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Ann Thorac Surg 1998;65:1342-1347
© 1998 The Society of Thoracic Surgeons

Cardiopulmonary Bypass Circuit Treated With Surface-Modifying Additives: A Clinical Evaluation of Blood Compatibility

^a Department of Cardiothoracic Surgery, Thorax Center, University Hospital Groningen, Groningen, the Netherlands

Accepted for publication December 26, 1997.

Address reprint requests to Dr van Oeveren, Blood Interaction Research, Dept. of Cardiothoracic Surgery, University Hospital Groningen, Hanzeplein 1, 9700 RB Groningen, the Netherlands

Background. 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.

Methods. 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.

Results. During CPB, platelet count and ß-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.

Conclusions. 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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