Intraoperative Embolus Formation During Cardiopulmonary Bypass Affects the Release of S100B

Abstract

Background: Intraoperative thromboembolism and the systemic inflammatory reaction are thought to play a role in causing cerebral dysfunction following cardiopulmonary bypass (CPB). Increased levels of S100B, an astroglial protein, have been linked to neuropsychological deficits after CPB. The present study investigated whether S100B release correlates with intraoperative embolus formation, thrombin formation, or the release of inflammatory parameters. Methods: 40 patients undergoing coronary artery bypass grafting were included. Blood samples were taken before, during, and after CPB, and levels of S100B, thrombin-anti-thrombin complex (TAT), complement C5a, and interleukin 8 were analysed. Embolus formation was assessed by Doppler ultrasound at the arterial line of CPB. Results: The release of S100B correlated with embolus count (r = 0.42; p = 0.009) and TAT formation (r = 0.71; p = 0.0001). The correlation of S100B with interleukin 8 (r = 0.58; p = 0.0001) was due to the dependence of both parameters on bypass time (r = 0.29; p = 0.075, partial correlation). A correlation of S100B with C5a formation could not be observed. Conclusions: S100B release is related to embolus and thrombin formation during CPB, indicating that thrombofibrinous embolism is involved in perioperative brain damage. Inflammatory parameters (i.e. interleukin 8 and C5a) seem to have no influence on S100B release.

Key words

Cardiopulmonary bypass - Intraoperative emboli - S100B - Cerebral dysfunction