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Ann Thorac Surg 2001;71:1925-1930
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

Lactate release during reperfusion predicts low cardiac output syndrome after coronary bypass surgery

^a Division of Cardiovascular Surgery and Department of Clinical Biochemistry, Toronto General Hospital, Centre for Cardiovascular Research and University of Toronto, Toronto, Ontario, Canada

Accepted for publication March 13, 2001.

Address reprint requests to Dr Weisel, Division of Cardiovascular Surgery, The Toronto Hospital, 200 Elizabeth St, E14215, Toronto, Ontario, Canada M5G 2C4
e-mail: richard.weisel{at}uhn.on.ca

	Abstract

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Background. Cardioplegic arrest induces anaerobic myocardial metabolism with a net production of lactate from glycolysis. However, persistent lactate release during reperfusion suggests a delayed recovery of normal aerobic metabolism and may lead to depressed myocardial function necessitating inotropic or intraaortic balloon pump support (low output syndrome [LOS]). We examined the relation between perioperative myocardial metabolism and postoperative clinical outcomes in patients undergoing isolated coronary artery bypass surgery (CABG).

Methods. We reviewed 623 patients who were enrolled in clinical studies evaluating perioperative myocardial metabolism between 1983 and 1996. Arterial and coronary sinus blood samples were obtained intraoperatively to assess myocardial metabolism. Clinical data regarding patient demographics and postoperative outcomes were prospectively collected and entered into our institutional database.

Results. Low output syndrome developed in 36 patients (5.8%). Myocardial lactate release was higher in these patients compared with those who did not develop postoperative LOS. Advanced age and poor preoperative left ventricular function were independent predictors of lactate release during reperfusion. Persistent lactate release after 5 minutes of reperfusion was the only independent predictor of postoperative LOS in this low-risk population.

Conclusions. Persistent lactate release during reperfusion occurs in a significant proportion of low-risk patients undergoing isolated CABG and is an independent predictor of postoperative low cardiac output syndrome. Persistent lactate release during reperfusion suggests a delayed recovery of aerobic myocardial metabolism and may be related to intraoperative misadventure or inadequate myocardial protection. Myocardial lactate release may be useful as an alternative end-point in clinical trials evaluating perioperative myocardial protection.

	Introduction

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Despite apparently adequate blood cardioplegic protection, sensitive indices reveal delayed myocardial metabolic and functional recovery after surgery [1–8]. In previous clinical trials at our institution [5–8], we have observed that aortic cross-clamping induces anaerobic myocardial metabolism with a net release of lactate. A return to normal aerobic lactate extraction may be delayed for as long as 4 hours after cross-clamp removal. Persistent anaerobic glycolysis during reperfusion may be associated with intraoperative ischemic injury.

Kobayashi and Neely [9] demonstrated that the activity of mitochondrial pyruvate dehydrogenase (PDH) was inhibited within 2 minutes of reperfusion after global ischemia. PDH regulates the conversion of pyruvate to acetyl-CoA and the inhibition of this metabolic pathway can lead to persistent lactate production with a resultant acidosis. In addition to the decreased efficiency of anaerobic ATP production, Weiss and colleagues [10] demonstrated that ATP produced by oxidative phosphorylation was preferentially utilized for myocardial contractile function. Therefore, it is possible that persisent anaerobic lactate release during reperfusion may lead to inadequate ventricular function in the early postoperative period.

We reviewed 623 patients who were enrolled in clinical trials at our institution evaluating various techniques of myocardial protection. Metabolic and clinical data were collected prospectively on all patients. We have previously identified the clinical predictors of low output syndrome (LOS) in 4,558 patients undergoing isolated coronary artery bypass grafting [11]. Our objective definition of LOS involves the use of inotropic or intraaortic balloon pump support for more than 30 minutes in the intensive care unit in order to maintain adequate hemodynamics after appropriate adjustment of preload and afterload. The development of LOS is associated with a higher prevalence of perioperative myocardial infarction and operative mortality. The current low rates of perioperative infarction and mortality associated with isolated CABG [12] have required large sample sizes in order to demonstrate clinically significant differences between myocardial protective strategies. The use of LOS as an alternative clinical outcome may improve the statistical power to observe differences between treatment groups. We believe that myocardial lactate release during reperfusion is a marker of perioperative ischemic injury, and may predict the development of postoperative LOS.

The purpose of this study was to examine the relationship between lactate release during reperfusion and postoperative LOS. We reviewed a predominantly low risk patient population in which significant morbidity and mortality was not anticipated in order to determine if myocardial lactate release can be used as a sensitive predictor of inadequate ventricular function in the early postoperative period.

	Material and methods

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Six hundred and twenty-three patients agreed to participate in prospective clinical trials at our institution evaluating alternate myocardial protective strategies between 1983 and 1996. All patients signed an informed consent form approved by our institutional ethics committee. Our conduct of operation and techniques of myocardial protection have been previously described in detail [5–8]. Cardioplegic arrest was achieved using a mixture of systemic blood and crystalloid cardioplegia in a 2:1 or 4:1 ratio. After initial antegrade arrest, cardioplegia was delivered either retrograde into the coronary sinus or antegrade into completed vein grafts. All distal and proximal coronary anastomoses were performed during a single aortic cross-clamp period. Arterial and coronary sinus blood samples were obtained during the cross-clamp period and at prespecified intervals during reperfusion. Specifically, samples were obtained immediately after aortic cross-clamp removal, 5 and 10 minutes after cross-clamp removal, and 5 and 10 minutes after discontinuation of cardiopulmonary bypass.

Low cardiac output syndrome
Low output syndrome was diagnosed if the patient required an intraaortic balloon pump either in the operating room or in the intensive care unit for hemodynamic compromise. Low output syndrome was also diagnosed if the patient required inotropic medication to maintain the systolic blood pressure greater than 90 mm Hg and the cardiac output greater than 2.2 L · min^-1 · m^-2 for at least 30 minutes in the intensive care unit after correction of all electrolyte and blood gas abnormalities, and after adjusting the preload to its optimal value [13]. Afterload reduction was also attempted when possible. Patients received either dopamine, dobutamine, milrinone or epinephrine. Patients who received less than 4 µg/kg of dopamine to increase renal perfusion were not considered to have LOS. Patients who received vasoconstricting medication because of a high cardiac output ( 2.5 L · min^-1 · m^-2) and low peripheral resistance were also not considered to have LOS.

Biochemical measurements
Arterial and coronary sinus blood samples were assayed to estimate the myocardial consumption of oxygen and production of lactate or acid. Oxygen content (O₂Con) was calculated from the formula O₂Con = 1.39Hgb x SaO₂ + 0.0031 x pO₂, where Hgb is the hemoglobin concentration, SaO₂ is the oxygen saturation and pO₂ is the partial pressure of oxygen. Myocardial oxygen extraction (O₂Ex) was calculated as the arterial or cardioplegic oxygen content minus the coronary venous oxygen content and myocardial oxygen consumption (MVO₂) determined after correcting for coronary flow. Measurements were made at 37°C and then corrected to the cardioplegic temperature at the time of sampling.

Blood lactate concentration was determined using a commercially available assay (Rapid Lactate Stat Pack kit; Calbiochem-Behring, La Jolla, CA). Lactate extraction (LEx) was calculated as the difference between arterial and coronary sinus lactate content. Negative lactate extraction is expressed as net lactate release. Lactate consumption or production (MVL) was determined after correcting lactate extraction for coronary blood flow.

The concentration of hydrogen ion (H+) in blood was determined by converting the measured pH value to [H+] by the formula: [H+] = antilog (-pH). Measurements were made at 37°C and corrected to the myocardial temperature at the time of sampling. Myocardial acid production was calculated as the difference in H+ concentration between arterial and coronary sinus blood corrected for coronary flow.

Creatine kinase measurement
An antibody inhibition technique was employed to measure the MB isozyme of creatine kinase (CK-MB). Sequential CK-MB measurements were performed at 2, 4, 8, 16, 24, and 48 hours after the removal of the aortic cross-clamp. Integration of the area under the concentration-time curve for CK-MB within the first 48 hours postoperatively allowed calculation of the total CK-MB release, expressed as units (IU) x hours.

Statistical analysis
Statistical analysis was performed using the SAS program (SAS Institute, Cary, NC). Categorical variables were analyzed with ² or Fisher’s exact test as appropriate. Continuous variables were analyzed using analysis of variance (ANOVA). Stepwise multiple logistic regression was employed to determine the independent predictors of LOS and lactate release during reperfusion. Variables were included in the multivariable model if their univariate p value was less than 0.15 or if they were of known clinical importance. Multivariable models were evaluated by comparing the Hosmer-Lemeshow goodness of fit statistic and the area under the receiver operating characteristic curve [11].

	Results

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Thirty-six patients (5.8%) developed postoperative LOS. Figure 1 illustrates the relationship between myocardial lactate release, oxygen extraction, and acid release and the development of postoperative LOS. Myocardial lactate release at cross-clamp removal was higher in patients who developed LOS (0.92 ± 0.2 mmol/L versus 0.45 ± 0.02, p < 0.01). Similarly, myocardial lactate release after 5 minutes of reperfusion was higher in patients who developed LOS (0.25 ± 0.07 mmol/L versus 0.06 ± 0.01 mmol/L, p < 0.05). Myocardial oxygen extraction or acid release were not different in patients who developed postoperative LOS. There were no differences between groups in any metabolic measurements during the cross-clamp period or beyond 10 minutes of reperfusion.

View larger version (28K): [in this window] [in a new window]   Fig 1. The relationship between myocardial lactate release, oxygen extraction, and acid release during reperfusion and the development of postoperative low output syndrome (LOS). Patients in whom LOS developed had significantly higher lactate release immediately after aortic cross-clamp removal (XCL OFF) and at 5 minutes of reperfusion (5'). However, net myocardial lactate release at 10 minutes of reperfusion (10') was not different between groups. There were no differences in myocardial oxygen extraction or acid release at any time point.

View larger version (28K): [in this window] [in a new window]   Fig 2. (A) The relationship between myocardial lactate release at 5 minutes of reperfusion and the development of postoperative low output syndrome (LOS). Arbitrary cut-points (POS = positive; NEG = negative) reveal an increased prevalence of LOS in those patients who released more than 0.4, 0.6 or 0.8 mmol/L of lactate. (B) A receiver operating characteristics (ROC) curve was constructed from the arbitrary cut-points used in panel A. The optimal balance between sensitivity and specificity for predicting postoperative LOS is determined at a cut-point of 0.4 mmol/L of lactate (the point closest to the upper left quadrant). The area under the ROC curve, which estimates the precision of the diagnostic test, is 0.6328.

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Advances in myocardial protection have led to lower risk-adjusted rates of morbidity and mortality after coronary bypass surgery [12]. However, the prevalence of postoperative LOS remains relatively high at approximately 9% [11]. In this series of 623 predominantly low risk patients, the overall incidence of LOS was 5.4%, despite an operative mortality of only 2.1% and a perioperative infarction rate of only 2.9%. In our institution, LOS is only diagnosed after an active intervention on the part of the surgeon or attending intensivist. The development of postoperative LOS, in the absence of an intraoperative misadventure, represents a failure of myocardial protection.

We have previously shown that LOS, which may be a transient event in some patients, is associated with an increased length of intensive care unit and hospital stay and a higher mortality [11]. There are several preoperative clinical predictors of LOS in a diversified surgical population. However, in the low-risk homogeneous populations often employed for clinical studies, these risk factors are no longer predictive. Furthermore, the low rates of perioperative myocardial infarction and operative mortality necessitate the recruitment of large numbers of patients in order to discriminate between treatment strategies. Alternative outcome measures are required to increase the feasibility of clinical trials in myocardial protection.

In previous clinical trials at our institution [5–8], we have observed a delayed recovery of myocardial metabolism after coronary bypass surgery. In particular, we have reported that anaerobic metabolism is induced by aortic crossclamping and cardioplegic arrest. However, in some patients, anaerobic metabolism persists even after cross-clamp removal and reperfusion. We hypothesized that persistent anaerobic metabolism, which we detect as net myocardial lactate release, is a marker of inadequate intraoperative myocardial protection and may predict early postoperative left ventricular dysfunction.

Predictors of LOS
Persistent lactate release during reperfusion was found to be the only multivariable predictor of LOS (odds ratio 5.85, 95% confidence interval 2.1 to 16.3). In a diversified surgical population, we have previously found that poor preoperative left ventricular function, repeat operation, urgent surgery for unstable angina, female gender, diabetes mellitus, age more than 70 years, left main disease, preoperative myocardial infarction, and triple vessel coronary artery disease to be independent predictors of postoperative LOS. None of these clinical risk factors predicted the development of LOS in this homogeneous study population. Although myocardial lactate release at 5 minutes of reperfusion had a poor predictive capability (area under ROC = 0.6328), it was the only significant risk factor for the development of postoperative LOS. The poor predictive capability may be due to the fact that in some patients with adequate myocardial protection, postoperative LOS may be a result of intraoperative technical problems. Lactate release during reperfusion may be highly predictive of LOS in patients who had an uneventful intraoperative course. Unfortunately, it is difficult to distinguish between the effects of inadequate myocardial protection and intraoperative misadventure as these two events may be highly correlated. For example, diffuse atherosclerotic coronary artery disease not easily amenable to bypass grafting would also preclude adequate distribution of cardioplegia. Nevertheless, the development of postoperative LOS in a patient who had an uneventful intraoperative course may be due to a delayed recovery of normal aerobic myocardial metabolism.

Relationship between lactate release and postoperative LOS
The relationship between contractile function and myocardial metabolism is not clear. Weiss and associates [10] in an isolated rabbit heart model demonstrated that aerobically produced ATP was preferentially used for contractile function while ATP produced by anaerobic glycolysis was preferentially used for sarcolemnal ion channel function. Our findings in this study support Weiss’ observation in that persistent anaerobic lactate release during reperfusion predicted early postoperative left ventricular dysfunction. There was no evidence of irreversible myocardial injury as assessed by CK-MB enzyme release, thus the metabolic abnormalities are likely transient and may be amenable to treatment. Ando and colleagues [14] found similar results in a smaller study involving 66 patients undergoing isolated CABG with or without left main coronary artery stenosis. In patients with left main disease, they observed net lactate release in the empty beating state prior to cardioplegic arrest. These patients displayed a depression in postoperative left ventricular stroke work index, suggesting that subtle changes in normal myocardial metabolism may affect postoperative functional recovery [15]. The effect of left ventricular mass on myocardial lactate release was not evaluated in this study. One would expect myocardial oxygen and lactate consumption to increase as mass increases. However, the conversion from anaerobic to aerobic metabolism (lactate consumption to production) is independent of left ventricular mass.

The exact mechanism of the derangement in normal myocardial metabolism remains unknown. Kobayashi and Neely [9] demonstrated that mitochondrial pyruvate dehydrogenase (PDH) activity was inhibited during early reperfusion after ischemia. As PDH regulates the conversion from pyruvate to acetyl-CoA, its inhibition would result in greater lactate production. Attempts to improve myocardial functional recovery after ischemia and reperfusion by stimulating mitochondrial PDH activity have been inconsistent [16–19]. Mazer and colleagues [16] employed dichloroacetate (DCA), a potent stimulator of PDH activity, in a porcine model and found improved oxidative metabolism but no effect on functional recovery. In contrast, Wahr and associates [17] demonstrated in an isolated rabbit heart model that DCA resulted in a significant improvement in left ventricular functional recovery after ischemia and reperfusion.

We have previously evaluated the effect of insulin on mitochondrial pyruvate dehydrogenase activity after simulated ischemia and reperfusion [20]. Inhibition of these enzymes would also impair normal oxidative phosphorylation and may result in inadequate functional recovery after surgery. Our results suggest that restoring normal aerobic metabolism during early reperfusion is crucial to preventing left ventricular dysfunction after surgery. We found that the metabolic differences that occurred in patients in whom LOS developed were attenuated within 10 minutes of reperfusion. In Kobayashi’s report [9], mitochondrial pyruvate dehydrogenase activity was inhibited within 2 minutes of reperfusion and remained depressed for 45 minutes. Preventing this early inhibition of mitochondrial PDH activity may prevent left ventricular dysfunction after cardioplegic arrest.

Summary
This study evaluated the relationship between myocardial metabolism and postoperative low cardiac output syndrome in patients undergoing coronary bypass surgery. We believe that this is the largest invasive study of intraoperative myocardial metabolism in patients undergoing coronary bypass surgery. The results of this study suggest that delayed recovery of normal aerobic myocardial metabolism can adversely affect the clinical results of surgery. We believe that myocardial lactate release during reperfusion is a marker of inadequate myocardial protection during cardioplegic arrest. Future clinical trials evaluating novel myoprotective strategies should aim to convert anaerobic lactate release during reperfusion to myocardial lactate extraction and oxidation. Our results suggest that improving the transition from anaerobic to aerobic metabolism after cardioplegic arrest may have a significant impact on clinical outcomes after coronary bypass surgery.

	Acknowledgments

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
This study was supported by the Medical Research Council of Canada (Grant MT1989) and the Heart and Stroke Foundation of Canada (HSFC). Joan Ivanov is a research fellow of the HSFC; Richard D. Weisel is a career investigator of the HSFC. The authors wish to thank the nursing staff of the cardiovascular intensive care unit and operating room for their cooperation with this study. The authors are indebted to the clinical perfusionists of The Toronto Hospital for their valuable assistance with the intraoperative measurements of myocardial metabolism. Laura Tumiati and Molly Mohabeer are acknowledged for their assistance in analyzing perioperative blood samples.

	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): Vivek Rao Richard D. Weisel Gideon Cohen Michael A. Borger Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rao, V. Articles by Mickle, D. A.G. Search for Related Content PubMed PubMed Citation Articles by Rao, V. Articles by Mickle, D. A.G. Related Collections Cardiac - physiology Myocardial protection