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Clinical Investigations: SURGERY |

Complement Activation in Coronary Artery Bypass Grafting Patients Without Cardiopulmonary Bypass*: The Role of Tissue Injury by Surgical Incision

Y. John Gu, MD, PhD; Massimo A. Mariani, MD, PhD; Piet W. Boonstra, MD, PhD; Jan G. Grandjean, MD, PhD; Willem van Oeveren, PhD
Author and Funding Information

*From the Department of Cardiothoracic Surgery, Thorax Center, University Hospital Groningen, The Netherlands.

Correspondence to: Willem van Oeveren, PhD, Blood Interaction Research, Department of Cardiothoracic Surgery, University Hospital Groningen, Hanzeplein 1, 9700 RB Groningen, The Netherlands



Chest. 1999;116(4):892-898. doi:10.1378/chest.116.4.892
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Study objectives: Complement activation is a trigger in inducing inflammation in patients who undergo coronary artery bypass grafting (CABG) and is usually thought to be induced by the use of cardiopulmonary bypass (CPB). In this study, we examined whether tissue injury caused by chest surgical incision per se contributes to complement activation in CABG patients.

Design: Prospective study.

Setting: Thorax center in university hospital.

Patients: Twenty-two patients undergoing CABG without CPB were prospectively divided into two groups: a small chest incision via an anterolateral thoracotomy representing a minimized tissue injury (lateral group, n = 8), and a conventional median sternotomy representing a large tissue injury (median group, n = 14). Biochemical markers indicating complement activation as well as systemic inflammatory response were determined before, during, and after the operation.

Measurements and results: Plasma concentrations of complement 3a increased in both the lateral and median groups right after chest incision (p < 0.01 and p < 0.05, respectively) and by the end of operation increased only in the median group (p < 0.01). The terminal complement complex 5b-9 did not increase in the lateral group, but it did increase in the median group both after incision and by the end of the operation (p < 0.05 and p < 0.05, respectively). During surgery, complement 4a did not increase, suggesting that it is the alternative rather than the classic pathway that is involved in complement activation by tissue injury. Postoperatively, interleukin-6 production was greater in the median group (p < 0.01) than the lateral group (p < 0.05), suggesting a more pronounced inflammatory response to a larger chest incision.

Conclusions: Tissue injury caused by surgical incision contributes to complement activation in CABG patients who are operated on without CPB. A small anterolateral thoracotomy is associated with reduced complement activation in comparison with a median sternotomy.

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