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Ann Thorac Surg 1996;62:1328
© 1996 The Society of Thoracic Surgeons

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Discussion

Discussion

See also page 1321.

DR PEER M. PORTNER (Stanford, CA): I congratulate Dr Slater and his colleagues for their excellent results and a nicely presented paper.

The issue of thrombogenicity is, as you know, a complex, multifactorial issue that extends beyond the blood-contacting surface of the device. It includes aspects of the flow, not only in the pump itself but also in the conduits, the valves, and other parts of the system, and of course the coagulation state. Based on the fact that this is a multifactorial issue, I would like to ask a couple of questions.

First, what objective evidence do you have that the textured surface of this device represents a critical contribution to what are obviously very nice results? Second, in a population of ambulatory patients who are outside the hospital and pursuing normal activities with a potential risk of disconnection, inadvertently or otherwise, of their batteries, do you not think that avoidance of anticoagulation poses an unacceptable risk independent of device thrombogenicity itself? We believe that a low therapeutic level of warfarin at an international normalized ratio of about 2.5, in addition to platelet modifiers, is not unreasonable for these patients.

DR SLATER: I thank Dr. Portner for his comments. I will attempt to answer his second question first. It may be problematic if a pump shuts down on a patient who is not anticoagulated, but we are not convinced that a patient who is adequately anticoagulated would be better off if the pump were to shut off for 5 or 10 minutes. To anticoagulate a patient to the point that they could tolerate this insult may be prohibitive.

The first question I feel less equipped to answer other than to say we document evidence of the biologic lining. We believe that this does become the blood-contacting surface and results in a low level of thromboembolic rates that we are seeing. As I demonstrated, we are using very, very little anticoagulation.

DR BRUCE A. REITZ (Stanford, CA): Except in those patients who have had embolic events, what are the other indications that you have had in the few patients who you have anticoagulated?

DR SLATER: As I mentioned, I cannot answer for the entire study for all 22 centers, but in our own center, atrial fibrillation and deep venous thrombosis are the two leading causes for anticoagulation. We have had a majority of patients receiving aspirin, an antiplatelet therapy, more from an empiric reason, trying to diminish platelet activity, but we are beginning to rethink even that.

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Low Thromboembolic Risk Without Anticoagulation Using Advanced-Design Left Ventricular Assist Devices

James P. Slater, Eric A. Rose, Howard R. Levin, O. H. Frazier, J. Kirk Roberts, Alan D. Weinberg, and Mehmet C. Oz
Ann. Thorac. Surg. 1996 62: 1321-1327. [Abstract] [Full Text]

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