Complement activation in coronary artery bypass grafting patients without cardiopulmonary bypass - The role of tissue injury by surgical incision

Citation
Yj. Gu et al., Complement activation in coronary artery bypass grafting patients without cardiopulmonary bypass - The role of tissue injury by surgical incision, CHEST, 116(4), 1999, pp. 892-898
Citations number
31
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CHEST
ISSN journal
00123692 → ACNP
Volume
116
Issue
4
Year of publication
1999
Pages
892 - 898
Database
ISI
SICI code
0012-3692(199910)116:4<892:CAICAB>2.0.ZU;2-7
Abstract
Study objectives: Complement activation is a trigger in inducing inflammati on in patients who undergo coronary artery bypass grafting (CABG) and is us ually thought to be induced by the use of cardiopulmonary bypass (CPB), In this study, we examined whether tissue injury caused by chest surgical inci sion per se contributes to complement activation in CABG patients. Design: Prospective study. Setting: Thorax center in university hospital. Patients: Twenty-two patient s undergoing CABG without CPB were prospectively divided into two groups: a small chest incision via an anterolateral thoracotomy representing a minim ized tissue injury (lateral group, n = 8), and a conventional median sterno tomy representing a large tissue injury (median group, n 14). Biochemical m arkers indicating complement activation as well as systemic inflammatory re sponse 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 t he median group (p < 0.01), The terminal complement complex 5b-9 did not in crease in the lateral group, but it did increase in the median group both a fter incision and by the end of the operation (p < 0.05 and p < 0.05, respe ctively). During surgery, complement 4a did not increase, suggesting that i t is the alternative rather than the classic pathway that is involved in co mplement activation by tissue injury. Postoperatively, interleukin-6 produc tion 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 ches t incision. Conclusions: Tissue injury caused by surgical incision contributes to compl ement 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.