CARDIOPULMONARY BYPASS CIRCUIT TREATED WITH SURFACE-MODIFYING ADDITIVES - A CLINICAL-EVALUATION OF BLOOD COMPATIBILITY

Citation
Yj. Gu et al., CARDIOPULMONARY BYPASS CIRCUIT TREATED WITH SURFACE-MODIFYING ADDITIVES - A CLINICAL-EVALUATION OF BLOOD COMPATIBILITY, The Annals of thoracic surgery, 65(5), 1998, pp. 1342-1347
Citations number
24
Categorie Soggetti
Surgery,"Cardiac & Cardiovascular System","Respiratory System
ISSN journal
00034975
Volume
65
Issue
5
Year of publication
1998
Pages
1342 - 1347
Database
ISI
SICI code
0003-4975(1998)65:5<1342:CBCTWS>2.0.ZU;2-E
Abstract
Background. The cardiopulmonary bypass (CPB) circuit induces blood act ivation and a systemic inflammatory response in cardiac surgical patie nts. The CPB circuit treated with surface-modifying additive (SMA) has been found to reduce blood activation by in vitro and ex vivo experim ents. This study evaluates the surface thrombogenicity and complement activation of SMA circuits during clinical CPB. Methods. Twenty patien ts undergoing corollary artery bypass grafting were randomly divided i nto two groups. In the SMA group (n = 10), all blood-contacting surfac es in the CPB circuit were treated or coated with SMA, whereas in the control group (n = 10) patients were perfused with an identical circui t without treatment. Results. During CPB, platelet count and beta-thro mboglobulin were found similar in both the SMA and the control groups. Prothrombin activation indicated by fragment F1+2 was found less in t he SMA group (p < 0.05). After CPB, platelet deposition on the CPB cir cuit was significantly less (p < 0.05) in the SMA group than in the co ntrol group as assessed by the labeled monoclonal antibody against pla telet glycoprotein IIIa. Complement activation identified by C3a and t erminal complex C5b-9 did not differ between the two groups, but C4a g eneration was less in the SMA group (p < 0.05). Leukocyte activation i dentified by elastase and cytokine release indicated by interleukin-8 were found uniformly in both groups. Postoperatively, chest tube drain age, blood transfusion, duration of ventilatory support, as well as th e intensive care unit and hospital stay were not significantly differe nt between the two groups. Conclusions. These preliminary clinical res ults suggest that SMA inhibits platelet interaction with the biomateri al surface of the CPB circuit. Complement activation assessed by the t erminal complement complex is not influenced by SMA. The clinical bene fit of this surface-modifying technique has yet to be assessed in a la rger population of patients undergoing cardiac operations. (C) 1998 by The Society of Thoracic Surgeons.