CD11b may be a less satisfactory indicator for cardiac ischemia-reperfusion injury in coronary artery bypass graft surgery with cardiopulmonary bypass than cardiac troponin I

Abstract

Study objectiveTo investigate whether CD11b on neutrophils can be used as a marker to predict myocardial ischemia-reperfusion injury for patients undergoing coronary artery bypass graft (CABG) surgery on cardiopulmonary bypass (CPB). DesignProspective, observational study. SettingUniversity teaching hospital and university hospital laboratories. PatientsTwelve adults, physical status II and III (American Society of Anesthesiologists) patients scheduled for elective CABG surgery on CPB. InterventionsAnesthesia and surgical interventions were performed according to standard procedures. Coronary sinus was cannulated for retrograde cardioplegia perfusion and for coronary sinus blood sampling. The blood samples were collected from systemic and coronary venous sinus blood respectively at several time points before CPB, during CPB, and after declamping of the ascending aorta. Measurements and main resultsCD11b expressions in systemic circulation blood increased significantly during CPB and maintained higher levels after cardiac reperfusion (P < .05); on the other hand, CD11b expressions in coronary sinus blood declined gradually and reached their lowest level at 5 minutes after aortic declamping. The differences in CD11b expressions between systemic circulatory blood and coronary sinus blood after cardiac reperfusion were significant (P < .05). Cardiac troponin I (cTnI) concentrations in both systemic circulatory blood and coronary sinus blood increased significantly after cardiac reperfusion (P < .05), and the concentrations of cTnI in coronary sinus blood increased much higher than the corresponding concentrations of cTnI at each time point (P < .05). ConclusionCD11b expression on neutrophils may not be a reliable predictor for myocardial ischemia-reperfusion injury in CABG surgery on CPB because of the possible sequestration of neutrophils in myocardium.