Peri-operative myocardial tissue injury and the release of inflammatory mediators in coronary artery bypass graft patients

Citation
Ej. Fransen et al., Peri-operative myocardial tissue injury and the release of inflammatory mediators in coronary artery bypass graft patients, CARDIO RES, 45(4), 2000, pp. 853-859
Citations number
18
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOVASCULAR RESEARCH
ISSN journal
00086363 → ACNP
Volume
45
Issue
4
Year of publication
2000
Pages
853 - 859
Database
ISI
SICI code
0008-6363(200003)45:4<853:PMTIAT>2.0.ZU;2-3
Abstract
Objective: This study was conducted to evaluate to what extent the ischemia -reperfusion injury resulting from the cardiopulmonary bypass (CPB) and aor tic 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-enzymati c proteins (FABP and myoglobin) as markers of myocardial tissue injury, bac tericidal permeability increasing protein (BPI) as an indicator of neutroph il activation, interleukin-6 (IL-6) as inducer of the acute phase response and lipopolysaccharide binding protein (LBP) as parameter of the acute phas e 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 betwee n 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-operativ e day (P<0.05). However, no correlations were found for any marker of peri- operative tissue damage with either early neutrophil activation, or acute p hase reactants. Conclusions: Perioperative myocardial injury resulting from CPB and aortic crossclamping in low-risk CABG patients does not contribute to the release of inflammatory mediators in these patients. (C) 2000 Elsev ier Science B.V. All rights reserved.