Effect of Pericardial Blood Processing on Postoperative Inflammation and the Complement Pathways

Background The objective of the present study was to determine the effect of processing of pericardial blood with a cell-saving device (CS) and vacuum-assisted cardiopulmonary bypass (VACPB) on reduction of postoperative inflammation. Methods One hundred patients who underwent on-pump coronary arter...

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Veröffentlicht in:The Annals of thoracic surgery 2008-02, Vol.85 (2), p.530-535
Hauptverfasser: Marcheix, Bertrand, MD, MS, Carrier, Michel, MD, Martel, Catherine, MS, Cossette, Mariève, MD, Pellerin, Michel, MD, Bouchard, Denis, MD, Perrault, Louis P., MD, PhD
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Sprache:eng
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Zusammenfassung:Background The objective of the present study was to determine the effect of processing of pericardial blood with a cell-saving device (CS) and vacuum-assisted cardiopulmonary bypass (VACPB) on reduction of postoperative inflammation. Methods One hundred patients who underwent on-pump coronary artery bypass grafting surgery were included in a prospective randomized study. Patients were randomly assigned into four groups of 25 patients, each in a two-by-two factorial design: group A had no CS and no VACPB, group B had VACPB alone, group C had CS alone, and group D had CS and VACPB. The complement factors C4a, C3a, and C5a, and the terminal complex sC5b-9, MBL (mannose-binding lectin), and Bb were measured in plasma preoperatively and at 30 and 240 minutes after termination of CPB. Results Mean age, CPB, and aortic cross-clamping times were similar in all groups. At 30 and 240 minutes after CPB, C3a, sC5b-9, and Bb were increased and C5a and MBL levels were decreased compared with preoperative levels in all groups. At 240 minutes, Bb levels were lower in patients with CS ( p = 0.0002). Conclusions The present study shows that contemporary CPB remains associated with a striking activation of all complement pathways and its terminal component. The use of CS decreases the activation of the complement alternative pathway.
ISSN:0003-4975
1552-6259
DOI:10.1016/j.athoracsur.2007.08.050