TY - JOUR
T1 - Anti-HLA antibodies and pulmonary valve allograft function after the ross procedure
AU - Matthias Bechtel, J. E.
AU - Marquardt, Anja
AU - Müller-Steinhardt, Michael
AU - Hanke, Thorsten
AU - Stierle, Ulrich
AU - Sievers, Hans Hinrich
PY - 2009/11
Y1 - 2009/11
N2 - Background and aim of the study: Rejection is a plausible cause of failure of allograft valves, but has not been demonstrated unequivocally in humans. A cross-sectional study has been conducted on the frequency of anti-human leukocyte antigen (HLA) antibodies in order to identify any correlation with allograft function in adult patients, following the Ross procedure. Methods: Anti-HLA antibodies were determined during regular follow up (median 1.1 years postoperatively) in a random sample of 197 patients (151 males, 46 females; mean age 46 ± 13 years). Panel-reactive antibodies (PRA) were determined by cytotoxicity testing; anti-HLA class 2 antibodies (HLA2AB) were determined by ELISA in a subgroup of 94 patients. Echocardiographic examinations were performed during the first visit and at a median of 6.8 years postoperatively. Results: The prevalence of positive antibody tests was 47% for PRA and 52% for HLA2AB. A slight deterioration of allograft valve function occurred between the two examinations (median maximal pressure gradient increased from 9 mmHg to 13 mmHg, p <0.001; median degree of regurgitation increased from zero to trivial, p = 0.020). The degree of regurgitation was slightly, but significantly, higher in PRA-positive patients at both examinations (p = 0.008 and p = 0.038). No relationship was observed between PRA status and pressure gradients, nor between HLA2AB status and allograft valve function. Neither were any other risk factors for allograft valve deterioration identified. Conclusion: Subtle, clinically irrelevant and temporally stable differences with regard to regurgitation across the allograft were observed between PRA-positive and -negative patients. These findings neither proved nor disproved rejection, but rather suggested that a slow deterioration of allograft valve function was complex, and most likely multifactorial.
AB - Background and aim of the study: Rejection is a plausible cause of failure of allograft valves, but has not been demonstrated unequivocally in humans. A cross-sectional study has been conducted on the frequency of anti-human leukocyte antigen (HLA) antibodies in order to identify any correlation with allograft function in adult patients, following the Ross procedure. Methods: Anti-HLA antibodies were determined during regular follow up (median 1.1 years postoperatively) in a random sample of 197 patients (151 males, 46 females; mean age 46 ± 13 years). Panel-reactive antibodies (PRA) were determined by cytotoxicity testing; anti-HLA class 2 antibodies (HLA2AB) were determined by ELISA in a subgroup of 94 patients. Echocardiographic examinations were performed during the first visit and at a median of 6.8 years postoperatively. Results: The prevalence of positive antibody tests was 47% for PRA and 52% for HLA2AB. A slight deterioration of allograft valve function occurred between the two examinations (median maximal pressure gradient increased from 9 mmHg to 13 mmHg, p <0.001; median degree of regurgitation increased from zero to trivial, p = 0.020). The degree of regurgitation was slightly, but significantly, higher in PRA-positive patients at both examinations (p = 0.008 and p = 0.038). No relationship was observed between PRA status and pressure gradients, nor between HLA2AB status and allograft valve function. Neither were any other risk factors for allograft valve deterioration identified. Conclusion: Subtle, clinically irrelevant and temporally stable differences with regard to regurgitation across the allograft were observed between PRA-positive and -negative patients. These findings neither proved nor disproved rejection, but rather suggested that a slow deterioration of allograft valve function was complex, and most likely multifactorial.
UR - http://www.scopus.com/inward/record.url?scp=77449089782&partnerID=8YFLogxK
M3 - Journal articles
C2 - 20099717
AN - SCOPUS:77449089782
SN - 0966-8519
VL - 18
SP - 673
EP - 681
JO - Journal of Heart Valve Disease
JF - Journal of Heart Valve Disease
IS - 6
ER -