Development of anti-major histocompatibility complex class I or II antibodies following left ventricular assist device implantation: Effects on subsequent allograft rejection and survival

Citation
Fd. Pagani et al., Development of anti-major histocompatibility complex class I or II antibodies following left ventricular assist device implantation: Effects on subsequent allograft rejection and survival, J HEART LUN, 20(6), 2001, pp. 646-653
Citations number
18
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF HEART AND LUNG TRANSPLANTATION
ISSN journal
10532498 → ACNP
Volume
20
Issue
6
Year of publication
2001
Pages
646 - 653
Database
ISI
SICI code
1053-2498(200106)20:6<646:DOAHCC>2.0.ZU;2-B
Abstract
Background: Previous reports have indicated that antibodies to HLA class I or II antigens develop in approximately 60% of patients following left: ven tricular assist device (LVAD) implantation, subsequent rates of allograft r ejection are higher, and survival is adversely affected. Methods: We performed an analysis of the incidence of antibody development to HLA class I or II antigens by panel reactive antibody (PRA) screening fo llowing implantation of the HeartMate LVAD in 38 patients from October 1, 1 996 to March 1, 2000 (6 LVAD deaths excluded from study). The occurrence of vascular or cellular rejection of International Society of Heart and Lung Transplantation grade greater than or equal to 3A, as determined by endomyo cardial biopsy following heart transplantation (HTX), were compared for pat ients with (n = 32, LVAD group) or without (n = 68, control group) preopera tive LVAD support. Results: After LVAD implantation, 9 patients (28%) in the LVAD group develo ped IgG antibodies to class I (n = 3), class II (n = 5), or both antigens ( n = 1) with PRA > 10%. The remaining 23 patients (72%) had either no detect able IgG antibody development or IgG antibody development with PRA < 10%. A t the time of HTX, only 4 patients in the LVAD group had persistent PRA > 1 0%. Only 3 patients (4%) in the control group had PRA > 10% at the time of HTX. The incidence of patients free from rejection at 6 and 12 months was 6 2% and 44% for the control group, and 49%, and 40% for the LVAD group, resp ectively (p not significant). The mean linearized rate plus or minus standa rd deviation of allograft rejection from 0 to 6 months and 7 to 12 months w as 0.13 +/- 0.21 and 0.09 +/- 0.14 episodes a month, respectively, for pati ents with no LVAD support, and 0.17 +/- .25 and 0.06 +/- 0.1 episodes a mon th, respectively, for those with LVAD support (p = not significant). Post-t ransplantation survival at 1 and 2 years was 90% and 90%, respectively, for the control group, and 97% and 92%, respectively, for the LVAD group (p no t significant). Conclusion: Patients with LVAD support before HTX do not appear to be at in creased risk for significant allograft rejection in the first year or for d eath within the first 2 years after transplantation.