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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Published inThe Annals of thoracic surgery Vol. 85; no. 2; pp. 530 - 535
Main Authors Marcheix, Bertrand, MD, MS, Carrier, Michel, MD, Martel, Catherine, MS, Cossette, Mariève, MD, Pellerin, Michel, MD, Bouchard, Denis, MD, Perrault, Louis P., MD, PhD
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.02.2008
Elsevier Science
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Summary: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.
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ISSN:0003-4975
1552-6259
DOI:10.1016/j.athoracsur.2007.08.050