Monitoring of Heparin-induced Anticoagulation with Kaolinactivated Clotting Time in Cardiac Surgical Patients Treated with Aprotinin

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Abstract
High-dose aprotinin appears to enhance the anticoagulant effects of heparin, as documented by increases in the activated clotting times (ACTs) during cardiopulmonary bypass; hence, some authorities have advocated reducing the dose of heparin in patients treated with aprotinin. An in vitro study by our group suggested that the increase of the ACT in the presence of aprotinin and heparin may be due to the use of celite as surface activator. We compared celite and kaolin as surface activators for the measurement of the ACT in cardiac surgical patients treated with aprotinin and in patients given no aprotinin. This double-blind, randomized, placebo-controlled study included 30 patients, of whom 14 received aprotinin and 16 received a placebo. Before, during, and after cardiopulmonary bypass, the ACT was measured with two Hemochron 400 systems with 12 mg of either celite (C-ACT) or kaolin (K-ACT) used as surface activator and with one Hepcon HMS system (HR-ACT), which uses kaolin as activator. The latter also was used for measurement of the blood heparin concentration. The ACTs of blood without heparin did not differ between aprotinin and control patients. During anticoagulation with heparin and cardiopulmonary bypass, the average C-ACTs were 784 ± 301 s (aprotinin) and 496 ± 120 s (control) (P < .001); the K-ACTs were 502 ± 131 s (aprotinin) and 458 ± 101 s (control) (P > .05); the HR-ACTs were 406 ± 87 s (aprotinin) and 423 ± 82 s (control) (P > .05), which was consistently less than C-ACT and K-ACT. Measurement with the Hepcon HMS system demonstrated no statistically significant difference in the circulating heparin concentration between the aprotinin and control groups. Our results indicate that the apparent increase in the ACT during heparin-induced anticoagulation in the presence of aprotinin was due to the use of celite as surface activator, rather than due to enhanced anticoagulation of heparin by aprotinin. We conclude that the ACT measured with kaolin provides better monitoring of heparin-induced anticoagulation in patients treated with high-dose aprotinin than does the ACT measured with celite. It appears that patients being treated with aprotinin should receive the usual doses of heparin and that the ACT should be assayed with kaolin as the activator.

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