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.
center in university hospital.
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.
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
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