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Eur J Cardiothorac Surg 1999;16:540-545
© 1999 Elsevier Science NL
a Bristol Heart Institute, Bristol Royal Infirmary, Bristol, UK
b Papworth Hospital NHS Trust, Papworth Everard, Cambridge, UK
Corresponding author. Mr Inderpaul Birdi, FRCS, MCh, Specialist Registrar in Cardiothoracic Surgery, Papworth Hospital NHS Trust, Papworth Everard, Cambridge, CB3 8RE, UK. Tel.: +44-1480-830-541, bleep 610; fax: +44-1480-364-610
e-mail: Inderuk{at}hotmail.com
Objectives: The inflammatory response to cardiopulmonary bypass is believed to play an important role in end organ dysfunction after open heart surgery and may be more profound after normothermic systemic perfusion. The aim of the present study was to investigate the effects of cardiopulmonary bypass temperature on the production of markers of inflammatory activity after coronary artery surgery. Methods: Forty-five low risk patients undergoing elective coronary artery surgery were prospectively randomized into three groups: hypothermia (28°C, n=15), moderate hypothermia (32°C, n=15), and normothermia (37°C, n=15). All patients received cold antegrade crystalloid cardioplegia and topical myocardial cooling with saline at 4°C. Serum samples were collected for the estimation of neutrophil elastase, interleukin 8, C3d, and IgG under ice preoperatively, 5 min after heparinisation, 30 min following start of CPB, at the end of CPB, 5 min after protamine administration, and 4, 12 and 24 h postoperatively. Results: Patients were similar with regard to preoperative and intraoperative characteristics (age, sex, severity of symptoms, number of grafts performed, aortic cross clamp time, cardiopulmonary bypass time). Neutrophil elastase concentration increased markedly as early as 30 min after the onset of cardiopulmonary bypass and peaked 5 min after protamine administration. Levels were not significantly different between the three groups. A similar finding was apparent for C3d release. Interleukin 8 concentrations also demonstrated a considerable increase related to cardiopulmonary bypass in all groups, but there was a significantly more rapid decline in interleukin 8 concentrations in the normothermic group in the postoperative period. Eluted IgG fraction showed a much earlier peak concentration than the other markers, occurring within 30 min of the start of cardiopulmonary bypass. Levels reached a plateau, before declining soon after the end of bypass and remained higher than preoperative values at 24 h. There was no difference between the three groups. The cumulative release of all markers was calculated from the concentration–time curves, and was not statistically different between groups. Conclusion: Normothermic systemic perfusion was not shown to produce a more profound inflammatory response compared to hypothermic and moderately hypothermic cardiopulmonary bypass.
Key Words: Cardiopulmonary bypass • Coronary artery surgery • Inflammatory mediators
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