was a significant predictor of mortality independent of epinephrine and inotrope use, which were both included in their analysis. Nevertheless, to minimize these potential confounding factors, we decided to examine the relationship between intraoperative peak serum glucose level, rather than postoperative glucose level, on adverse outcomes.
From a treatment standpoint, van den Berghe and associates
6
and Lazar and coworkers
5
provide the most convincing evidence to date that the establishment of postoperative euglycemia reduces morbidity and mortality. Van den Berghe and associates
6
randomized 1548 surgical ICU patients, of which 63% had undergone cardiac surgery, to receive intensive insulin therapy versus conventional therapy for hyperglycemia. Insulin therapy resulted in a one-third reduction in serum glucose levels and lowered mortality from 8.0% to 4.6% (P < .04). The mortality reduction was most notable in those patients who required an extended stay in the ICU (ie, >5 days). Lazar and coworkers
5
randomized 141 diabetic patients and avoided hyperglycemia in the treatment group by using a modified glucose-insulin-potassium (GIK) protocol. These investigators demonstrated less atrial fibrillation and a shorter length of stay in the hospital and fewer recurrent ischemic events in the follow-up period in the GIK-treated patients. These patients also had lower glucose levels than control subjects. In contrast, there are several reports demonstrating improved cardiac outcomes with systemic GIK infusions, despite the fact that these solutions resulted in hyperglycemia.
1,15
Thus it is still not clear whether hyperglycemia is a risk factor in itself and whether its effect is the same in diabetic and nondiabetic patients.
Hyperglycemia might be linked to adverse outcome through direct or indirect mechanisms. Hyperglycemia interferes with monocyte and neutrophil function, affects endothelial function, and induces the expression of proinflammatory cytokines.
16-18
These events might be responsible for a directly negative effect of hyperglycemia, including the facilitation of wound infection or sepsis with or without multiorgan failure.
6,13
Indirectly, hyperglycemia might be a surrogate parameter for insulin resistance. Chronic insulin resistance is considered to be a risk factor for coronary artery disease, left ventricular hypertrophy, and diabetic cardiomyopathy.
14,19
The potential mechanisms for these associations include the inhibition of the insulin signaling cascade by free fatty acids
20
or by inflammatory cytokines, such as TNF-
.
21
Insulin resistance during surgical intervention is thought to be caused by endogenous release of catecholamines and cortisone as part of the body's stress response.
22
However, it is reasonable to assume that the mechanisms behind chronic insulin resistance also apply to the acute setting. Heparin, administered before the commencement of CPB, causes a drastic and sudden increase in circulating free fatty acids,
23
and the use of CPB is linked to a massive production of inflammatory cytokines, including TNF-.
24
Thus it might be hypothesized that an acute impairment of certain pathways of the insulin signaling network could affect outcome.
We analyzed the effect of peak glucose levels during CPB on postoperative morbidity and mortality in both diabetic and nondiabetic patients. We measured glucose levels during CPB because they are not influenced by the administration of post-CPB glucogenic drugs. There was no significant association between the type of the procedure (coronary artery bypass grafting, valve with or without coronary artery bypass grafting, and other procedures) and peak glucose level. It is therefore reasonable to conclude that peak glucose level during CPB is not a surrogate parameter for the effects of a certain intervention or procedure but is more likely to reflect the activation of endogenous mechanisms leading to the clinical picture of insulin resistance.
The presence of such new-onset insulin resistance or the aggravation of chronic insulin resistance during CPB is supported by our analysis in several ways. First, many diabetic and nondiabetic patients reached peak glucose levels of greater than 20 mmol/L, even though insulin boluses were administered when glucose levels exceeded 15 mmol/L. Second, nearly all patients undergoing cardiac surgery had at least mild increases of serum glucose levels (>9.0 mmol/L) during CPB, a finding that has been described by several other investigators.
1,8,25
Third, insulin secretion from the pancreas during CPB does not appear to be impaired.
1
Finally, the relationship between peak glucose level and CPB and aortic crossclamp times (Figure 2) was poor, suggesting that peak glucose level is not solely influenced by the complexity of the operative procedure or the amount of glucose-containing cardioplegia administered.
However, other factors might have influenced our findings. Nondiabetic patients with peak glucose levels of greater than 20 mmol/L had significantly more risk factors (Table 1), suggesting that this patient population might have experienced impaired insulin signaling before their operation. Unfortunately, we do not know the preoperative serum glucose, circulating insulin, or HbA1c levels from our database analysis and therefore cannot conclusively address this issue. However, the percentage of patients with diabetes in our study and our mode of arriving at the diagnosis is similar to that presented in other studies in this field.
5,6
We also do not know in how many of the surviving nondiabetic patients DM developed after the operation. However, the same relationship between peak glucose level and mortality existed in diabetic patients, in whom the risk profile was not different in patients with and without severe (>20 mmol/L) hyperglycemia. Although it has to be considered that the lack of different outcomes between diabetic and nondiabetic patients might have been caused by the intravenous insulin infusions administered to the diabetic patients, the multivariate analysis identified peak glucose level as an independent predictor of death in both groups. We therefore hypothesize that an impairment of (preoperative) insulin sensitivity during surgical intervention might be associated with poor outcome.
Several studies in the literature support our hypothesis that insulin resistance might be the main cause for adverse outcomes rather than the presence of hyperglycemia alone. Booth and colleagues
26
demonstrated that hyperglycemia (25 mmol/L) increases the rolling and adherence of leukocytes in the mesenteric microvasculature of rats. The application of physiologic doses of insulin without altering glucose levels completely blocked these effects of hyperglycemia. Clinical support for our hypothesis can also be obtained from several GIK cardiac surgery trials.
8,27,28
In these studies intravenous GIK is administered in the perioperative period, often resulting in very high levels of serum glucose at supraphysiologic levels of circulating insulin.
15
The GIK studies report normal or reduced rates of wound infection and generally improved cardiac outcome, despite the presence of hyperglycemia.
8,29
Our hypothesis and the GIK study findings are not contradictory with those studies establishing a link between hyperglycemia and wound infection because the groups with high glucose levels and high rates of wound infection in those studies did not receive larger doses of insulin.
12,13
These findings support the notion that impairment of the insulin signaling pathways (ie, insulin resistance) might be an underlying cause for the observed relationship between hyperglycemia and adverse outcome. It might be hypothesized from our findings that either exogenous hyperglycemia (as induced by many GIK protocols) is less harmful or that the presence of insulin during times of hyperglycemia is protective. Either way, application of adequate dosages of insulin (which might be high) should be recommended during postoperative hyperglycemia. The latter point is the most important conclusion that can be made from the current study.
The current study demonstrates that peak hyperglycemia during CPB is associated with adverse postoperative outcomes in both diabetic and nondiabetic patients. We suggest that hyperglycemia during CPB reflects a state of insulin resistance developing during surgical intervention and that this insulin resistance contributes to poor outcome, rather than hyperglycemia alone. We speculate that the treatment of insulin resistance might improve outcomes in all patients undergoing cardiac surgery.
|
Appendix E1 |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix E1References |
|---|
Sex
Age
Left ventricular grade: left ventricular ejection fraction, as assessed by means of angiography or 2-dimensional echocardiography, where grade 1 is greater than 60%, grade 2 is 40% to 59%, grade 3 is 20% to 39%, and grade 4 is less than 20%.
Recent (<30 days) myocardial infarction
Timing: elective, semiurgent (operation during same hospitalization for cardiac event), urgent (operation <72 hours of cardiac event), and emergency (operation <12 hours of cardiac event).
Canadian Cardiovascular Society Angina Class
New York Heart Association Heart Failure Class
Congestive heart failure: history of hospital admission for congestive heart failure.
Shock: requirement for preoperative inotropes
Renal failure: serum creatinine level greater than 200 µmol/L or history of renal failure.
Diabetes mellitus: history of type I or type II diabetes mellitus
Hypertension
Hypercholesterolemia
Chronic obstructive pulmonary disease
Peripheral vascular disease: history of peripheral or carotid vascular disease
Previous stroke or transient ischemic attack
History of syncope
Type of procedure: coronary bypass, valve with or without coronary bypass, or other procedure (including heart transplant, aneurysmectomy, ascending aortic replacement)
Prior cardiac operation
Prior coronary artery bypass grafting
Cardiopulmonary bypass time
Aortic crossclamp time
Cardiopulmonary bypass temperature
Cardioplegia temperature
Cardioplegia delivery: antegrade, retrograde, or combined (antegrade and retrograde) cardioplegia
Number of diseased vessels
Number of bypass grafts
Use of left internal thoracic artery
Use of multiple arterial conduits
Highest and lowest glucose level during cardiopulmonary bypass
|
Acknowledgments |
|---|
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionAppendix E1References |
|---|
This article has been cited by other articles:
|
|
 |
|
  Z. Yang, V. E. Laubach, B. A. French, and I. L. Kron Acute hyperglycemia enhances oxidative stress and exacerbates myocardial infarction by activating nicotinamide adenine dinucleotide phosphate oxidase during reperfusion. J. Thorac. Cardiovasc. Surg., March 1, 2009; 137(3): 723 - 729. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. L. Lazar, M. McDonnell, S. R. Chipkin, A. P. Furnary, R. M. Engelman, A. R. Sadhu, C. R. Bridges, C. K. Haan, R. Svedjeholm, H. Taegtmeyer, et al. The society of thoracic surgeons practice guideline series: blood glucose management during adult cardiac surgery. Ann. Thorac. Surg., February 1, 2009; 87(2): 663 - 669. [Full Text] [PDF]
|
|
|
|
 |
|
 A. Polito, R. R. Thiagarajan, P. C. Laussen, K. Gauvreau, M. S.D. Agus, M. A. Scheurer, F. A. Pigula, and J. M. Costello Association Between Intraoperative and Early Postoperative Glucose Levels and Adverse Outcomes After Complex Congenital Heart Surgery Circulation, November 25, 2008; 118(22): 2235 - 2242. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Ascione, C.A. Rogers, C. Rajakaruna, and G.D. Angelini Inadequate Blood Glucose Control Is Associated With In-Hospital Mortality and Morbidity in Diabetic and Nondiabetic Patients Undergoing Cardiac Surgery Circulation, July 8, 2008; 118(2): 113 - 123. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Albacker, G. Carvalho, T. Schricker, and K. Lachapelle High-Dose Insulin Therapy Attenuates Systemic Inflammatory Response in Coronary Artery Bypass Grafting Patients Ann. Thorac. Surg., July 1, 2008; 86(1): 20 - 27. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Lecomte, L. Foubert, F. Nobels, J. Coddens, G. Nollet, F. Casselman, P. V. Crombrugge, G. Vandenbroucke, and G. Cammu Dynamic Tight Glycemic Control During and After Cardiac Surgery Is Effective, Feasible, and Safe Anesth. Analg., July 1, 2008; 107(1): 51 - 58. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Gandhi, B. A. Finegan, and A. S. Clanachan Role of glucose metabolism in the recovery of postischemic LV mechanical function: effects of insulin and other metabolic modulators Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2576 - H2586. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Doenst, H. Bugger, M. Schwarzer, G. Faerber, M. A. Borger, and F. W. Mohr Three good reasons for heart surgeons to understand cardiac metabolism Eur. J. Cardiothorac. Surg., May 1, 2008; 33(5): 862 - 871. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Kramer, R. Groom, D. Weldner, P. Gallant, B. Heyl, R. Knapp, and A. Arnold Glycemic Control and Reduction of Deep Sternal Wound Infection Rates: A Multidisciplinary Approach Arch Surg, May 1, 2008; 143(5): 451 - 456. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Doenst, M. A. Borger, R. D. Weisel, T. M. Yau, M. Maganti, and V. Rao Relation between aortic cross-clamp time and mortality -- not as straightforward as expected Eur. J. Cardiothorac. Surg., April 1, 2008; 33(4): 660 - 665. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Puskas, H. P. Grocott, W. D. White, J. P. Mathew, M. F. Newman, and S. Bar-Yosef Intraoperative Hyperglycemia and Cognitive Decline After CABG Ann. Thorac. Surg., November 1, 2007; 84(5): 1467 - 1473. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. D'Alessandro, P. Leprince, J. L. Golmard, A. Ouattara, S. Aubert, A. Pavie, I. Gandjbakhch, and N. Bonnet Strict glycemic control reduces EuroSCORE expected mortality in diabetic patients undergoing myocardial revascularization J. Thorac. Cardiovasc. Surg., July 1, 2007; 134(1): 29 - 37. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Urban, D. Redford, and D. F. Larson Insulin binding to the cardiopulmonary bypass biomaterials Perfusion, May 1, 2007; 22(3): 207 - 210. [Abstract] [PDF]
|
|
|
|
 |
|
 G. Y. Gandhi, G. A. Nuttall, M. D. Abel, C. J. Mullany, H. V. Schaff, P. C. O'Brien, M. G. Johnson, A. R. Williams, S. M. Cutshall, L. M. Mundy, et al. Intensive Intraoperative Insulin Therapy versus Conventional Glucose Management during Cardiac Surgery: A Randomized Trial Ann Intern Med, February 20, 2007; 146(4): 233 - 243. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. G. Shann, D. S. Likosky, J. M. Murkin, R. A. Baker, Y. R. Baribeau, G. R. DeFoe, T. A. Dickinson, T. J. Gardner, H. P. Grocott, G. T. O'Connor, et al. An evidence-based review of the practice of cardiopulmonary bypass in adults: A focus on neurologic injury, glycemic control, hemodilution, and the inflammatory response. J. Thorac. Cardiovasc. Surg., August 1, 2006; 132(2): 283 - 290.e3. [Full Text] [PDF]
|
|
|
|
 |
|
 P. Hans, A. Vanthuyne, P. Y. Dewandre, J. F. Brichant, and V. Bonhomme Blood glucose concentration profile after 10 mg dexamethasone in non-diabetic and type 2 diabetic patients undergoing abdominal surgery Br. J. Anaesth., August 1, 2006; 97(2): 164 - 170. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. H. Jones The Year in Cardiovascular Surgery J. Am. Coll. Cardiol., May 16, 2006; 47(10): 2094 - 2107. [Full Text] [PDF]
|
|
|
|
|
|
H. L. Lazar Hyperglycemia during cardiac surgery J. Thorac. Cardiovasc. Surg., January 1, 2006; 131(1): 11 - 13. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
