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Ann Thorac Surg 1994;58:734-741
© 1994 The Society of Thoracic Surgeons
Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania USA
Accepted for publication December 7, 1993.
* Address reprint requests to Dr Wagner, Presbyterian University Hospital, C-813, Pittsburgh, PA 15213.
This prospective, randomized study involving patients undergoing isolated coronary artery bypass grafting investigated whether the use of heparin-coated bypass circuits with an uncoated cardiotomy reservoir (n = 10) compared with standard uncoated bypass circuits (n = 10) resulted in differences in patient outcome and hemostatic alterations. There were no differences in postoperative blood loss, transfusion requirements, and routine coagulation test results between groups. Immunoassays for platelet alpha-granule constituents platelet factor 4 and beta-thromboglobulin, thrombin generation byproduct F1.2, fibrinopeptide A, thrombin-antithrombin complex, and fibrinolysis by-product D-dimer also demonstrated no significant differences between groups, although trends for lower platelet secretion with heparin coating were noted. Increases were found in betathromboglobulin and platelet factor 4 concentrations at 10 (p < 0.03) and 30 minutes (p < 0.001) of CPB, respec tively, and continuing throughout CPB (p < 0.001) for both groups versus values measured before incision. No significant differences were seen between levels 5 minutes prior to aortic cross-clamp release and those obtained 8 and 45 minutes after cross-clamp release. Conversely, no significant increases in F1.2, thrombin-antithrombin complex, and D-dimer were seen prior to release of the aortic cross-clamp, but afterward increases occurred that were highly significant (p < 0.001). The temporal data suggest that platelet activation occurs primarily as a result of contact with the cardiopulmonary bypass circuitry, whereas thrombin generation and fibrinolytic activity are not significant until reperfusion of the heart and lungs. This latter effect may be due to reperfusion injury, humoral mediators generated by blood—biomaterial contact, or rewarming and increased use of cardiotomy suction and return of shed mediastinal blood.
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