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Ann Thorac Surg 1996;62:410-418
© 1996 The Society of Thoracic Surgeons
Department of Cardiothoracic Surgery, Boston University Medical Center, Boston, Massachusetts
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Abstract |
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Methods. A prospective randomized trial was undertaken to test the hypothesis that "tip-to-tip" heparin-bonded cardiopulmonary bypass circuits (HBC) can further enhance blood conservation and clinical outcomes in patients undergoing primary coronary artery bypass grafting. Two hundred thirty-four patients were treated with either HBC and lower anticoagulation therapy (activated clotting time >280 seconds) or with conventional, nonheparin-bonded circuits and full anticoagulation therapy (activated clotting time >480 seconds).
Results. Preoperative and intraoperative risk profiles and characteristics were similar in both groups, with 69.7% of the patients undergoing nonelective coronary artery bypass grafting. Compared with the group with nonheparin-bonded circuits, patients treated with HBC had a lower chest tube output in the first 24 hours (561 ± 257 versus 651 ± 403; p = 0.04), were less likely to receive blood products (31.6% versus 47.9%; p = 0.01), and required substantially fewer homologous donor units (1.98 ± 4.8 versus 4.29 ± 10.1; p = 0.029). Patients treated with HBC required a shorter duration of ventilatory support (13.2 ± 16.9 versus 23.4 ± 50.0 hours; p = 0.04), spent less time in the surgical intensive care unit (20.7 ± 17.4 versus 35.5 ± 61.7 hours; p = 0.01), spent fewer days in the hospital (6.0 ± 2.5 versus 7.3 ± 5.2 days; p = 0.02), and had fewer postoperative complications (25.6% versus 39.3%; p = 0.03). The use of HBC with a lower anticoagulation protocol was not associated with any adverse events.
Conclusions. This study demonstrates that the use of HBC with a lower anticoagulation protocol in primary coronary artery bypass grafting safely and effectively reduces the incidence and magnitude of homologous transfusion, the duration of ventilation, and surgical intensive care unit and hospital stays.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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As many as 30% to 70% of patients undergoing coronary artery bypass grafting (CABG) require homologous transfusions [1]. Many blood-conservation strategies are currently being used during CABG, including cell saving [1], use of large-bore directional cannulas to decrease shear rates [2], routine use of antifibrinolytic agents [3, 4], normothermic bypass to decrease coagulopathy [5], closed venous reservoir and membrane oxygenators to decrease the blood-air interface [6], low cardiopulmonary bypass (CPB) prime to decrease dilution of coagulation factors, precise heparin and protamine titration [7, 8], stricter transfusion threshold protocols, and postoperative reinfusion of shed blood. Despite the efficacy of these individual strategies, they have not been applied uniformly because of their perceived complexity and cost.
Full systemic anticoagulation with heparin to achieve a target activated clotting time (ACT) greater than 480 seconds has been the "gold standard" of practice during CPB [9]. Recently, investigators have questioned this standard and suggested that an ACT of greater than 300 seconds is equally safe [10, 11]. Heparin, independent of CPB, could cause postoperative platelet dysfunction and fibrinolysis [8]. If lower doses of heparin could be given safely without an increased thromboembolic risk, less postoperative hemostatic disturbance may occur.
The bonding of heparin to all the surfaces that come into contact with blood during CPB was developed in an attempt to limit the blood-material reaction, enhance biocompatibility and thromboresistance, and limit the postperfusion syndrome [11–16]. The few large clinical studies of heparin-bonded bypass circuits (HBC) have demonstrated a decrease in chest tube drainage and autologous blood reinfusion without thromboembolic events [11, 12]. There was no substantial impact on homologous transfusion or other relevant end points. Therefore, the use of HBC has been limited to high-risk patients.
The failure of previous studies to demonstrate a definitive clinical benefit from the use of HBC was possibly due to its application in an elective, low-risk patient group that did not require any homologous transfusions [11, 12]. This study was designed to answer the question of whether using HBC with a lower anticoagulation protocol could further improve blood conservation and clinical outcomes in a consecutive group undergoing primary CABG.
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Material and Methods |
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A prospective, randomized study was undertaken to include all patients undergoing primary CABG. Only catheterization laboratory emergencies and reoperations were excluded (these patients were treated with HBC and lower anticoagulation protocols exclusively). The study was not double blinded to the operating surgeons, but was blinded to the nurses and the surgical intensive care unit (SICU) team. Standardized transfusion thresholds and protocol, extubation protocol, and SICU and hospital management pathways were applied uniformly to all patients. To eliminate variability among surgeons and perfusionists, all the components, configuration, and techniques of CPB were standardized. The study was reviewed and approved by the Boston University Medical Center Institutional Review Board (IRB protocol number 3610, approved July 1994).
Patients undergoing primary CABG were randomly assigned to one of two treatment groups: HBC with lower anticoagulation therapy (ACT >280 seconds) or an identical, conventional nonheparin-bonded circuit (NHBC) with full anticoagulation (ACT >480 seconds). The HBC group was equally divided between the ionically bonded heparin circuits (Duraflo II; Baxter, Irvine, CA) and the covalently bound heparin circuits with end-point attachment (Carmeda; Medtronic Inc, Minneapolis, MN). Two hundred fifty-six consecutive patients undergoing CABG within a 6-month period were evaluated and 234 patients were randomized, representing an accrual of 91.4% of eligible patients. Nine patients refused randomization (were treated with NHBC), and 13 others were treated off protocol with HBC at their surgeon's request (9 Jehovah's Witnesses and 4 with recent cerebrovascular accident or acute gastrointestinal bleeding requiring transfusion within a month of CABG). Differences in treatment protocol between the HBC and NHBC patients are delineated later.
Cardiopulmonary Bypass Circuit
In the HBC group, the entire CPB circuit ("tip-to-tip") was heparin bonded. The HBC consisted of a two-stage venous cannula (34/48F), a directional arterial cannula (20/22F), cardioplegia multiple perfusion set, cardioplegia antegrade and retrograde administration catheters (DLP Inc, Grand Rapids, MI), all the CPB tubing and connectors, low prime (1,200 to 1,500 mL), and membrane oxygenator with closed venous reservoir, cardiotomy reservoir, and suckers. In the control group, identical conventional NHBC were used. Centrifugal pumps were used exclusively in both groups.
Anticoagulation Protocol and Cardiopulmonary Bypass Technique
In the HBC group, the heparin dose was measured by a dose-response assay using the Hepcon Heparin Management System (Medtronic Inc) titrated to achieve and maintain an ACT greater than 280 seconds. In the control (NHBC) group, the heparin dose was measured by a dose-response assay using the Hepcon Heparin Management System titrated to achieve and maintain an ACT greater than 480 seconds. In both groups, the ACT was checked every 20 minutes throughout CPB. We initiated CPB slowly with an empty (closed) venous reservoir and a low volume (1,200 to 1,500 mL) of Plasmalyte prime (Travenol, Baxter). Once the venous reservoir was filled, flow was increased to maintain venous saturation of 60% to 75%. Core temperature was not allowed to drift below 34°C, and active cooling was avoided. During the entire procedure, all field drainage was directed to a cell-saving device (Haemonetics Corp, Braintree, MA). In both groups, no discard suckers were used; all sponges were soaked in saline solution, wrung into a sterile reservoir by the scrub nurse, and directed to the cell-saving device. Cardiotomy pump suckers were used sparingly and only in the event of substantial and active bleeding.
Myocardial Protection
Myocardial protection techniques were identical in the HBC and NHBC groups. In both groups, priming of the blood cardioplegia line was performed on CPB with blood; we avoided crystalloid priming. Cold (4°C) blood cardioplegia was administered in an antegrade fashion in all patients and was supplemented with retrograde cardioplegia in most patients. In all patients, cardioplegia was also administered down the saphenous grafts. Cardioplegia was readministered every 20 minutes while the cross clamp was applied. In the HBC group, before each cardioplegia dose, 50 to 100 mL of cardioplegia, presumed to be stagnant in the tubing, was discarded to the operative field and directed to the cell-saving device. Topical cooling with cold saline solution was used to supplement myocardial protection in both groups.
Weaning From Cardiopulmonary Bypass and Reversal of Anticoagulation
Patients were actively warmed to a core temperature of 37°C before weaning from CPB. Once they were weaned from bypass, a test dose of protamine was administered (Elkins-Sunn, Cherry Hill, NJ) and the cannulas were removed promptly. To avoid blood stagnation in the HBC group after line clamping, the circuit was continuously recirculated. After hemodynamic stability was confirmed (after the protamine test dose), the arterial, venous, pump sucker, and cardioplegia lines were quickly drained of blood by retrograde siphoning, the lines were refilled (and air was removed) with crystalloid, and the blood was directed to the cell-saving device. A crystalloid primed circuit was thus available in the event of hemodynamic deterioration. In both groups, the protamine reversal dose were verified and titrated by the Hepcon Heparin Management System. In the NHBC group, Amicar (American Reagent, Shirley, NY) was administered as a 10-g intravenous infusion loading dose administered after heparin administration and before initiation of CPB. The dose was given over 30 minutes and was followed by a 10-g intravenous continuous infusion administered over 5 hours. In the HBC group, Amicar was administered as a 10-g intravenous infusion loading dose begun after protamine administration and decannulation. This dose was given over 30 minutes, followed by a 10-g intravenous continuous infusion administered over 5 hours. Aprotinin was not used in either treatment group.
Transfusion Practice
Patients had red blood cell transfusion if the intraoperative hematocrit during CPB fell below 20% or if the postoperative (SICU) hematocrit decreased to less than 25%. After protamine administration, the ACT was checked, and circulating heparin was identified and reversed with doses titrated by the Hepcon Heparin Management System. All operatively correctable bleeding was carefully addressed. Persistent postoperative bleeding in excess of 300 mL in the first hour or 500 mL in the first 2 hours was considered an indication for transfusion of platelets (5 to 10 U) and fresh frozen plasma (2 U).
Statistics
All data and figures are presented as mean ± standard deviation. Continuous variables were evaluated by Student's t test or analysis of variance, and categoric variables were tested by 
2 or Fisher's exact test, where appropriate. Absolute p values were reported. Data were considered significant at p < 0.05.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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). No statistical differences between preoperative and discharge hematologic indices were noted between the treatment groups (Table 2). Both the initial heparin dose (148 ± 46 versus 263 ± 62 USP/kg; p = 1.45 x 10-40; 44% reduction) and the total heparin dose (175.71 ± 61.91 versus 409.69 ± 292.14 USP/kg; p = 2.7 x 10-15; 57.1% reduction) were significantly lower in the HBC group. The protamine dose also differed significantly between the HBC and NHBC groups (123 ± 52 versus 222 ± 82 mg; p = 5.21 x 10-23; 45% reduction). The ACT values at the initiation of CPB and at the end of CPB were significantly lower in the HBC group (initial: 385 ± 73 versus 556 ± 98 seconds, p = 1.4 x 10-32; end: 294 ± 48 versus 403 ± 54 seconds, p = 2.5 x 10-36). The total amount of shed pleural and mediastinal blood measured from the time of sternal closure was lower in the HBC patients at 12 hours (408 ± 197 versus 476 ± 342 mL; p = 0.05) and at 24 hours (561 ± 257 versus 651 ± 403 mL; p = 0.04). Compared with patients treated with NHBC, patients treated with HBC were less likely to have transfusions (31.6% versus 47.0%, p = 0.016; 33% reduction). The transfusion requirements for homologous packed red blood cells and fresh frozen plasma were significantly lower in the HBC group (Table 3). The total homologous donor exposure was significantly reduced in the HBC group (1.98 ± 4.7 versus 4.3 ± 10.1 U, p = 0.026; 54% reduction). The magnitude of homologous transfusion (total unit exposure) was reduced both in patients treated with aspirin and heparin before CABG (2.72 ± 3.51 versus 5.16 ± 8.50 U, p = 0.05; 47% reduction) and in patients not treated with aspirin or heparin before CABG (0.18 ± 0.63 versus 2.43 ± 5.80 U, p = 0.026; 94% reduction) (Table 4). Patients treated with HBC had a shorter duration of ventilatory support (13.2 ± 16.9 versus 23.4 ± 50.0 hours; p = 0.038), as well as shorter SICU stay (20.7 ± 17.4 versus 35.5 ± 61.1 hours; p = 0.01) and overall hospital stay (6.03 ± 2.50 versus 7.31 ± 5.23 days; p = 0.018).
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). The unadjusted mortality rate and other comorbidities did not reach statistical significance, but all tended to be lower in the HBC group (Table 5).
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We analyzed the effects of the magnitude of homologous transfusion and the duration of ventilatory support on hospital stay for all 234 patients (HBC plus NHBC) to understand better how the use of HBC improved hospital stays. In these 234 patients, we were able to demonstrate a relation between the magnitude of homologous transfusion and hospital length of stay. Patients who did not receive any homologous transfusions were discharged on postoperative day 5.39 ± 1.47; those receiving one to two transfusions of homologous blood were discharged on postoperative day 7.30 ± 3.90 (p < 0.001 versus no transfusion, by analysis of variance); those receiving more than five homologous blood units were discharged on postoperative day 10.19 ± 7.69 (p < 0.0001 versus no transfusion) (Table 6). The magnitude of homologous transfusion was also related to postoperative weight gain (presented as a percentage of preoperative weight). Patients who received no homologous transfusions gained less weight than patients who received more than 5 U (4.24% ± 2.99% versus 8.17% ± 5.93%; p < 0.001). The effects of reduced homologous transfusions and shorter SICU and hospital stays translated into substantial cost savings (Table 7). Total hospital charges were also substantially lower in patients treated with HBC ($39,332 ± $10,998 versus $44,777 ± $20,209; p < 0.05).
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Comment |
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Several approaches to minimize blood activation during CPB have been used, including: (1) pharmacologic intervention, (2) alteration of blood flow characteristics, and (3) alteration of the materials and surfaces of the CPB circuit. This investigation was designed to use all these strategies to enhance biocompatibility.
Pharmacologic Intervention
The most commonly used pharmacologic intervention during CPB is systemic anticoagulation therapy with heparin to achieve the "gold standard" target ACT of greater than 480 seconds [9]. Recently, investigators have suggested that an ACT greater than 300 seconds is equally safe and effective [10, 11].
Additional pharmacologic interventions target post-CPB fibrinolysis. Contact with artificial biomaterial surfaces activates factor XII, leading to activation of the intrinsic coagulation system, the fibrinolytic, and the complement systems. The antifibrinolytic agent Amicar (
-aminocaproic acid), with its demonstrated efficacy to decrease perioperative blood loss and transfusion requirement, was used routinely in all patients [3]. Protocols differed in this study depending on the type of extracorporeal circuit used. Concerns regarding the promotion of coagulation with Amicar in the presence of lower heparin doses in the HBC patients led to Amicar administration only after weaning from CPB, decannulation, and protamine reversal. Previous investigations suggested that a post-CPB protocol with conventional CPB is less effective than a pre-CPB administration protocol. Therefore, our findings of diminished blood drainage and a reduced incidence and magnitude of homologous transfusion in the HBC-treated patients appear to have added importance because the more effective Amicar administration protocol was used in the NHBC-treated patients. Aprotinin (Trasylol; Bayer-Miles, Inc, West Haven, CT) was not used in this study because of considerations of cost and safety with HBC [4, 21–23].
Alteration in Blood Flow Characteristics
Advances in the design of CPB devices have streamlined blood flow to minimize stagnation. In addition, we attempted to improve blood flow characteristics further to minimize shear stresses. This was accomplished by using large-bore venous cannulas (to facilitate drainage), large-bore directional arterial cannulas, and centrifugal pumps. The air-blood interface was also minimized by using closed venous reservoirs and hollow-fiber membrane oxygenators, as well as by strictly limiting the use of cardiotomy suction.
Alterations in Materials and Surfaces of the Cardiopulmonary Bypass Circuit
Because of the inherent thrombogenicity of the CPB circuit, numerous attempts have been made to improve biocompatibility by immobilizing various antithrombotic agents such as heparin, hirudin, urokinase, and prostacyclin. The demonstration that some materials, particularly nylon, preferentially activate C3a and C5a [24] led to the removal of these materials from cardiotomies and bubble oxygenators. Platelet depletion, fibrin formation, and high pressure drops across nylon arterial filters were also demonstrated, which led to the replacement of this material with less thrombogenic polyester [25].
Immobilization of heparin, first described by Gott and associates [26], appears to be most promising. Heparin causes a change in the configuration of antithrombin III, increasing its inhibitory effect on factors IIa and Xa (which are formed in the later stages of the coagulation cascade) by 1,000-fold. The effects of heparin on factor XIIf, kallikrein, and factor XIa are substantially weaker. Even in the presence of full anticoagulation (ACT >480 seconds), thrombin generation (as measured by F1.2, fibrinopeptide A, and thrombin-antithrombin complexes) [12, 18, 27] increases slowly but progressively during CPB in proportion to the duration of extracorporeal perfusion. Thrombin generation is noted to increase further after the release of the aortic cross-clamp. The amount of thrombin formed during CPB is nonetheless small, particularly when compared with the 5- to 10-fold increase in thrombin generation noted 2 to 4 hours after the termination of CPB [28].
Heparin, immobilized onto the CPB circuit, catalyzes antithrombin III activity but is not consumed. Surface-immobilized heparin circuits have been demonstrated to inhibit complement activation [29], neutrophil activation, and sequestration; to improve platelet preservation and function (decreasing adhesion and pulmonary sequestration of platelets, fibrinopeptide A, and platelet factor 4 release) [16, 30, 31]; and to decrease thromboembolic debris [14].
Plasma proteins are adsorbed onto the surfaces of CPB within seconds after the initiation of CPB. It is this blood-adsorbed protein interaction that determines the character of the response to CPB [17, 18]. Adsorbed fibrinogen is highly reactive, causing platelet adherence and activation and promoting thrombus formation [32]. Whereas protein adsorption may neutralize some of the beneficial effects of coating, fibrinogen adsorption was demonstrated to be significantly diminished on the surface of HBC compared with NHBC and may contribute to its diminished thrombogenicity [33]. These differences in the surface protein mosaic are thought to be responsible for the biologic differences among various surfaces. Clinically, investigators have demonstrated either no change or diminished thrombin formation (measured by thrombin-antithrombin and F1.2) [12, 18, 30–32, 34] when HBC were compared with NHBC and full anticoagulation. No studies have demonstrated increased thrombin formation with HBC. Moreover, no significant changes in the generation of thrombin-antithrombin, F1.2, ß-thromboglobulin, D-dimer, fibrinogen, fibrinolytic activity, or platelet activation were noted when lower anticoagulation therapy (ACT >250 seconds) was compared with full anticoagulation therapy (ACT >450 seconds) when HBC were used [12, 34]. Thus, both experimental and clinical studies have suggested that HBC improve biocompatibility, as reflected in the reduction in complement, neutrophil, and platelet activation, with no increased thromboembolic complications even in the presence of lower anticoagulation protocols.
This study demonstrated a decrease in shed pleural and mediastinal blood, confirming previous studies. More important, this study demonstrated a significant decrease in the incidence and magnitude of homologous transfusions in patients undergoing primary CABG treated with HBC and a lower anticoagulation protocol. The use of HBC also resulted in a diminished duration of ventilatory support, as well as shorter SICU and hospital stays. The exact mechanism for these findings is unknown. The relation between the need for and magnitude of transfusion and clinical outcomes was striking. In these 234 patients, an important relation existed between the magnitude of homologous transfusion and the hospital length of stay. Even patients receiving only one to two homologous units had a longer hospital stay than patients who did not receive any homologous blood. The duration of ventilation and the ability to extubate patients before 12 hours postoperatively were also related to the length of hospital stay. The data suggest that the decreased duration of ventilatory support and the decrease in the SICU and hospital stays in patients treated with HBC may reflect the diminished inflammatory response to CPB with its resultant pulmonary dysfunction [20], the lower incidence and magnitude of homologous transfusion, and the fewer postoperative complications. The effects of reduced transfusion and shorter SICU and hospital stays translated into substantial cost savings, which must be weighed against the cost of the circuits.
The use of HBC and a lower anticoagulation protocol in this study was not associated with any adverse events. Furthermore, the incidence of perioperative myocardial infarction, postoperative inotropic support, thromboembolic complications (myocardial infarction plus cerebrovascular accident/transient ischemic attack), excessive ventilatory support, and the overall incidence of complications were statistically lower in patients treated with HBC and with lower anticoagulation. The use of HBC with lower anticoagulation therapy has evolved to ensure efficacy and patient safety. However, the limitations of the technique should be clearly understood [11, 12]. These concerns are common to all CPB modalities, but may be accentuated in the presence of lower anticoagulation treatment. Identification of patients with antithrombin III deficiencies or patients with other hypercoagulable states, avoidance of blood stagnation, and avoidance of intraoperative administration of drugs that may shift the balance of hemostasis and promote thrombosis are essential to avoid complications while preserving the benefits this study has demonstrated.
In summary, the use of HBC with a lower anticoagulation protocol was compared in a prospective, randomized study with the use of conventional NHBC with full anticoagulation in patients undergoing CABG. The use of HBC with lower anticoagulation treatment was safe and effective in reducing both the incidence and magnitude of homologous transfusions. This resulted in significant improvements in the duration of ventilatory support and in SICU and hospital stays, and in a substantial reduction of hospital costs. The use of these circuits need not be restricted to the higher-risk CPB patient, but should be considered for all appropriate patients.
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Acknowledgments |
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We thank Mrs Regina Lynch for her secretarial assistance in coordinating this study and in the preparation of the manuscript.
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Address reprint requests to Dr Aldea, Department of Cardiothoracic Surgery, Boston University Medical Center, 88 E Newton, Boston, MA 02118-2393.
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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S. Svenmarker, E. Sandstrom, T. Karlsson, S. Haggmark, E. Jansson, M. Appelblad, R. Lindholm, and T. Aberg Neurological and general outcome in low-risk coronary artery bypass patients using heparin coated circuits Eur. J. Cardiothorac. Surg., January 1, 2001; 19(1): 47 - 53. [Abstract] [Full Text] [PDF]
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C. Olsson, A. Siegbahn, E. Halden, B. Nilsson, P. Venge, and S. Thelin No benefit of reduced heparinization in thoracic aortic operation with heparin-coated bypass circuits Ann. Thorac. Surg., March 1, 2000; 69(3): 743 - 749. [Abstract] [Full Text] [PDF]
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O. M. Shapira, G. Akopian, A. Hussain, M. Adelstein, H. L. Lazar, G. S. Aldea, and R. J. Shemin Improved clinical outcomes in patients undergoing coronary artery bypass grafting with coronary endarterectomy Ann. Thorac. Surg., December 1, 1999; 68(6): 2273 - 2278. [Abstract] [Full Text] [PDF]
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S. Wan, J.-L. LeClerc, M. Antoine, J.-M. DeSmet, A. P.C. Yim, and J.-L. Vincent Heparin-coated circuits reduce myocardial injury in heart or heart-lung transplantation: a prospective, randomized study Ann. Thorac. Surg., October 1, 1999; 68(4): 1230 - 1235. [Abstract] [Full Text] [PDF]
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H. Kumano, S. Suehiro, K. Hattori, T. Shibata, Y. Sasaki, M. Hosono, and H. Kinoshita Coagulofibrinolysis during heparin-coated cardiopulmonary bypass with reduced heparinization Ann. Thorac. Surg., October 1, 1999; 68(4): 1252 - 1256. [Abstract] [Full Text] [PDF]
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H. L. Lazar, Y. Bao, J. Gaudiani, S. Rivers, and H. Marsh Total Complement Inhibition : An Effective Strategy to Limit Ischemic Injury During Coronary Revascularization on Cardiopulmonary Bypass Circulation, September 28, 1999; 100(13): 1438 - 1442. [Abstract] [Full Text] [PDF]
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H. P. Wendel and G. Ziemer Coating-techniques to improve the hemocompatibility of artificial devices used for extracorporeal circulation Eur. J. Cardiothorac. Surg., September 1, 1999; 16(3): 342 - 350. [Abstract] [Full Text] [PDF]
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M. M.H. Khan, N. Gikakis, S. Miyamoto, A. K. Rao, S. L. Cooper, L. H. Edmunds Jr, and R. W. Colman Aprotinin inhibits thrombin formation and monocyte tissue factor in simulated cardiopulmonary bypass Ann. Thorac. Surg., August 1, 1999; 68(2): 473 - 478. [Abstract] [Full Text] [PDF]
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C. B. Mahoney and G. M. Lemole Transfusion after coronary artery bypass surgery: the impact of heparin-bonded circuits Eur. J. Cardiothorac. Surg., August 1, 1999; 16(2): 206 - 210. [Abstract] [Full Text] [PDF]
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P. M. McCarthy, J.-P. P. Yared, R. C. Foster, D. A. Ogella, J. A. Borsh, and D. M. Cosgrove III A prospective randomized trial of Duraflo II heparin-coated circuits in cardiac reoperations Ann. Thorac. Surg., May 1, 1999; 67(5): 1268 - 1273. [Abstract] [Full Text] [PDF]
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O. M. Shapira, G. S. Aldea, S. M. Cutter, C. A. Fitzgerald, A.N.P. H. L. Lazar, and R. J. Shemin Improved clinical outcomes after operation of the proximal aorta: a 10-year experience Ann. Thorac. Surg., April 1, 1999; 67(4): 1030 - 1037. [Abstract] [Full Text] [PDF]
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G. S. Aldea, J. M. Gaudiani, O. M. Shapira, A. K. Jacobs, J. Weinberg, A. L. Cupples, H. L. Lazar, and R. J. Shemin Effect of gender on postoperative outcomes and hospital stays after coronary artery bypass grafting Ann. Thorac. Surg., April 1, 1999; 67(4): 1097 - 1103. [Abstract] [Full Text] [PDF]
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G. S. Aldea Heparin-Bonded Circuits Decrease Thromboembolic Complications and Improve Outcomes in Patients Undergoing Coronary Artery Bypass Graft Surgery Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 1999; 3(1): 9 - 16. [Abstract] [PDF]
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F. D. Rubens, R. S. Labow, G. R. Lavallee, M. I. Watson, J. A. Robblee, M. E. Voorhees, and H. J. Nathan Hematologic evaluation of cardiopulmonary bypass circuits prepared with a novel block copolymer Ann. Thorac. Surg., March 1, 1999; 67(3): 689 - 696. [Abstract] [Full Text] [PDF]
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L. H. Edmunds Jr Inflammatory response to cardiopulmonary bypass Ann. Thorac. Surg., November 1, 1998; 66(90050): S12 - 16. [Abstract] [Full Text] [PDF]
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O. M. Shapira Reply Ann. Thorac. Surg., September 1, 1998; 66(3): 987 - 988. [Full Text] [PDF]
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C B. Mahoney Heparin-bonded circuits: clinical outcomes and costs Perfusion, May 1, 1998; 13(3): 192 - 204. [Abstract] [PDF]
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H. L. Lazar, T. Hamasaki, Y. Bao, S. Rivers, S. A. Bernard, and R. J. Shemin Soluble Complement Receptor Type I Limits Damage During Revascularization of Ischemic Myocardium Ann. Thorac. Surg., April 1, 1998; 65(4): 973 - 977. [Abstract] [Full Text] [PDF]
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O. M. Shapira, G. S. Aldea, P. R. Treanor, R. M. Chartrand, K. M. DeAndrade, H. L. Lazar, and R. J. Shemin Reduction of Allogeneic Blood Transfusions After Open Heart Operations by Lowering Cardiopulmonary Bypass Prime Volume Ann. Thorac. Surg., March 1, 1998; 65(3): 724 - 730. [Abstract] [Full Text] [PDF]
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G. S. Aldea, P. O'Gara, O. M. Shapira, P. Treanor, A. Osman, E. Patalis, C. Arkin, R. Diamond, V. Babikian, H. L. Lazar, et al. Effect of Anticoagulation Protocol on Outcome in Patients Undergoing CABG With Heparin-Bonded Cardiopulmonary Bypass Circuits Ann. Thorac. Surg., February 1, 1998; 65(2): 425 - 433. [Abstract] [Full Text] [PDF]
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H. L. Lazar, X. Zhang, T. Hamasaki, C. A. Memmelo, P. Treanor, S. Rivers, G. S. Aldea, S. A. Bernard, and R. J. Shemin Heparin-Bonded Circuits Decrease Myocardial Ischemic Damage: An Experimental Study Ann. Thorac. Surg., June 1, 1997; 63(6): 1701 - 1705. [Abstract] [Full Text]
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M. Ranucci, E. Ovrum, and V. Videm Antithrombin III, Leukocyte Activation, and Low Systemic Heparinization Ann. Thorac. Surg., April 1, 1997; 63(4): 1211 - 1212. [Full Text]
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