Early Assessment of Cardiac Allograft Vasculopathy Risk Among Recipients of Hepatitis C Virus-infected Donors in the Current Era.

CAV HCV Heart transplant cardiac allograft vasculopathy donor

Journal

Journal of cardiac failure
ISSN: 1532-8414
Titre abrégé: J Card Fail
Pays: United States
ID NLM: 9442138

Informations de publication

Date de publication:
29 Oct 2023
Historique:
received: 03 06 2023
revised: 22 09 2023
accepted: 27 09 2023
pubmed: 1 11 2023
medline: 1 11 2023
entrez: 31 10 2023
Statut: aheadofprint

Résumé

Transplantation of hearts from hepatitis C virus (HCV)-positive donors has increased substantially in recent years following development of highly effective direct-acting antiviral therapies for treatment and cure of HCV. Although historical data from the pre-direct-acting antiviral era demonstrated an association between HCV-positive donors and accelerated cardiac allograft vasculopathy (CAV) in recipients, the relationship between the use of HCV nucleic acid test-positive (NAT+) donors and the development of CAV in the direct-acting antiviral era remains unclear. We performed a retrospective, single-center observational study comparing coronary angiographic CAV outcomes during the first year after transplant in 84 heart transplant recipients of HCV NAT+ donors and 231 recipients of HCV NAT- donors. Additionally, in a subsample of 149 patients (including 55 in the NAT+ cohort and 94 in the NAT- cohort) who had serial adjunctive intravascular ultrasound examination performed, we compared development of rapidly progressive CAV, defined as an increase in maximal intimal thickening of ≥0.5 mm in matched vessel segments during the first year post-transplant. In an unadjusted analysis, recipients of HCV NAT+ hearts had reduced survival free of CAV ≥1 over the first year after heart transplant compared with recipients of HCV NAT- hearts. After adjustment for known CAV risk factors, however, there was no significant difference between cohorts in the likelihood of the primary outcome, nor was there a difference in development of rapidly progressive CAV. These findings support larger, longer-term follow-up studies to better elucidate CAV outcomes in recipients of HCV NAT+ hearts and to inform post-transplant management strategies.

Sections du résumé

BACKGROUND BACKGROUND
Transplantation of hearts from hepatitis C virus (HCV)-positive donors has increased substantially in recent years following development of highly effective direct-acting antiviral therapies for treatment and cure of HCV. Although historical data from the pre-direct-acting antiviral era demonstrated an association between HCV-positive donors and accelerated cardiac allograft vasculopathy (CAV) in recipients, the relationship between the use of HCV nucleic acid test-positive (NAT+) donors and the development of CAV in the direct-acting antiviral era remains unclear.
METHODS AND RESULTS RESULTS
We performed a retrospective, single-center observational study comparing coronary angiographic CAV outcomes during the first year after transplant in 84 heart transplant recipients of HCV NAT+ donors and 231 recipients of HCV NAT- donors. Additionally, in a subsample of 149 patients (including 55 in the NAT+ cohort and 94 in the NAT- cohort) who had serial adjunctive intravascular ultrasound examination performed, we compared development of rapidly progressive CAV, defined as an increase in maximal intimal thickening of ≥0.5 mm in matched vessel segments during the first year post-transplant. In an unadjusted analysis, recipients of HCV NAT+ hearts had reduced survival free of CAV ≥1 over the first year after heart transplant compared with recipients of HCV NAT- hearts. After adjustment for known CAV risk factors, however, there was no significant difference between cohorts in the likelihood of the primary outcome, nor was there a difference in development of rapidly progressive CAV.
CONCLUSIONS CONCLUSIONS
These findings support larger, longer-term follow-up studies to better elucidate CAV outcomes in recipients of HCV NAT+ hearts and to inform post-transplant management strategies.

Identifiants

pubmed: 37907147
pii: S1071-9164(23)00381-0
doi: 10.1016/j.cardfail.2023.09.015
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2023 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors have no relevant conflicts of interest to declare.

Auteurs

Kaushik Amancherla (K)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Irene D Feurer (ID)

Departments of Surgery and Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee.

Scott A Rega (SA)

Vanderbilt Transplant Center, Nashville, Tennessee.

Andrew Cluckey (A)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Mohamed Salih (M)

Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Jonathan Davis (J)

Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Dawn Pedrotty (D)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Henry Ooi (H)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Aniket S Rali (AS)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Hasan K Siddiqi (HK)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Jonathan Menachem (J)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Douglas M Brinkley (DM)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Lynn Punnoose (L)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Suzanne B Sacks (SB)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Sandip K Zalawadiya (SK)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Mark Wigger (M)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Keki Balsara (K)

Department of Cardiac Surgery, Medstar Washington Hospital Center, Washington, DC.

John Trahanas (J)

Department of Cardiac Surgery, Vanderbilt University Medical Center, Nashville, Tennessee.

William G McMaster (WG)

Department of Cardiac Surgery, Vanderbilt University Medical Center, Nashville, Tennessee.

Jordan Hoffman (J)

Division of Cardiothoracic Surgery, University of Colorado, Aurora, Colorado.

Chetan Pasrija (C)

Department of Cardiac Surgery, Vanderbilt University Medical Center, Nashville, Tennessee.

Joann Lindenfeld (J)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.

Ashish S Shah (AS)

Department of Cardiac Surgery, Vanderbilt University Medical Center, Nashville, Tennessee.

Kelly H Schlendorf (KH)

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address: kelly.h.schlendorf@vumc.org.

Classifications MeSH