Late-gadolinium enhancement is common in older pediatric heart transplant recipients and is associated with lower ejection fraction

Abstract

Background: Chronic graft failure and cumulative rejection history in pediatric heart transplant recipients (PHTR) are associated with myocardial fibrosis on endomyocardial biopsy (EMB). Cardiovascular magnetic resonance imaging (CMR) is a validated, non-invasive method to detect myocardial fibrosis via the presence of late gadolinium enhancement (LGE). In adult heart transplant recipients, LGE is associated with increased risk of future adverse clinical events including hospitalization and death. We describe the prevalence, pattern, and extent of LGE on CMR in a cohort of PHTR and its associations with recipient and graft characteristics. Methods: This was a retrospective study of consecutive PHTR who underwent CMR over a 6-year period at a single center. Two independent reviewers assessed the presence and distribution of left ventricular (LV) LGE using the American Heart Association (AHA) 17-segment model. LGE quantification was performed on studies with visible fibrosis (LGE+). Patient demographics, clinical history, and CMR-derived volumetry and ejection fractions were obtained. Results: Eighty-one CMR studies were performed on 59 unique PHTR. Mean age at CMR was 14.8 ± 6.2 years; mean time since transplant was 7.3 ± 5.0 years. The CMR indication was routine surveillance (without a clinical concern based on laboratory parameters, echocardiography, or cardiac catheterization) in 63% (51/81) of studies. LGE was present in 36% (29/81) of PHTR. In these LGE + studies, patterns included inferoseptal in 76% of LGE + studies (22/29), lateral wall in 41% (12/29), and diffuse, involving > 4 AHA segments, in 21% (6/29). The mean LV LGE burden as a percentage of myocardial mass was 18.0 ± 9.0%. When reviewing only the initial CMR per PHTR (n = 59), LGE + patients were older (16.7 ± 2.9 vs. 12.8 ± 4.6 years, p = 0.001), with greater time since transplant (8.3 ± 5.4 vs. 5.7 ± 3.9 years, p = 0.041). These patients demonstrated higher LV end-systolic volume index (LVESVI) (34.7 ± 11.7 vs. 28.7 ± 6.1 ml/m2, p = 0.011) and decreased LV ejection fraction (LVEF) (56.2 ± 8.1 vs. 60.6 ± 5.3%, p = 0.015). There were no significant differences in history of moderate/severe rejection (p = 0.196) or cardiac allograft vasculopathy (CAV) (p = 0.709). Conclusions: LV LGE was present in approximately one third of PHTR, more commonly in older patients with longer time since transplantation. Grafts with LGE have lower LVEF. CMR-derived LGE may aid in surveillance of chronic graft failure in PHTR.