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Perfusion, Vol. 18, No. 2, 95-105 (2003)
DOI: 10.1191/0267659103pf649oa

Leucocyte depletion in cardiopulmonary bypass: a comparison of four strategies

Piya Samankatiwat

Department of Cardiothoracic Surgery, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Hammersmith Campus, London, UK

Ioannis Samartzis

Department of Cardiothoracic Surgery, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Hammersmith Campus, London, UK

Panuwat Lertsithichai

Department of Surgery, Faculty of Medicine, Mahidol University, Ramathibodi Hospital, Bangkok, Thailand

Demetrios Stefanou

Department of Cardiothoracic Surgery, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Hammersmith Campus, London, UK

Prakash P Punjabi

Department of Cardiothoracic Surgery, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Hammersmith Campus, London, UK

Kenneth M Taylor

Department of Cardiothoracic Surgery, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Hammersmith Campus, London, UK

Terence Gourlay

Department of Cardiothoracic Surgery, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Hammersmith Campus, London, UK

Leucocytes have been shown to play a fundamental role in the pathophysiology of inflammation. This prospective, randomized, controlled study was designed to identify the most advantageous leucocyte depletion technique in terms of reduction in systemic inflammatory response syndrome and myocardial ischaemia reperfusion injury associated with cardiopulmonary bypass (CPB). Forty consecutive patients undergoing elective coronary artery bypass graft (CABG) surgery were randomly allocated to one of four groups. The four groups consisted of a control group, a systemic leucocyte depletion (SLD) group, a cardioplegic leucocyte depletion (CLD) group and a total leucocyte depletion (TLD) group. There were 10 patients in each group. Lactoferrin (marker of neutrophil activation) and troponin-I (marker of myocardial ischaemia reperfusion injury) were measured at six time points: post induction, 5 min on CPB, 5 min before releasing the aortic crossclamp, 15 min after releasing the clamp and 1 and 24 hours after the discontinuation of CPB.

Plasma lactoferrin levels increased rapidly in every group after the commencement of CPB, subsequently reached a peak after releasing the aortic crossclamp and gradually declined after the discontinuation of CPB. The lowest lactoferrin concentration was observed in the TLD (range 2.15-141.9 ng/mL) and CLD groups (7.469-114.6 ng/mL). Regarding myocardial injury, plasma cardiac troponin-I levels did not differ significantly between groups; but troponin-I concentrations rose dramatically after releasing the aortic crossclamp in all groups. Nevertheless, the CLD group had the lowest troponin-I level (1.37-5.55 ng/mL).

In conclusion, it is believed that myocardial ischaemia is probably a major contributor to the inflammatory response. Although there is no clear statistical significance shown in this pilot study, the data tend to support the cardioplegic leucocyte depletion strategy as the optimal method for attenuating neutrophil activation and myocardial ischaemia reperfusion injury.


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