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Eur J Cardiothorac Surg 2005;27:727
© 2005 Elsevier Science NL
Letter to the Editor |
Department of Anaesthesiology and Intensive Care Medicine, Charité—University Hospital Berlin, Campus Charité Mitte, Schumannstr. 20-21, D-10117 Berlin, Germany
Received 29 November 2004; accepted 12 January 2005.
* Corresponding author. Tel.: +49 30 450 531012; fax: +49 30 450 531911. (E-mail: christian.von_heymann{at}charite.de).
Key Words: Heparin • ACT • Cardiopulmonary bypass • Blood loss • Activation • Coagulation
We read with interest the article of Shuhaibar et al. ‘How much heparin do we really need to go on pump? A rethink of current practices’ in the November 2004 issue of the European Journal of Cardiothoracic Surgery [1].
The authors showed that a heparin dose of 250IU/kg achieved an activated coagulation time (ACT)>480s in 81.5% of patients which was associated with less blood loss compared to higher doses of heparin. The heparin dose correlated linearily with blood loss in the first 24h. These results require further comment:
It is well known and approved by the authors that the ACT shows a great heparin dose response-variability [2], making the ACT somehow unreliable to monitor effective inhibition of thrombin generation during CPB. Furthermore, studies of Despotis and Koster [3,4] have shown that higher heparin doses—based on an automated heparin dose response assay—led to lower levels of thrombin–antithrombin complexes and D-dimers and higher activities of FV and FVIII after CPB. In these studies postoperative blood loss was not increased in the higher heparin group and an indirect evidence for a better preservation of the coagulation system by higher heparin doses was postulated.
Neither heparin levels nor certain parameters activating the coagulation cascade were measured by Shuhaibar and colleagues which may have substantiated the reduced blood loss in the lower heparin group. Based on the ACT alone, no statements regarding the inhibition of thrombin generation and activity of coagulation factors can be made and no conclusions regarding postoperative blood loss should be drawn as they may be misleading [3,4].
Furthermore, no preoperative coagulation lab tests or platelet function monitoring were presented as the patients have been on aspirin until the day before surgery. We assume that preoperative coagulation lab tests and platelet function were not different between groups, but further studies should present these data to exclude any bias. In patients taking aspirin until the day prior to surgery a valid platelet function monitoring is required as the aspirin-induced platelet inhibition shows a high interindividual variability [5] which may influence postoperative blood loss.
Unfortunately, the protamine protocol to neutralize the heparin effect was not presented. We assume that a heparin dose-dependent protamine approach was used. As far as the increased postoperative blood loss in the higher heparin group is concerned, the missing protamine protocol opens the door for speculations such as insufficient heparin reversal or other investigator bias.
Taken all these considerations together, we disagree with the conclusion of Shuhaibar and colleagues that less postoperative blood loss is caused by a lower heparin dose. Too many confounding factors have not been controlled to draw this conclusion.
As these results may be misleading in clinical practice, we need to know much more about inhibition of thrombin generation and clotting factor consumption during CPB. The ‘ideal’ heparin dose should result in a low activation of coagulation, less consumption of clotting factors and less postoperative blood loss. More randomized and double-blind designed trials are needed to answer this question.
References
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