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Ann Thorac Surg 1992;53:477-481
© 1992 The Society of Thoracic Surgeons
a Department of Cardiac Surgery and the Maurice and Gabriela Goldschleger Eye Research Institute, The Chaim Sheba Medical Center, Tel Hashomer, Israel
b The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Accepted for publication August 30, 1991.
* Address reprint requests to Dr Goor, Department of Cardiac Surgery, The Chaim Sheba Medical Center, Tel Hashomer 52621, Israel.
To evaluate the functional integrity of platelets in patients administered the proteinase inhibitor aprotinin during cardiopulmonary bypass, 20 patients undergoing a complicated and prolonged open heart operation were studied. They were randomized to receive either a high dose of aprotinin (total dose, 6 to 7 x 106 KIU) before and during cardiopulmonary bypass (10 patients) or a placebo (10 patients). Blood samples were collected preoperatively, at the termination of bypass, and 90 minutes thereafter to assess platelet count and aggregation on extracellular matrix, which was studied by scanning electron microscopy. On a scale of 1 to 4, mean preoperative platelet aggregation grades were similar in both groups (3.5 ± 0.5). Postoperatively, at the termination of cardiopulmonary bypass and 90 minutes thereafter, all 10 patients treated with aprotinin revealed normal, unchanged platelet aggregation (grade, 3.5 ± 0.5), whereas all placebo-treated patients showed severely disturbed aggregation (grade, 1.4 ± 0.5) (p < 0.001). The platelet count was similar in both groups before and after operation (preoperatively, 182 ± 75 x 109/L and 146 ± 30 x 109/L, and postoperatively, 87 ± 13 x 109/L and 80 ± 27 x 109/L for the aprotinin and placebo groups, respectively). Total 24-hour postoperative bleeding and blood requirement were significantly lower in the aprotinin group (371 ± 84 mL and 2 ± 0.7 units, respectively) compared with the placebo group (608 ± 28 mL and 3.4 ± 1.3 units, respectively) (p < 0.01). These results demonstrate that improved postoperative hemnstatis is directly related to the complete preservation of platelet function achieved by the protective properties of aprotinin.
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