Key result
HCV NAT+ donor hearts treated with DAAs show no excess CAV risk versus NAT- hearts.
Why the study?
Direct-acting antiviral therapy has renewed interest in transplanting HCV-viremic donor hearts, but long-term outcomes and the risk of cardiac allograft vasculopathy remain limited.
Does heart transplantation from HCV NAT+ donors followed by DAA therapy increase the risk of cardiac allograft vasculopathy in adult heart transplant recipients?
Cohort (n=131)
No
Does heart transplantation from HCV NAT+ donors followed by DAA therapy increase the risk of cardiac allograft vasculopathy in adult heart transplant recipients?
Heart transplantation from HCV-viremic donors followed by direct-acting antiviral therapy does not appear to increase the intermediate-term risk of cardiac allograft vasculopathy compared to non-viremic donors.
Supports expanded use of HCV NAT+ donor hearts; leaves open need for randomized confirmation of long-term safety.
Background: Cardiac allograft vasculopathy (CAV) is a leading cause of death in heart transplant (HTx) recipients. Chronic hepatitis C virus (HCV) infection has been associated with increased inflammation and accelerated CAV. The advent of direct-acting antiviral (DAA) therapy has renewed interest in transplanting HCV-viremic donors, though long-term outcomes remain limited. Methods: We conducted a single-center retrospective study of adult HTx recipients at UC San Diego from 2015 to 2019 who underwent routine intravascular ultrasound (IVUS) surveillance. Recipients were stratified by donor HCV nucleic acid amplification test (NAT) status. Donor-derived HCV infection was treated with DAA therapy. We used multivariable-adjusted Cox regression to evaluate the primary endpoint of developing CAV, defined as maximal intimal thickness (MIT) ≥ 0.5 mm, and endpoints of MIT ≥ 0.7 mm and a composite outcome of incident acute coronary syndrome, percutaneous coronary intervention (PCI), and all-cause mortality. Conclusion: In the modern DAA era, transplantation of HCV NAT+ donor hearts is not associated with increased risk of CAV or adverse clinical outcomes over intermediate-term follow-up.
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Paternostro et al. (2025) conducted a cohort in Heart transplantation (n=131). HCV NAT+ donor heart (with direct-acting antiviral therapy) vs. HCV NAT- donor heart was evaluated on Development of cardiac allograft vasculopathy (maximal intimal thickness ≥ 0.5 mm) (HR 0.89, 95% CI 0.52-1.53, p=0.673). Transplantation of HCV NAT+ donor hearts followed by direct-acting antiviral therapy was not associated with a higher risk of cardiac allograft vasculopathy compared to HCV NAT- hearts (adjusted HR 0.89).
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