Murray H Kwon1, Jennifer Q Zhang2, Joanna M Schaenman3, Martin Cadeiras4, David W Gjertson2, Carolyn A Krystal5, Hillel Laks6, Abbas Ardehali6, Mario C Deng4, Richard J Shemin6, Elaine F Reed2. 1. Division of Cardiothoracic Surgery, Department of Surgery, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, Calif. Electronic address: mkwon@mednet.ucla.edu. 2. University of California, Los Angeles Immunogenetics Center, University of California, Los Angeles, Los Angeles, Calif. 3. Division of Immunology, Department of Medicine, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, Calif. 4. Division of Cardiology, Department of Medicine, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, Calif. 5. David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, Calif. 6. Division of Cardiothoracic Surgery, Department of Surgery, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, Calif.
Abstract
OBJECTIVE: Ventricular assist devices (VADs) are associated with increased anti-human leukocyte antigen antibody production. The purpose of this study is to characterize differences in sensitization patterns in patients receiving axial flow, implantable VADs versus pulsatile, paracorporeal biventricular assist devices (BIVADs) as bridges to transplantation. METHODS: The study is a retrospective review of 68 patients who were bridged to transplantation with either a VAD or a BIVAD, as described, from January 2007 to June 2010, at a university medical center. RESULTS: Five of 15 (33.3%) VAD patients became sensitized during treatment, compared with 30 of 53 (56.6%) BIVAD patients, P = .15. Multivariable analysis comparing BIVAD with VAD, while controlling for previous cardiac surgery, pregnancy, and packed red blood cell transfusion produced an odds ratio of 2.99, P = .14. Of sensitized patients, all 5 (100%) of the VAD patients had pre-existing antibodies before VAD placement, compared with 9 of 30 (30.0%) BIVAD patients, P = .006. Maximum cumulative mean fluorescence intensities for BIVAD were 46,259 ± 66,349 versus 42,540 ± 12,840 for VAD, P = .90. Time to maximum antibody expression was shorter for the VAD group (34 ± 28 days vs 5.8 ± 9 days, P = .04). CONCLUSIONS: Device type was not a factor in patient sensitization after implantation. However, VAD patients required pre-existing sensitization before implantation to produce antibodies during their treatment interval, whereas more than two thirds of BIVAD patients developed de novo antibodies. These data suggest that the mechanism of sensitization between VAD and BIVAD patients may differ, and further mechanistic studies into the impact of device types on patient sensitization are warranted.
OBJECTIVE: Ventricular assist devices (VADs) are associated with increased anti-human leukocyte antigen antibody production. The purpose of this study is to characterize differences in sensitization patterns in patients receiving axial flow, implantable VADs versus pulsatile, paracorporeal biventricular assist devices (BIVADs) as bridges to transplantation. METHODS: The study is a retrospective review of 68 patients who were bridged to transplantation with either a VAD or a BIVAD, as described, from January 2007 to June 2010, at a university medical center. RESULTS: Five of 15 (33.3%) VAD patients became sensitized during treatment, compared with 30 of 53 (56.6%) BIVADpatients, P = .15. Multivariable analysis comparing BIVAD with VAD, while controlling for previous cardiac surgery, pregnancy, and packed red blood cell transfusion produced an odds ratio of 2.99, P = .14. Of sensitized patients, all 5 (100%) of the VAD patients had pre-existing antibodies before VAD placement, compared with 9 of 30 (30.0%) BIVADpatients, P = .006. Maximum cumulative mean fluorescence intensities for BIVAD were 46,259 ± 66,349 versus 42,540 ± 12,840 for VAD, P = .90. Time to maximum antibody expression was shorter for the VAD group (34 ± 28 days vs 5.8 ± 9 days, P = .04). CONCLUSIONS: Device type was not a factor in patient sensitization after implantation. However, VAD patients required pre-existing sensitization before implantation to produce antibodies during their treatment interval, whereas more than two thirds of BIVADpatients developed de novo antibodies. These data suggest that the mechanism of sensitization between VAD and BIVADpatients may differ, and further mechanistic studies into the impact of device types on patient sensitization are warranted.
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