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Adult congenital heart disease (ACHD) patients have the potential for increased sensitization and complications deriving from repeated interventions. Donor-derived cell-free-DNA (dd-cfDNA) test is a non-invasive method for surveillance of allograft injury. We sought to characterize dd-cfDNA in ACHD recipients and its impact on post-heart transplant (HT) outcomes. We performed a retrospective analysis of patients who underwent HT in our institution between January 2005 and January 2021, and who had at least one dd-cfDNA result. Multiorgan recipients were excluded. Patients with a history of ACHD were compared to adult HT recipients with no history of ACHD (control group). Dd-cfDNA was considered positive if >0.12%. Samples reported as <0.12% were analyzed as 0.11%. A total of 418 patients were identified; 23 ACHD patients and 395 control patients were included. ACHD patients were younger (38 years vs. 56 years, p <0.001) and the majority (73%) were male. The median dd-cfDNA did not differ between the groups (p=0.49). Endomyocardial biopsy proven allograft rejection, graft dysfunction, formation of donor specific antibody, and cardiac allograft vasculopathy did not differ between the groups during the follow-up period (2100 days in the ACHD group vs 1430 days in the control group, p=0.09). In this retrospective single center study, HT recipients with a history of ACHD did not demonstrate significantly elevated dd-cfDNA levels as compared to control. ACHD patients similarly did not have a higher incidence of endomyocardial biopsy proven allograft rejection or graft dysfunction. [ABSTRACT FROM AUTHOR]

Background: Cardiac allograft vasculopathy (CAV) causes impaired blood flow in both epicardial coronary arteries and the microvasculature. A leading cause of post-transplant mortality, CAV affects 50% of heart transplant recipients within 10 years of heart transplant., Objectives: This analysis examined the outcomes of heart transplant recipients with reduced myocardial blood flow reserve (MBFR) and microvascular CAV detected by 13 N-ammonia positron emission tomography (PET) myocardial perfusion imaging., Methods: A total of 181 heart transplant recipients who underwent PET to assess for CAV were included with a median follow-up of 4.7 years. Patients were classified into 2 groups according to the total MBFR: >2.0 and ≤2.0. Microvascular CAV was defined as no epicardial CAV detected by PET and/or coronary angiography, but with an MBFR ≤2.0 by PET., Results: In total, 71 (39%) patients had an MBFR ≤2.0. Patients with an MBFR ≤2.0 experienced an increased risk for all outcomes: 7-fold increase in death or retransplantation (HR: 7.05; 95% CI: 3.2-15.6; P < 0.0001), 12-fold increase in cardiovascular death (HR: 12.0; 95% CI: 2.64-54.12; P = 0.001), and 10-fold increase in cardiovascular hospitalization (HR: 10.1; 95% CI: 3.43-29.9; P < 0.0001). The 5-year mean survival was 302 days less than those with an MBFR >2.0 (95% CI: 260.2-345.4 days; P < 0.0001). Microvascular CAV (adjusted HR: 3.86; 95% CI: 1.58-9.40; P = 0.003) was independently associated with an increased risk of death or retransplantation., Conclusions: Abnormal myocardial blood flow reserve, even in the absence of epicardial CAV, identifies patients at a high risk of death or retransplantation. Measures of myocardial blood flow provide prognostic information in addition to traditional CAV assessment., Competing Interests: Funding Support and Author Disclosures Dr Clerkin has been supported by National Institutes of Health K23 HL148528. Dr Topkara has been supported by National Institutes of Health K08 HL146964. Dr Colombo has received consulting fees from Abbott. Dr Einstein has received speaker fees from Ionetix; has received consulting fees from W. L. Gore and Associates; and his institution has grants/grants pending from Canon Medical Systems, GE Healthcare, Roche Medical Systems, and W. L. Gore and Associates. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)