Cardiopulmonary bypass circuit treated with surface-modifying additives: A clinical evaluation of blood compatibility

University of Groningen, Groningen, Groningen, Netherlands
The Annals of Thoracic Surgery (Impact Factor: 3.85). 05/1998; 65(5):1342-7. DOI: 10.1016/S0003-4975(98)00223-9
Source: PubMed

ABSTRACT The cardiopulmonary bypass (CPB) circuit induces blood activation and a systemic inflammatory response in cardiac surgical patients. The CPB circuit treated with surface-modifying additive (SMA) has been found to reduce blood activation by in vitro and ex vivo experiments. This study evaluates the surface thrombogenicity and complement activation of SMA circuits during clinical CPB.
Twenty patients undergoing coronary artery bypass grafting were randomly divided into two groups. In the SMA group (n = 10), all blood-contacting surfaces in the CPB circuit were treated or coated with SMA, whereas in the control group (n = 10) patients were perfused with an identical circuit without treatment.
During CPB, platelet count and beta-thromboglobulin were found similar in both the SMA and the control groups. Prothrombin activation indicated by fragment F1 + 2 was found less in the SMA group (p < 0.05). After CPB, platelet deposition on the CPB circuit was significantly less (p < 0.05) in the SMA group than in the control group as assessed by the labeled monoclonal antibody against platelet glycoprotein IIIa. Complement activation identified by C3a and terminal complex C5b-9 did not differ between the two groups, but C4a generation was less in the SMA group (p < 0.05). Leukocyte activation identified by elastase and cytokine release indicated by interleukin-8 were found uniformly in both groups. Postoperatively, chest tube drainage, blood transfusion, duration of ventilatory support, as well as the intensive care unit and hospital stay were not significantly different between the two groups.
These preliminary clinical results suggest that SMA inhibits platelet interaction with the biomaterial surface of the CPB circuit. Complement activation assessed by the terminal complement complex is not influenced by SMA. The clinical benefit of this surface-modifying technique has yet to be assessed in a larger population of patients undergoing cardiac operations.

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Available from: Wim van Oeveren, Dec 30, 2013
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    • "The whole body response to CPB may lead to organ dysfunction [4], and cause temporary biochemical disorders in every patient. Due to major advances in oxygenator technology [5], current research focuses on the biocompatibility of CPB [6], and speci®cally on reducing the pathogenicity of CPB surfaces by coating [7] or modi®cation [8]. Additional technologies such as leucocyte or particle ®ltration are evolving concepts to prevent CPB-related pathogenicity. "
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    ABSTRACT: Complications associated with cardiopulmonary bypass (CPB) have gained more attention due to increased interest in coronary artery bypass grafting without CPB. The impact of heparin coating of CPB circuits has been discussed controversially. The present study examines if the treatment of the oxygenator surface with a synthetic protein may serve as an alternative to a completely heparin coated circuit. Fifty-eight patients undergoing coronary artery bypass grafting with CPB were randomly assigned to completely heparin coated circuits or synthetic protein treated oxygenators in a double blind protocol, focussing on the inflammatory reaction resulting in membrane damage, coagulation changes and markers of cerebral injury or dysfunction. Treatment groups did not differ as to preoperative demographics, and intraoperative clinical data. Patients with any neurologic disease or risk factors for cerebral dysfunction were not included in the study. Postoperative clinical data did not differ between groups. Both surface treatments resulted in similar coagulation activation, hyperfibrinolysis and disseminated intravascular coagulation. Platelet count displayed a difference in favour of the heparin coated group (P = 0.029). Increased leukocyte activation reflected by rising myeloperoxidase concentrations on CPB was present in both synthetic protein and heparin coating groups. Interleukins 6 and 8 reacted similarly, but interleukin 8 increased significantly more (P = 0.0061) at the end of surgery in patients treated with protein treated oxygenators. The same pattern was observed for complement activation as determined by total complement complex (P = 0.006). Both surface changes resulted in moderately increased S-100B protein and neuron specific enolase, without difference between groups. Both markers did not reach concentrations associated with clinical manifestation of cerebral injury. These results in routine patients with short bypass time, imply that protein treated oxygenators are associated with a limited increase of biochemical markers similar to heparin coating. However, significantly lower interleukin 8 release and complement activation can be achieved by heparin coating. The protein treatment is a standard feature of the oxygenator examined in both groups. It is not associated with additional cost and therefore appropriate for use in routine patients.
    European Journal of Cardio-Thoracic Surgery 09/1999; 16(2):211-7. DOI:10.1016/S1010-7940(99)00143-8 · 3.30 Impact Factor
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    ABSTRACT: Objective: Blood contact with synthetic surfaces during cardiopulmonary bypass (CPB), inevitably results in the activation of a variety of interrelated pathways of inflammation and coagulation that may contribute to postoperative complications in cardiac surgery patients. The objective of this trial was to evaluate clinical events and complement activation related to the use of a novel biomaterial, into which a surface modifying additive had been incorporated into the polymer used to prepare the bypass circuit. Methods: A prospective, double-blind trial was carried out with 34 patients randomized to surgery, with either a standard circuit or a circuit treated (`tip to tip') with the surface modifying additive. Variables recorded included perioperative haemodynamics, volume replacement, α-agonist and inotrope use. Terminal complement complex (SC5b-9) was measured using an ELISA. Results: Upon initiation of bypass, there was a decrease in mean arterial pressure (MAP) in the control group, not seen in the test group (P=0.0005, ANOVA). There was a decrease in the total volume of replacement fluid given intraoperatively in the test group as compared with the control group (total plus prime; control 5.3±1.2 L, test 4.4±1.9 L, P=0.03, Mann–Whitney test). There was a trend to decreased need for inotrope infusion in the test group after CPB (test 1/17, control 6/17, Fisher exact test; P=0.085). No difference was seen in the generation of terminal complement complex between the groups either during or after CPB. Conclusions: The decrease in blood pressure in the control group, upon the initiation of CPB, did not occur in patients undergoing CPB with the circuit prepared with the surface modifying additive. The decrease in blood pressure was likely associated with the increase in total administered fluids intraoperatively (approximately 1 l/patient) and perhaps the trend towards higher use of inotropes in the control patients as opposed to the test patients. These haemodynamic changes did not appear to be related to complement activation early in CPB.
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