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J Thorac Cardiovasc Surg 1996;112:1090-1097
© 1996 Mosby, Inc.


CARDIOPULMONARY BYPASS,
MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

ACTIVATION OF COAGULATION AND FIBRINOLYTIC PATHWAYS IN PATIENTS WITH LEFT VENTRICULAR ASSIST DEVICES

Talia Spanier, MDa, Mehmet Oz, MDa, Howard Levin, MDb, Alan Weinberg, MSc, Kathy Stamatis, MSc, David Stern, MDa,d, Eric Rose, MDa, Ann Marie Schmidt, MDa,b

Supported by grants from the U.S. Public Health Service (AG00602), the American Heart Association (New York affiliate), and The American Association for Thoracic Surgery (Evarts A. Graham Traveling Fellowship). Dr. Oz is an Irving Scholar at Columbia University.

Received for publication Jan. 18, 1996 Revisions requested March 5, 1996; revisions received May 22, 1996 Accepted for publication May 23, 1996 Address for reprints: Talia Spanier, MD/Ann Marie Schmidt, MD, Columbia University College of Physicians and Surgeons, 630 W. 168 St., P&S 11-518, New York, NY 10032.

Abstract

Left ventricular assist devices have provided successful supportive therapy for patients awaiting cardiac transplantation for extended periods of time. Although thromboembolic events have complicated support with these devices, the HeartMate left ventricular assist device developed by Thermo Cardiosystems, Inc., Woburn, Massachusetts, was specifically designed with a textured blood-contacting surface to minimize this risk. Clinical experience with this device has been encouraging, inasmuch as minimal thromboembolic complications have occurred despite the absence of anticoagulation. The coagulation and fibrinolytic pathways in these individuals were investigated to better understand the hematologic status of patients treated with the Thermo Cardiosystems device. Despite apparently normal prothrombin and activated partial thromboplastin times, as well as platelet counts, evidence of significant thrombin generation and fibrinolysis was present. To eliminate underlying cardiac failure as the responsible factor for these abnormalities, we made similar measurements in patients with end-stage heart failure who were not supported by an assist device or anticoagulation. These measurements revealed no evidence of thrombin generation or fibrinolysis. These data demonstrate that patients supported with a left ventricular assist device, while successfully sustained without systemic anticoagulation, nevertheless have evidence of activation of coagulation. These phenomena appear to be related to the presence of the device rather than to the underlying cardiac abnormalities. Although procoagulant and fibrinolytic pathways are apparently balanced in these patients, these data underscore the potential for the development of bleeding or thrombosis in clinically relevant settings. (J THORAC CARDIOVASC SURG 1996;112:1090-7)




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