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Risk of heparin-induced thrombocytopenia from heparin-bonded vascular prostheses
Leila Mureebe1, Joseph A Graham, Ruth L Bush
1Division of Vascular Surgery, New York Presbyterian Hospital, Columbia University Medical Center, New York, NY 10034, USA. leila.mureebe@duke.edu
Heparin can be bonded to vascular devices to improve their patency. The purpose of this study was to determine if a clinically utilized heparin-bonded Dacron((R)) graft (HBG) places patients at risk for heparin-induced thrombocytopenia (HIT) and its complications. A commercially available HBG was divided into 1 cm long segments, which were incubated in platelet-poor plasma (PPP) for 24 hr at 37 degrees C. Control segments of non-heparin-bonded Dacron graft were similarly treated. After incubation, aliquots of PPP were assayed for heparin content. Additional graft segments were immersed in PPP from HIT-positive patients to determine if the effluent from the HBG led to platelet activation. Heparin was discharged from the HBG (1.82 +/- 0.08 units/cc) but not from the control group (0.00 units/cc, p < 0.05). Platelet aggregation occurred in 85.7% of the plasma samples with leached heparin when mixed with normal donor platelets and plasma containing heparin antiplatelet antibodies (HAAbs). None of the control grafts caused any type of aggregation. HBG may contribute to the development of HAAb that can lead to HIT in previously unaffected patients, and HIT causes a prothrombotic state which counteracts the theoretic advantages of an HBG. Patients receiving an HBG should be made aware of these possibilities.
Heparin can be bonded to vascular devices to improve their patency. The purpose of this study was to determine if a clinically utilized heparin-bonded Dacron((R)) graft (HBG) places patients at risk for heparin-induced thrombocytopenia (HIT) and its complications. A commercially available HBG was divided into 1 cm long segments, which were incubated in platelet-poor plasma (PPP) for 24 hr at 37 degrees C. Control segments of non-heparin-bonded Dacron graft were similarly treated. After incubation, aliquots of PPP were assayed for heparin content. Additional graft segments were immersed in PPP from HIT-positive patients to determine if the effluent from the HBG led to platelet activation. Heparin was discharged from the HBG (1.82 +/- 0.08 units/cc) but not from the control group (0.00 units/cc, p < 0.05). Platelet aggregation occurred in 85.7% of the plasma samples with leached heparin when mixed with normal donor platelets and plasma containing heparin antiplatelet antibodies (HAAbs). None of the control grafts caused any type of aggregation. HBG may contribute to the development of HAAb that can lead to HIT in previously unaffected patients, and HIT causes a prothrombotic state which counteracts the theoretic advantages of an HBG. Patients receiving an HBG should be made aware of these possibilities.
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