ArticleESC heart failure2026
Myocardial testosterone glucuronide and disease phenotypes in hypertrophic cardiomyopathy.
Article in ESC heart failure, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Metabolomic biomarkers and metabolic remodelling in genetically characterised hypertrophic cardiomyopathy: a systematic review.Metabolomics : Official journal of the Metabolomic Society · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors.
Funding
Abstract
introductionThe relationship between myocardial lipid metabolism and disease phenotypes, genetic variation, and prognostic factors in patients with hypertrophic cardiomyopathy (HCM) remains largely unexplored. This study aimed to clarify how metabolic remodelling relates to disease phenotypes in HCM. We used desorption electrospray ionization imaging mass spectrometry (DESI-IMS) to compare myocardial lipid signatures in patients who required septal reduction therapy (SRT) and those who did not.
methodsIn this prospective study, patients with HCM undergoing either right-ventricular biopsy or surgical septal myectomy were enrolled. Frozen 10 µm sections were analysed using DESI-IMS, and mass spectra were compared with volcano plots after signal-intensity normalization. Candidate ions showing |log2 fold change| ≥ 1 and P < .05 were annotated using the Human Metabolome Database.
resultsOverall, 61 patients were analysed (34 [55.7%] were female; mean age 64.5 ± 15.9 years). Of these, 43 (70.5%) had obstructive HCM and 20 underwent SRT (SRT, n = 20; non-SRT, n = 41). The SRT group displayed a 3.3-fold higher signal for m/z 463.23, identified as testosterone glucuronide (P < .001). SRT remained the only predictor of elevated testosterone-glucuronide intensity in confirmatory regression (β = 1.991, P = .004), even after adjusting for age at diagnosis and the presence of hypertension, which significantly differed in baseline characteristics between the SRT and non-SRT groups.
conclusionDESI-IMS revealed selective accumulation of testosterone glucuronide in hypertrophied myocardium from patients needing SRT, suggesting that androgen-linked metabolic remodelling plays a role in advanced obstructive physiology in HCM.
Indexed as
Identifiers
What 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.