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Ann Thorac Surg 2002;73:1897-1904
© 2002 The Society of Thoracic Surgeons

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Original article: cardiovascular

Aprotinin in coronary operation with cardiopulmonary bypass: does "low-dose" aprotinin inhibit the inflammatory response?

^a Department of Cardiovascular Surgery, University Hospital (Inselspital), Berne, Switzerland

Accepted for publication February 15, 2002.

* Address reprint requests to Dr Englberger, Department of Cardiovascular Surgery, Inselspital University Hospital, Freiburgstrasse 3010, Berne, Switzerland
e-mail: lars.englberger{at}insel.ch

Background. Cardiopulmonary bypass induces a systemic inflammatory response. Aprotinin, a nonspecific proteinase inhibitor is known to improve postoperative hemostasis and may modify the inflammatory reaction. This study evaluates the effects of low-dose aprotinin on inflammatory markers in patients scheduled for elective coronary artery bypass grafting.

Methods. Patients were prospectively randomized into two groups: the control group (C) (n = 14) and the low-dose aprotinin group (A) (n = 15) with (2 x 10⁶ KIU = 280 mg) aprotinin added to the pump prime. Cytokine response (interleukin-6, soluble TNF II receptor), terminal complement production (SC5b-9), and neutrophil activation (lactoferrin) were assessed up to 6 hours postoperatively. Clinical data and hemostatic factors including fibrinopeptide A, thrombin-antithrombin complex, D-dimer, and plasmin/₂-antiplasmin were investigated.

Results. In both study groups, a significant increase of all inflammatory markers was seen (IL-6, sTNF-IIR, SC5b-9, lactoferrin), p less than 0.001. Peak levels of complement production occurred after protamine administration, whereas cytokine increases were more pronounced postoperatively with marked elevation up to 6 hours. The markers did not differ significantly between groups throughout the study period (p > 0.05 at each time of determination). However, after protamine administration reduced fibrinolysis (D-dimer, plasmin/₂-antiplasmin) was detected in group A. Measurements for coagulation (fibrinopeptide A, thrombin-antithrombin complex) were not significantly influenced by aprotinin. The total amount of blood loss during the first 24 hours was significantly reduced in group A (p < 0.02).

Conclusions. Low-dose aprotinin added to the pump prime does not inhibit the inflammatory response caused by cardiopulmonary bypass, but improves postoperative hemostasis. A potential effect of high-dose aprotinin on inflammatory markers remains to be elucidated.

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