Key result
Specific dried blood spot metabolites identify pediatric heart failure with ~98% accuracy versus healthy controls.
Why the study?
Pediatric heart failure causes substantial morbidity and mortality, but the metabolic derangements underlying myocardial energy failure in children remain incompletely characterized.
Does targeted dried blood spot acylcarnitine and amino acid profiling discriminate between pediatric heart failure patients and healthy controls?
Case-Control (n=60)
No
Does targeted dried blood spot acylcarnitine and amino acid profiling discriminate between pediatric heart failure patients and healthy controls?
Targeted dried blood spot metabolomic profiling reveals coordinated decreases in medium-chain/dicarboxylic acylcarnitines and specific amino acids in pediatric heart failure, offering a potential low-cost, minimally invasive candidate biomarker panel pending external validation.
Answers are grounded in this paper and cite their sources.
Distinct metabolite reductions discriminate pediatric HF cases from controls; hypothesis-generating for biomarkers but requires prospective validation before any clinical use.
Pediatric heart failure (HF) causes substantial morbidity and mortality, yet the metabolic derangements underlying myocardial energy failure in children remain incompletely characterized. We performed targeted dried blood spot (DBS) acylcarnitine and amino acid profiling in 30 children with HF of mixed etiology and 30 age- and sex-frequency-matched healthy controls, quantifying 44 metabolites by flow-injection tandem mass spectrometry. Seven metabolites were significantly decreased in HF patients (p < 0.05, FDR < 0.05): hexanoylcarnitine/adipoylcarnitine (C6DC), tyrosine, octenoylcarnitine (C8:1), glutamate, decadienoylcarnitine (C10:2), proline, and dodecanoylcarnitine (C12), with decreases of 23.9–48.8%. Hydroxyoctadecanoic acid (C18OH) showed the largest overall decrease (57.7%) but did not reach FDR significance. Multivariate modeling using the full metabolite panel achieved excellent, permutation-validated discrimination between groups (PLS-DA accuracy 98%, Q²=0.82; OPLS-DA R²Y = 0.835, Q²=0.708); six metabolites (C6DC, tyrosine, C8:1, glutamate, C10:2, and proline) emerged as the top contributors to this discrimination and are proposed as an exploratory minimal candidate panel, warranting dedicated validation of its own discriminatory performance in larger, independent cohorts. Pathway enrichment highlighted catecholamine biosynthesis, thyroid hormone synthesis, and aromatic amino acid metabolism, without enrichment of fatty-acid β-oxidation or carnitine-synthesis pathways. These findings indicate that pediatric HF involves a coordinated decrease in medium-chain/dicarboxylic acylcarnitines and selected amino acids alongside enrichment of catecholaminergic and aromatic amino-acid pathways, consistent with a myocardial shift away from fatty-acid oxidation. A small, low-cost DBS-based panel may hold promise as a non-invasive adjunct for pediatric HF assessment, pending external validation.
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Abdolahpour et al. (2026) conducted a case-control in Pediatric heart failure (n=60). Pediatric heart failure (targeted dried blood spot acylcarnitine and amino acid profiling) vs. Age- and sex-frequency-matched healthy controls was evaluated on Targeted dried blood spot concentrations of 44 acylcarnitine and amino acid metabolites and multivariate group discrimination (23.9% to 48.8% decrease in 7 metabolites (PLS-DA accuracy 98%, Q²=0.82; OPLS-DA R²Y=0.835, Q²=0.708), p=<0.05 (FDR <0.05)). Pediatric heart failure was associated with 23.9–48.8% reductions in 7 acylcarnitines and amino acids (FDR<0.05), enabling 98% PLS-DA discrimination from healthy controls.
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