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


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.
Gu
Y J
YJ
Department of Cardiothoracic Surgery, Thorax Center, University Hospital Groningen, The Netherlands.
Boonstra
P W
PW
Rijnsburger
A A
AA
Haan
J
J
van Oeveren
W
W
D001792:Blood Platelets / Q000187:drug effects*; D002315:Cardiopulmonary Bypass / Q000009:adverse effects / Q000295:instrumentation*; D003167:Complement Activation / Q000187:drug effects*; D015926:Complement C3a / Q000032:analysis; D015934:Complement C4a / Q000032:analysis; D015938:Complement Membrane Attack Complex / Q000032:analysis; D001026:Coronary Artery Bypass; D005069:Evaluation Studies as Topic; D005260:Female; D006801:Humans; D016209:Interleukin-8 / Q000097:blood; D019272:Leukocyte Elastase / Q000097:blood; D007962:Leukocytes / Q000502:physiology; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000032:analysis; D010973:Platelet Adhesiveness / Q000187:drug effects; D010976:Platelet Count / Q000187:drug effects; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000032:analysis; D011516:Prothrombin / Q000032:analysis / Q000502:physiology; D013501:Surface-Active Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology; D013927:Thrombosis / Q000209:etiology / Q000517:prevention & control*; D001620:beta-Thromboglobulin / Q000032:analysis
D015938:Complement Membrane Attack Complex; D016209:Interleukin-8; D010446:Peptide Fragments; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D013501:Surface-Active Agents; D001620:beta-Thromboglobulin; C045879:prothrombin fragment 1.2; D015926:Complement C3a; D015934:Complement C4a; D011516:Prothrombin; D019272:Leukocyte Elastase