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Ann Thorac Surg 1997;64:1221-1222
© 1997 The Society of Thoracic Surgeons
Section of Cardiovascular and Thoracic Surgery, West Virginia University, Robert C. Byrd Health Sciences Center N, PO Box 9238, Morgantown, WV 26506-9238
To the Editor:
I read with interest the article entitled, "Low Heparinization with Heparin-Bonded Bypass: Is It A Safe Strategy?" by Bannan and colleagues [1]. I would agree that platelet and white blood cell activation markers are significantly lower in heparin-bonded circuits when compared with nonheparin-bonded circuits [1]. In addition, the markers of thrombin generation are significantly lower as a result of the heparin-bonded system. However, Bannan and colleagues state that evidence of contact activation in the heparin-bonded circuits was found after 120 minutes, indicating that anticoagulation in the system was not adequate. They thought this was important clinically, where the extrinsic pathway of coagulation is involved [1]. I would agree that coagulation probably does begin to take place in the system that they have designed. Binding of antithrombin III to the heparin-coated surfaces would be expected because the reaction takes place with the bonded heparin on the surface. Their protocol maintained flow within the circuits at 1 L/min for 6 hours. In doing clinical work and clinical studies using the heparin-bonded circuits and low heparin anticoagulation, my colleagues and I tend to keep the activated clotting times at approximately 200 to 400 seconds. This usually requires about 5,000 units of heparin before the initiation of bypass. The pump runs are usually short, ie, 60 to 120 minutes, and we never let the flow go to less than 2 L/min. Indeed, when weaning from cardiopulmonary bypass, bypass is discontinued when the flow reaches 2 L/min and then the circuit is reconnected and recirculated [2]. When the flow is reduced to the extent that was done in the article by Bannan and colleagues, one most likely would expect to see evidence of coagulation.
References
Molecular Vascular Medicine, G-Floor, Martin Wing, Leeds General Infirmary, Leeds LS1 3EX, UK
Department of Cardiothoracic Surgery, Killingbeck Hospital, Leeds LS14 6UQ, UK
To the Editor:
We thank Dr Hill for his comments on our article concerning low heparinization and heparin-bonded cardiopulmonary bypass circuits [1]. Such in vitro work bears the difficulty of using the findings to make judgements on clinical protocols. Conversely, the design of an in vitro model is open to more possibilities and we used this to our advantage in this study.
In theory, there should be a hemostatic benefit of using heparin-bonded surfaces for cardiopulmonary bypass, but clinical studies that have measured thrombin generation with heparin-bonded circuits have not found a significant reduction compared with untreated circuits [2, 3]. A study reporting in vitro work with heparin-bonded circuits in conjunction with low heparinization failed to demonstrate a reduction in thrombin generation with the treated surface [4]. Our in vitro work sought a definitive answer as to whether or not cell activation and thrombin generation were reduced with heparin-bonded cardiopulmonary bypass circuits and low heparinization. A flow rate in the region of that used for pediatric full heparinization operations was used in our model. This was to produce an additional insult to that of the intrinsic pathway alone because additional factors also contribute to the adverse reactions in vivo. The model enabled us to conclude that heparin bonding for cardiopulmonary bypass circuits caused a reduction in cell activation and in thrombin generation. Our speculations as to how these results could be applied to the clinical situation were intended to focus particularly on pediatric patients and longer perfusion periods.
References
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