© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Peri-operative myocardial tissue injury and the release of inflammatory mediators in coronary artery bypass graft patients
aDepartment of Cardiothoracic Surgery, University Hospital Maastricht, Maastricht, The Netherlands
bCardiovascular Research Institute Maastricht, Maastricht, The Netherlands
cDepartment of General Surgery, University Hospital Maastricht, Maastricht, The Netherlands
* Corresponding author. Tel.: +31-43-387-7068; fax: +31-43-387-5075 efr{at}scpc.azm.nl
Objective: This study was conducted to evaluate to what extent the ischemia-reperfusion injury resulting from the cardiopulmonary bypass (CPB) and aortic cross-clamping procedures during coronary artery bypass grafting (CABG) contributes to the systemic inflammatory response generally found in these patients. Methods: Serum levels of enzymes (CK and CK-MB) and non-enzymatic proteins (FABP and myoglobin) as markers of myocardial tissue injury, bactericidal permeability increasing protein (BPI) as an indicator of neutrophil activation, interleukin-6 (IL-6) as inducer of the acute phase response and lipopolysaccharide binding protein (LBP) as parameter of the acute phase response were measured in 15 low-risk CABG patients with cardiopulmonary bypass (CPB), and 17 low-risk CABG patients without CPB. Results: Already 0.5 h after reperfusion significantly increased plasma levels of all markers of myocardial tissue injury were noted in patients having surgery with CPB, but not in non-CPB patients. No significant differences were found between both groups for BPI and IL-6 levels in the early reperfusion period. BPI and IL-6 levels were higher in the non-CPB group on the first post-operative day (P<0.05). However, no correlations were found for any marker of peri-operative tissue damage with either early neutrophil activation, or acute phase reactants. Conclusions: Perioperative myocardial injury resulting from CPB and aortic cross-clamping in low-risk CABG patients does not contribute to the release of inflammatory mediators in these patients.
KEYWORDS Cardiovascular surgery; Ischemia; Reperfusion; Enzyme (kinetics); Cytokines
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