ArticleResuscitation plus2025
An untargeted metabolomics analysis suggests pathophysiological changes for post cardiac arrest syndrome.
Article in Resuscitation plus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cardiac arrest (CA) is a significant cause of mortality worldwide. However, the differences of untargeted metabolomics of CA patients have rarely been described. Methods: CA patients and controls were enrolled at the Emergency Department of Peking University Third Hospital between September 2022 and August 2023 in this prospective cohort study. Medical record data were utilized, and blood samples were analyzed via ultrahigh-performance liquid chromatography-tandem mass spectrometry. Comparison was made between CA patients vs controls and survivors vs non- survivors. Multivariate feature selection by sparse partial least squares discriminant analysis and metabolite set enrichment analysis were used to identify metabolites and biological pathways.Correlation analysis between these metabolites included in Significant enrichment pathways and clinical laboratory indicators was conducted. Results: 23 controls and 23 CA patients met the inclusion criteria. Principal component analysis and partial least squares discriminant analysis indicated a clear separation between the patients with CA and the healthy controls. A total of 348 differentially abundant metabolites, consisting of 132 upregulated metabolites and 216 downregulated metabolites, were screened between the above two groups. The CA group included 16 non-survivors and 7 survivors. Compared with non-survivors, 85 differentially abundant metabolites in survivors were upregulated, and 283 metabolites were downregulated. Choline metabolism in cancer and glycerophospholipid metabolism, were upregulated and enriched by Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis, whereas tryptophan metabolism, steroid hormone biosynthesis and alanine, aspartate and glutamate metabolism, and were downregulated. L-kynurenine, PLCs, cortisol and L-glutamate were correlated with some laboratory indicators. Conclusions: Differentially abundant metabolites and pathways discovered by metabolomics analysis may explained the pathophysiological changes of post CA syndrome. Some metabolites were hopeful to be prognostic biomarkers for post CA syndrome. Further pre-clinical and clinical researches need to study the mechanism of these findings.
Indexed as
Identifiers
What Socratic 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 Socratic graph.