ArticlePediatric radiology2026
Examination of elevated myocardial extracellular volume and exercise capacity in pediatric Fontan patients at moderate altitude.
Article in Pediatric radiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiffuse myocardial fibrosis, as measured by T1 (longitudinal relaxation time) mapping and extracellular volume, may be associated with ventricular dysfunction in the Fontan circulation. However, the relationship between diffuse myocardial fibrosis and exercise tolerance, an early and clinically meaningful marker of Fontan physiology, remains incompletely characterized, particularly in pediatric populations.
objectiveTo evaluate the association between CMR-derived markers of diffuse myocardial fibrosis (native T1 and ECV) and exercise tolerance in pediatric patients with Fontan circulation compared with healthy controls. MATERIALS AND
methodsA retrospective cohort study of pediatric patients with Fontan circulation who underwent clinically indicated cardiovascular magnetic resonance (CMR) with native and post-contrast T1 mapping between 2019 and 2022 was performed. Global native T1 and ECV were quantified and compared with age- and scanner-matched controls. Cardiopulmonary exercise testing-derived VO₂ max and catheterization parameters obtained within 24 months of CMR were analyzed. Associations between myocardial fibrosis markers and functional measures were assessed using correlation analyses.
resultsA cohort of 64 pediatric Fontan patients (median age 11.0 years, interquartile range 7.0-14.0; age range <18 years), and 41 pediatric controls, was stratified by field strength and ventricular dominance. Fontan patients demonstrated increased native T1 values across varying field strengths of 1.5 T (1,035.9 ± 48.7 ms vs 983.8 ± 29.0 ms, P<0.001) and 3 T (1,292.8 ± 53.5 ms vs 1,257.8 ± 41.5 ms, P=0.033), and significantly elevated ECV compared to controls (25.6 ± 3.5% vs 23.2 ± 2.1%, P=0.007). There was no significant difference in native T1 or ECV between dominant right and left ventricles. VO₂ max was markedly reduced in Fontan patients compared to controls (1.2 ± 0.4 liters per minute (LPM) vs 2.5 ± 0.7 LPM, P<0.001). While a broad-inverse correlation between ECV and VO₂ max did not reach statistical significance across the full cohort (R=-0.19, P>0.05), time since Fontan surgery was inversely correlated with ECV (R=-0.27, P<0.05), and localized subgroup correlations emerged between native T1 and exercise capacity.
conclusionsMarkers of myocardial fibrosis were elevated among Fontan patients compared to healthy controls. Fontan patients were shown to have reduced exercise tolerance compared to controls as measured by VO2 max. While myocardial ECV is elevated in pediatric Fontan patients, its relationship with impaired exercise capacity is complex and subgroup-specific, suggesting a need for additional study and functional decline may be driven by multifactorial etiologies.
Indexed as
Identifiers
42233987What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.