Gene expression profiling and racial disparities in outcomes after heart transplantation.


Journal

The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation
ISSN: 1557-3117
Titre abrégé: J Heart Lung Transplant
Pays: United States
ID NLM: 9102703

Informations de publication

Date de publication:
08 2019
Historique:
received: 27 02 2019
revised: 24 04 2019
accepted: 18 05 2019
pubmed: 16 6 2019
medline: 20 11 2020
entrez: 16 6 2019
Statut: ppublish

Résumé

African Americans (AAs) have lower survival rates after heart transplantation (HTx) than Caucasians. The aim of this analysis was to evaluate racial differences in gene expression and their associations with survival and the composite outcome of death, retransplant, rejection with hemodynamic compromise, and graft dysfunction in the Outcomes AlloMap Registry. Registry participants included low-risk Caucasian and AA heart transplant recipients with a baseline and at least 1 follow-up gene expression test (AlloMap(C)) within the first year after HTx. The Kaplan-Meier method with delayed entry was used to describe differences in outcomes. Multivariable Cox hazard regression was used to evaluate the associations of overall gene expression profiling score, MARCH8 and FLT3 expression, and tacrolimus levels with each outcome, and stratified Cox models were developed to quantify race-specific associations. Among 933 eligible recipients, 737 (79%) were Caucasian and 196 (21%) were AA. Compared with Caucasians, AAs were significantly younger (55 vs 59 years, p < 0.001), with higher rates of non-ischemic cardiomyopathy (68% vs 50%, p < 0.001), sensitization (>10% panel reactive antibody, 16% vs 9.1%, p = 0.009), and human leukocyte antigen mismatches (7 vs 7, p = 0.01), but less frequent primary cytomegalovirus serostatus mismatch (14.31% vs 27.3%, p < 0.001). Overall, AAs had an increased adjusted mortality risk (hazard ratio [HR] 4.13, p = 0.007). Higher tacrolimus levels were associated with decreased mortality in AAs (HR 0.62, p = 0.009). Overall gene expression profiling score was associated with increased mortality among Caucasians (HR 1.21, p = 0.048). In Caucasians, but not AAs, overexpression of MARCH8 was associated with increased mortality (HR 2.90, p = 0.001). FLT3 upregulation was associated with increased mortality (HR 2.42, p = 0.033) in AAs. There was an inverse relationship between FLT3 expression and tacrolimus levels (-0.029 and -0.176, respectively) in Caucasians and AAs. AAs have a significantly higher mortality risk after HTx than Caucasians, even in the low-risk Outcomes AlloMap Registry population. AAs and Caucasians had differential outcomes based upon the varying expression of MARCH8 and FLT3 genes following HTx.

Sections du résumé

BACKGROUND
African Americans (AAs) have lower survival rates after heart transplantation (HTx) than Caucasians. The aim of this analysis was to evaluate racial differences in gene expression and their associations with survival and the composite outcome of death, retransplant, rejection with hemodynamic compromise, and graft dysfunction in the Outcomes AlloMap Registry.
METHODS
Registry participants included low-risk Caucasian and AA heart transplant recipients with a baseline and at least 1 follow-up gene expression test (AlloMap(C)) within the first year after HTx. The Kaplan-Meier method with delayed entry was used to describe differences in outcomes. Multivariable Cox hazard regression was used to evaluate the associations of overall gene expression profiling score, MARCH8 and FLT3 expression, and tacrolimus levels with each outcome, and stratified Cox models were developed to quantify race-specific associations.
RESULTS
Among 933 eligible recipients, 737 (79%) were Caucasian and 196 (21%) were AA. Compared with Caucasians, AAs were significantly younger (55 vs 59 years, p < 0.001), with higher rates of non-ischemic cardiomyopathy (68% vs 50%, p < 0.001), sensitization (>10% panel reactive antibody, 16% vs 9.1%, p = 0.009), and human leukocyte antigen mismatches (7 vs 7, p = 0.01), but less frequent primary cytomegalovirus serostatus mismatch (14.31% vs 27.3%, p < 0.001). Overall, AAs had an increased adjusted mortality risk (hazard ratio [HR] 4.13, p = 0.007). Higher tacrolimus levels were associated with decreased mortality in AAs (HR 0.62, p = 0.009). Overall gene expression profiling score was associated with increased mortality among Caucasians (HR 1.21, p = 0.048). In Caucasians, but not AAs, overexpression of MARCH8 was associated with increased mortality (HR 2.90, p = 0.001). FLT3 upregulation was associated with increased mortality (HR 2.42, p = 0.033) in AAs. There was an inverse relationship between FLT3 expression and tacrolimus levels (-0.029 and -0.176, respectively) in Caucasians and AAs.
CONCLUSIONS
AAs have a significantly higher mortality risk after HTx than Caucasians, even in the low-risk Outcomes AlloMap Registry population. AAs and Caucasians had differential outcomes based upon the varying expression of MARCH8 and FLT3 genes following HTx.

Identifiants

pubmed: 31201087
pii: S1053-2498(19)31512-8
doi: 10.1016/j.healun.2019.05.008
pii:
doi:

Types de publication

Comparative Study Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

820-829

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2019 International Society for Heart and Lung Transplantation. All rights reserved.

Auteurs

Yasbanoo Moayedi (Y)

Section of Heart Failure, Cardiac Transplant, and Mechanical Circulatory Support, and Department of Medicine, Stanford University, Stanford, California; Ted Rogers Centre of Excellence for Heart Research, Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada.

Chun-Po S Fan (CS)

Ted Rogers Centre of Excellence for Heart Research, Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada.

Robert J H Miller (RJH)

Section of Heart Failure, Cardiac Transplant, and Mechanical Circulatory Support, and Department of Medicine, Stanford University, Stanford, California.

Maxime Tremblay-Gravel (M)

Section of Heart Failure, Cardiac Transplant, and Mechanical Circulatory Support, and Department of Medicine, Stanford University, Stanford, California.

Juan G Duero Posada (JGD)

Ted Rogers Centre of Excellence for Heart Research, Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada.

Cedric Manlhiot (C)

Section of Heart Failure, Cardiac Transplant, and Mechanical Circulatory Support, and Department of Medicine, Stanford University, Stanford, California.

David Hiller (D)

CareDx, Brisbane, California.

James Yee (J)

CareDx, Brisbane, California.

Robert Woodward (R)

CareDx, Brisbane, California.

Jennifer A McCaughan (JA)

Division of Nephrology, Belfast City Hospital, Belfast, Ireland.

Michael A Shullo (MA)

West Virginia University, Morgantown, West Virginia.

Shelley A Hall (SA)

Center for Advanced Heart and Lung Disease, Baylor University Medical Center, Dallas, Texas.

Sean Pinney (S)

Mount Sinai Hospital, New York City, New York.

Kiran K Khush (KK)

Section of Heart Failure, Cardiac Transplant, and Mechanical Circulatory Support, and Department of Medicine, Stanford University, Stanford, California.

Heather J Ross (HJ)

Ted Rogers Centre of Excellence for Heart Research, Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada.

Jeffrey J Teuteberg (JJ)

Section of Heart Failure, Cardiac Transplant, and Mechanical Circulatory Support, and Department of Medicine, Stanford University, Stanford, California. Electronic address: jeff.teuteberg@stanford.edu.

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