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Ann Thorac Surg 1998;66:747-754
© 1998 The Society of Thoracic Surgeons
a Division of Cardiothoracic Surgery, Emory University, Atlanta, Georgia, USA
b Division of Cardiology, Emory University, Atlanta, Georgia, USA
c Department of Biostatistics, Emory University, Atlanta, Georgia, USA
d Department of Pediatrics, Emory University, Atlanta, Georgia, USA
e Carlyle Fraser Heart Center, Crawford Long Hospital of Emory University, Atlanta, Georgia, USA
Address reprint requests to Dr Gott, Cardiac Surgery, Crawford Long Hospital, Emory University School of Medicine, 550 Peachtree St NE, Suite 7700, Atlanta, GA 30365
Presented at the Forty-fourth Annual Meeting of the Southern Thoracic Surgical Association, Naples, FL, Nov 6–8, 1997.
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Abstract |
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Methods. Four state-of-the-art strategies were studied in a prospective, randomized, preoperatively risk stratified, 400-patient study comprising primary (n = 358), reoperative (n = 42), coronary (n = 307), valve (n = 27), ascending aortic (n = 9), and combined operations (n = 23). Groups were as follows: standard, roller pump, membrane oxygenator, methylprednisolone (n = 112); aprotinin, standard plus aprotinin (n = 109); leukocyte depletion, standard plus a leukocyte filtration strategy (n = 112); and heparin-bonded circuitry, centrifugal pumping with surface modification (n = 67).
Results. Analysis of variance, linear and logistic regression, and Pearson correlation were applied. Actual mortality (2.3%) was less than half the risk stratification predicted mortality (5.7%). The treatment strategies effectively attenuated markers of the inflammatory response to extracorporeal circulation. Compared with the other groups the heparin-bonded circuit had highly significantly decreased complement activation (p = 0.00001), leukocyte filtration blunted postpump leukocytosis (p = 0.043), and the aprotinin group had less fibrinolysis (p = 0.011). Primary end points, length of stay, and hospital charges, were positively correlated with operation type, age, pump time, body surface area, stroke, pulmonary sequelae, predicted risk for stroke, predicted risk for mortality, and risk strata/treatment group interaction (p = 0.0001). In low-risk patients, leukocyte filtration reduced length of stay by 1 day (p = 0.02) and mean charges by $2,000 to $6,000 (p = 0.05). For high-risk patients, aprotinin reduced mean length of stay up to 10 fewer days (p = 0.02) and mean charges by $6,000 to $48,000 (p = 0.0007).
Conclusions. These pharmacologic and mechanical strategies significantly attenuated the inflammatory response to extracorporeal circulation. This translated variably into improved patient outcomes. The increased cost of treatment was offset for selected strategies through the added value of significantly reduced risk.
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Material and methods |
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Patients were randomized to one of four study limbs. The standard group had intravenous corticosteroid given before cardiopulmonary bypass (CPB). Methylprednisolone, 250 mg (Upjohn, Kalamazoo, MI), was given 30 to 60 minutes before standard CPB using a roller pump, membrane oxygenator (Cobe Cardiovascular, Inc, Arvada, CO), and red cell salvage (Cobe BRAT).
The aprotinin limb was the same as the standard group with the addition of a half-Hammersmith aprotinin protocol [2] (Trasylol; Bayer Corp, Pharmaceutical Division, West Haven, CT).
The leukocyte depletion strategy was based on the standard CPB protocol with addition of leukocyte filtration of the arterial line (Leukoguard AL; Pall Biomedical Products Comp, East Hills, NY), and cardioplegia delivery line (BC1B, Pall). All blood products, both intraoperatively and postoperatively, including autologous (RS1; Pall) and homologous red cells (RC400; Pall), platelets (PXLAR, Pall), and fresh frozen plasma (LPS; Pall) were filtered.
The fourth study limb used heparin-bonded circuitry, membrane oxygenator, and a centrifugal pump (Carmeda, Medtronic Inc, Minneapolis, MN). Methylprednisolone was given preoperatively, as it was in all groups.
The temperature of all patients was allowed to drift to 32° to 34°C on CPB. Cardioplegic arrest technique was uniform across groups and among the surgeons. Blood cardioplegia was given antegrade for arrest with maintenance cardioplegia delivered continuously retrograde for the duration of the cross-clamp period.
Data collection, definitions, and statistical methods
The sample included all patients who presented to Crawford Long Hospital for cardiac operation between August 1995 and April 1996 who met eligibility criteria and chose to participate. Those excluded were less than 18 years of age, unable to give consent, undergoing an emergent operation, pregnant, suspected to be allergic to aprotinin, had a previously documented coagulation diathesis, declined receipt of blood products if needed, could not meet the requirements of the uniform myocardial protection scheme, required mechanical circulatory support other than an intraaortic balloon pump, or were having a planned period of circulatory arrest. Three quarters of the way through the study the Carmeda heparin-bonded circuitry was withdrawn from the market. Randomization was then converted to three limbs for the remainder of the study. Nine patients became ineligible after enrollment when intraoperative decisions by the surgeons led to a change in the myocardial protection plan. Nine additional patients were enrolled and randomized to reach the goal of 400 patients.
Preoperative data collected on all patients included complete blood count and creatinine, demographic information (age, sex, body surface area, and proposed operation), risk stratification, and an electrocardiogram. Static and dynamic lung compliance was recorded before and after closure of the sternotomy and 4 hours after arrival in the intensive care unit. In a subsample of patients in each group, indicators of activation of the inflammatory response and coagulation system were measured. Transfusion requirements were documented. The duration of CPB and aortic cross-clamp time were recorded. Serial cardiac isoenzyme levels were measured on arrival to the intensive care unit, and at 8 and 16 hours after cross-clamp removal. Electrocardiograms were done on arrival at the intensive care unit, 12 and 24 hours after the removal of the aortic cross-clamp.
Chest tube drainage was recorded at 6, 12, and 24 hours postoperatively. The hemoglobin level, hematocrit, red blood cell count, platelet count, and creatinine level were measured on postoperative days 1 and 4 and at discharge. The leukocyte count was measured immediately before and after CPB, postoperative days 1 and 4, and at the time of discharge if delayed.
Neurologic, cardiac, pulmonary, renal, and hematologic variables, rhythm disturbances, and infections were assessed as composite end points. These definitions follow: neurologic composite morbidity: transient or permanent new focal central nervous system deficit; cardiac: perioperative infarction as determined by correlation of serial cardiac isoenzyme levels and electrocardiogram interpretation by a cardiologist blinded to patient identification, new postoperative heart failure, prolonged (>48 hours) inotropic support, or balloon counterpulsation after CPB; pulmonary: ventilatory support for more than 48 hours, pneumonia, hypoxemia, pleural effusion, pneumothorax, prolonged air leak, or aspiration; renal: any increase in creatinine level from normal to >2 mg/dL or a new dialysis requirement; infection: wound or urinary tract infection, bacteremia, or bronchitis; rhythm: any arrhythmia requiring treatment; hematologic: platelet, fresh frozen plasma, or cryoprecipitate transfusion or reentry for bleeding.
Mortality rate, length of stay, and hospital charges were compiled. Measures of central tendency described the sample and the independent variables. The effect of randomization on groups was assessed. The groups were risk stratified and compared by treatment group and risk using analysis of variance and Tukey’s HSD. Comparisons were made to detect differences among groups regarding the composite clinical end points. Repeated measures analysis of variance was used as means to detect differences among groups in the laboratory values collected over time. Linear multiple regression was used to identify independent predictors and a predictor model for both length of stay and hospital charges. The multiple R and F statistic for the model are reported. The semipartial r2 and the respective 
are reported and represent the unique variance accounted for by each independent variable. Logistic multiple regression was used to generate a model of mortality yielding an odds ratio predictive of mortality within the context of the independent variables.
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Hematologic complications did not demonstrate a group effect. However, excessive bleeding significantly increased length of stay and hospital charges. Chest tube drainage was significantly lower for the aprotinin group (Fig 2 ).
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The electrocardiographic determination of postoperative myocardial infarct and the level of creatine kinase isoenzyme correlated (p = 0.001); however, there was no significant treatment group association. Cardiac morbidity was low and not significantly associated with increased length of stay or charges.
Multivariate analysis of hospital charges generally paralleled the findings for length of stay (Table 4 and Fig 4 ). After identification of group effect, Tukey’s HSD was used to isolate where significance lay. For low-risk patients, leukocyte filtration demonstrated significant advantage compared with standard (Fig 4). For medium-risk patients, there was no statistically significant treatment difference detected. For the high-risk group, aprotinin had a powerful effect in both reduction of hospital charges and length of stay with most of the difference being accounted for in comparison with the heparin-coated circuit limb.
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Comment |
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Each of the antiinflammatory strategies in the study has a constituency. The existing literature does not clearly support one of these strategies for universal application or for a specific group of patients [3–6]. As only a few multiple comparisons such as this study exist, it is difficult to reconcile the purported advantages and disadvantages of each technique and develop a rational clinical strategy. This study was designed to include multiple leading-edge treatments and examine effects over a range of patient types.
The premise that the conditions of exposure to extracorporeal circulation are closely correlated with patient outcome was integral to the study design. Time on the heart-lung machine was assumed to be a critical determinant of the degree of diffuse inflammatory injury. Therefore, the design was inclusive of a broad spectrum of adult cardiac operations.
A second premise was that all patients do not present the same inherent risk. Some patients have risk approaching zero, for example, the low-risk, young, otherwise healthy, atrial septal defect patient, versus the failing, elderly, multivalve, coronary bypass patient at the other end of the risk spectrum. This study design incorporated a mechanism to examine these patient-specific effects.
Risk recognition and risk stratification have received wide acceptance in cardiac surgery over the past decade. The next logical step was to focus on factors associated with patient risk and develop and test strategies designed to improve the margin of safety and lead to risk neutralization. The evolution of myocardial protection techniques is such a model. Previous laboratory and clinical research and development led to the application of a cardioplegic technique suitable for 98% of those enrolled in this study. Cardiac morbidity in the context of increased charges or length of stay was conspicuously absent as a risk factor in the multivariate analyses here.
The key advantage of corticosteroid use is an extremely inexpensive, generalized immunosuppression [7]. Potential disadvantages include exacerbation of glucose intolerance, gastritis, impaired wound healing, and increased risk of infection. Advances in understanding of glucocorticosteroid use suggest areas for improvement in this strategy as it relates to prophylaxis against extracorporeal circulation injury. Revision of the timing of administration of corticosteroid to 8 to 12 hours before CPB should allow the antiinflammatory effect to coincide with the insult [8].
The beneficial effects of aprotinin for reduction of postoperative bleeding were evident here [2, 9, 10]. Chest tube output was significantly less and hemoglobin level significantly higher on the first postoperative day compared with the other groups. The pronounced antifibrinolytic effect was corroborated by the significant reduction in d-dimer formation seen here. The results in the high-risk stratum imply that the mechanism of benefit of aprotinin exceeds its important role in protection of coagulation after extracorporeal circulation through a more generalized inhibition of inflammation [3]. The significant improvement in length of stay and tandem suppression of hospital charges for the high-risk patient far outweigh the initial cost of this treatment.
Leukoreduction of transfused blood products has been shown to reduce infection postoperatively [11–13]. Leukocyte depletion has been demonstrated clinically to improve myocardial protection in some settings [14–17]. The clinical practicality of incorporating leukocyte filtration into the CPB circuit has been demonstrated [18, 19]. A leukocyte depletion strategy was developed incorporating all of these approaches. The strategy was effective in eliminating the increase in leukocyte count after CPB compared with the other three strategies. For the low-risk stratum there was a significantly beneficial effect on length of stay and hospital charges. As with the other strategies, questions about mechanism remain. The study design does not allow firm statements about whether suppression of the usual leukocytosis associated with extracorporeal circulation is a mechanism by which benefit was derived. The beneficial effect may be related not so much to decreasing the count, but to removal of a certain activated leukocyte subpopulation, known to be a culprit in the inflammatory reaction to extracorporeal circulation [20]. Another unanswered question is why the benefit of leukoreduction was not as profound in the medium- and high-risk strata. No deleterious effects were recognized from this prevention of the characteristic leukocytosis usually associated with extracorporeal circulation.
The suppression of the inflammatory response to extracorporeal circulation has been demonstrated using CPB circuit surface modification with covalently or ionically bound heparin [21, 22]. The question of degree of translation of this phenomenon into patient benefit remains open. The interpretation of this limb of this trial should be in the light of three special issues: a reduced number of patients compared with other strategies because of the unforeseen interruption of clinical availability of the technology during this study, no modification of systemic heparinization protocol that may have tended to negate potential reduction of postoperative bleeding [23, 24], and an insignificant trend toward longer CPB duration in this limb of the study. Complement activation was highly significantly reduced in the heparin-bonded circuit group. This did not translate into a recognized clinical benefit. The postpump protection of pulmonary function seen in animal models was not duplicated here in patients. Perioperative static and dynamic pulmonary compliance studies showed no comparative advantage for heparin-bonded circuitry. The higher initial cost and inability to demonstrate added value relegates this technology at present to a secondary role.
These data point clearly to areas of weakness in current protective strategies for extracorporeal circulation. The pulmonary, central nervous system, and hematologic systems remain prime targets for risk and expenditure reduction. Strategies that significantly reduce the diffuse inflammatory response to extracorporeal circulation do not uniformly translate into improved clinical outcomes for patients. There is great value in this risk stratification design for comparative evaluation of new strategies. The potential for beneficial synergism between strategies warrants study.
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R. C. Landis, D. O. Haskard, and K. M. Taylor New antiinflammatory and platelet-preserving effects of aprotinin Ann. Thorac. Surg., November 1, 2001; 72(5): S1808 - 1813. [Abstract] [Full Text] [PDF]
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H. A. Hennein Inflammation After Cardiopulmonary Bypass: Therapy for the Postpump Syndrome Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2001; 5(3): 236 - 255. [Abstract] [PDF]
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G Matheis, M Scholz, A Simon, O. Dzemali, and A Moritz Leukocyte filtration in cardiac surgery: a review Perfusion, September 1, 2001; 16(5): 361 - 370. [Abstract] [PDF]
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S J Morris Leukocyte reduction in cardiovascular surgery Perfusion, September 1, 2001; 16(5): 371 - 380. [PDF]
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G. Asimakopoulos, E. A. Lidington, J. Mason, D. O. Haskard, K. M. Taylor, and R. C. Landis Effect of aprotinin on endothelial cell activation J. Thorac. Cardiovasc. Surg., July 1, 2001; 122(1): 123 - 128. [Abstract] [Full Text] [PDF]
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J. Boldt, C. Brosch, A. Lehmann, G. Haisch, J. Lang, and F. Isgro Prophylactic use of pentoxifylline on inflammation in elderly cardiac surgery patients Ann. Thorac. Surg., May 1, 2001; 71(5): 1524 - 1529. [Abstract] [Full Text] [PDF]
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 E. C. Vamvakas and M. A. Blajchman Deleterious clinical effects of transfusion-associated immunomodulation: fact or fiction? Blood, March 1, 2001; 97(5): 1180 - 1195. [Full Text] [PDF]
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J. P. Gott Leukodepletion and aprotinin improve clinical outcome after extracorporeal circulation Perfusion, January 1, 2001; 16(1_suppl): 5 - 9. [Abstract] [PDF]
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G Matheis, M Scholz, A Simon, D Henrich, G Wimmer-Greinecker, and A Moritz Timing of leukocyte filtration during cardiopulmonary bypass Perfusion, January 1, 2001; 16(1_suppl): 31 - 37. [Abstract] [PDF]
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M. B Patel, K. S Kilgore, G. A Ortolano, C. L Gryboski, M. A Qureshi, P. Marcovitz, K. B Naylor, J. L Park, B. Wenz, N. Gikakis, et al. Conditioned blood reperfusion during angioplasty (CoBRA) treatment of acute myocardial infarction Perfusion, January 1, 2001; 16(1_suppl): 39 - 49. [Abstract] [PDF]
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M. S. Ali, M. Harmer, and R. Vaughan Serum S100 protein as a marker of cerebral damage during cardiac surgery Br. J. Anaesth., August 1, 2000; 85(2): 287 - 298. [Abstract] [Full Text] [PDF]
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A. D. Sharma, G. Sreeram, T. Erb, H. P. Grocott, and T. F. Slaughter Leukocyte-Reduced Blood Transfusions: Perioperative Indications, Adverse Effects, and Cost Analysis Anesth. Analg., June 1, 2000; 90(6): 1315 - 1323. [Full Text] [PDF]
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G. Asimakopoulos, A. Kohn, D. C. Stefanou, D. O. Haskard, R. C. Landis, and K. M. Taylor Leukocyte integrin expression in patients undergoing cardiopulmonary bypass Ann. Thorac. Surg., April 1, 2000; 69(4): 1192 - 1197. [Abstract] [Full Text] [PDF]
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R. Ascione, C. T. Lloyd, M. J. Underwood, A. A. Lotto, A. A. Pitsis, and G. D. Angelini Inflammatory response after coronary revascularization with or without cardiopulmonary bypass Ann. Thorac. Surg., April 1, 2000; 69(4): 1198 - 1204. [Abstract] [Full Text] [PDF]
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M. A. Chaney, M. P. Nikolov, M. Sumida, and M. Kawamata Methylprednisolone and the Systemic Inflammatory Response Syndrome • Response Anesth. Analg., November 1, 1999; 89(5): 1333 - 1333. [Full Text] [PDF]
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G. Asimakopoulos, P. L.C. Smith, C. P. Ratnatunga, and K. M. Taylor Lung injury and acute respiratory distress syndrome after cardiopulmonary bypass Ann. Thorac. Surg., September 1, 1999; 68(3): 1107 - 1115. [Abstract] [Full Text] [PDF]
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 J. E. Jordan, Z.-Q. Zhao, and J. Vinten-Johansen The role of neutrophils in myocardial ischemia-reperfusion injury Cardiovasc Res, September 1, 1999; 43(4): 860 - 878. [Abstract] [Full Text] [PDF]
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J. D. Puskas, C. E. Wright, R. S. Ronson, W. M. Brown III, J. P. Gott, and R. A. Guyton Off-pump multivessel coronary bypass via sternotomy is safe and effective Ann. Thorac. Surg., September 1, 1998; 66(3): 1068 - 1072. [Abstract] [Full Text] [PDF]
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0.004). (C) The antifibrinolytic effect of aprotinin was evidenced by significantly lower d-dimer levels after extracorporeal circulation (*p = 0.01). (A = aprotinin; H = heparin-bonded circuitry; L = leukocyte depletion; S = standard.)