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Director, Cardiac Anesthesia, Department of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, MA, alerner{at}bidmc.harvard.edu
To the Editor:
In a recent editorial, Drs. Hogue and London (1) state "... that aprotinin could artifactually prolong the celite-based activated clotting time (ACT)."
While it is clear from numerous studies that aprotinin independently prolongs celite activated ACT (2,3), there is no reason to think that this effect is simply an artifact. Aprotinin, as a serine protease inhibitor and inhibitor of kallikrein, is an inhibitor of contact activation of the coagulation system (4). The prolongation of PTT by aprotinin that has also been demonstrated further demonstrates this effect (5). As suggested by Dietrich et al., (6) in the presence of aprotinin the celite ACT "is not artificially prolonged," but, in fact, the kaolin ACT is "artificially shortened" by the binding of aprotinin to kaolin.
Aprotinin may also have heparin sparing effects during cardiopulmonary bypass (6). However, a small number of prospective studies (7) of thromboembolic complications that may or may not be related to aprotinin have suggested that clinicians, disregard the anticoagulant effect of aprotinin until further study of this issue is performed. Hunt et al. (8) suggested using this strategy by recommending a threshold of 750 s when using celite-based ACT in the presence of aprotinin. This number was not based on clinical study but rather the authors expert opinion that this represented an adequate heparin effect.
The "bottom line" is that aprotinins effect on celite-based ACT is real. What remains to be answered is the importance of this effect in vivo and how this effect interacts with aprotinins pro-hemostatic effects in individual patient situations.
REFERENCES
This article has been cited by other articles:
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C. W. Hogue and M. J. London Aprotinin's Effect on ACT is Not an Artifact Anesth. Analg., May 1, 2007; 104(5): 1302 - 1303. [Full Text] [PDF] |
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