Intermediate-term risk of cardiac allograft vasculopathy following heart transplantation from hepatitis C viremic donors in the era of direct-acting antiviral therapy.

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. Results: Among 131 recipients, 22 received HCV NAT+ hearts. Baseline donor and recipient characteristics were similar, except for recipients of HCV NAT- hearts were younger (53.7 years vs 61.0 years; P = 0.022). Over a median follow-up of 6.6 years, HCV NAT+ status was not associated with a higher risk of CAV (MIT ≥ 0.5 mm: adjusted HR 0.89, 95% confidence interval (CI), 0.52-1.53; p = 0.673; MIT ≥ 0.7 mm: adjusted HR 0.91, 95% CI 0.51-1.61; p = 0.750), nor the composite outcome (adjusted HR 1.23, 95% CI, 0.45-3.40; p = 0.690). 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.