ArticleBMC cardiovascular disorders2026
Comprehensive age-specific metabolic phenotyping in myocardial infarction.
Article in BMC cardiovascular disorders, 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
16 authors.
Funding
Abstract
Aging is a main risk factor for the development of myocardial infarction (MI), with worse clinical outcomes. However, the understanding of age-related metabolic profiles in MI remains unclear. This study aimed to identify the clinical implications of age-specific metabolic phenotyping in the MI population. MI patients were classified into two categories as > 65 years (n = 142) and ≤ 65 years (n = 139). Comprehensive metabolic profiles, including hydrophilic and lipid metabolites, were quantified and compared in MI patients aged > 65 vs. ≤ 65 years. The primary clinical outcome was 3-year major adverse cardiac event (MACE), defined as the composite of cardiac death, non-fatal MI, and any revascularization. Overall, 88 aging-specific metabolites were identified in MI, specifying pathways of insulin resistance, lipolysis in adipocytes, and phenylalanine metabolism. Within the 3-year follow-up, 3-O-Methyldopa (3-OMD), Phenylacetyl-L-Glutamine (PAGln), Taurolithocholic acid (TLCA), and TG (10:0_16:0_18:1) were significantly associated with MACE. In multivariable analysis, 3-OMD (HR = 5.5, [95% CI 1.6–19.2], p = 0.007) and PAGln (HR = 3.8, [95% CI 1.3–11.4], p = 0.02) were the independent predictors of MACE. OCT examination was performed in the majority of MI patients (271/281, 96.4%); plaque rupture was diagnosed in 188 patients, and plaque erosion was identified in 77 patients. 3-OMD and PAGln were significant predictors of MACE in patients with plaque rupture but not in those with plaque erosion. In conclusion, in elderly MI patients, pathways of insulin resistance, lipolysis in adipocytes, and phenylalanine metabolism were activated. 3-OMD and PAGln indicate the poor clinical outcomes in MI patients with plaque rupture.
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.