Background Left ventricular assist devices (LVAD) as a bridge (BTT) to heart transplantation (HTX) may be limited by the formation of anti-HLA antibodies. Whether sensitization occurs with continuous axial flow LVAD implant as assessed by Single Antigen Bead (SAB) assay is unknown. Methods Cytotoxic panel reactive antibody (PRA) and SAB assays were analyzed in HTX recipients undergoing LVAD implant as a BTT. Sensitization was defined as peak anti-HLA antibody values of >2000 mean fluorescent intensity as these values have been found to correlate with flow cytometric crossmatch results. Results LVADs were implanted as BTT in 30 patients. There were 7% (2/30) of patients prior to and no patients after LVAD implant with PRA >10%. However, 20% (6/30) of patients prior to and 53% (16/30) after LVAD were sensitized as measured by SAB (p=0.024). At HTX, 47% (14/30) of patients remained sensitized. A positive virtual crossmatch was observed in 28% (4/14) of the sensitized patients at HTX. There was no difference between the sensitized and non-sensitized groups (p>0.4 for all) in usage of blood products (64 11 vs. 63 39 units), time to HTX (286 63 vs. 257 48 days) and 1 year after HTX, there were no differences in rejection (total rejection score 0.30 vs. 0.37) and survival (93% vs. 88%). Conclusion Allosensitization after LVAD is common despite cytotoxic PRA being negative. One year after HTX, this sensitization does not translate into increased acute cellular or antibody mediated rejection or reduced survival.

Background Acute allograft dysfunction (AAD) is an important cause of morbidity among heart transplant recipients. The role of donor specific antibodies (DSA) in AAD, with the increasing use of Single Antigen Bead (SAB) assays that have improved the ability to detect DSA, remains unclear. Methods We retrospectively reviewed 329 heart transplant recipients followed at our institution. AAD was defined as an acute decline in left ventricular ejection fraction to <50% and a decrement of ≥10% compared to baseline in the absence of cellular rejection. AAD patients were compared with matched 30 heart transplant controls. Results There were 10 (3%) patients with AAD, 4 (40%) had DSA detectable by SAB assay compared to 16 (53%) controls (p=0.43). Peak DSA mean fluorescent intensity levels (MFI) were significantly higher at baseline (class I and class II) in AAD compared to controls. DSA MFI values increased at the time of AAD and returned to baseline values in follow-up for these AAD patients (p<0.05), but remained unchanged over time for controls. Six (60%) patients and 1 (3%) control had antibody-mediated rejection (AMR) by endomyocardial biopsy (p<0.01). There were 4 (40%) AAD patients with no DSA or AMR. Conclusions AAD after heart transplant is a heterogeneous process characterized by: 1) AMR and DSA, 2) AMR but no DSA, and 3) No AMR or DSA. The presence of DSA is not associated with AAD but quantity assessed by MFI levels may play a role.

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