Observational studyJournal of the American Heart Association2025
Accelerated Vascular Aging as a Possible Mechanism of Troponin I Release in the Absence of Clinically Manifested Myocardial Injury.
Observational study in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00741728 (Heart Rate, Baroreflex Sensitivity and Cardiovascular Morbidity and Mortality in the Population. The Paris Prospective Study III), which is not on this map. Cited by 2 papers.
What it found
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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.
Heart Rate, Baroreflex Sensitivity and Cardiovascular Morbidity and Mortality in the Population. The Paris Prospective Study III
Who cites it
2 citing papers in PubMed.
- Associations of High-Sensitivity Cardiac Troponin T, D-Dimer, and N-Terminal Pro-B-Type Natriuretic Peptide with Subclinical Cardiovascular Dysfunction in the General Population: A Retrospective Cross-Sectional Study.Vascular health and risk management · 2026Article
- Correlation Between Cardiac Troponin Serum Concentration and Selected Parameters of Subclinical Cardiovascular Dysfunction in Patients With and Without Arterial Hypertension: Retrospective Cross-Sectional Analysis of Real-World Data.Journal of clinical medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe examined the association between clusters of vascular aging manifestations and ultrasensitivity cardiac troponin I in individuals without cardiovascular disease. METHODS AND
resultsA cross-sectional analysis was conducted using baseline data from PPS-3 (Paris Prospective Study III), a French cohort of 10 157 participants. Cardiac troponin I was measured with an ultrasensitive immunoassay with a limit of detection of 0.013 pg/mL. Vascular aging manifestations were assessed via echotracking of the right common carotid artery to measure structural and functional parameters. Hierarchical clustering was used to identify clusters of vascular aging. Multinomial regression assessed the association between vascular aging clusters and cardiac troponin I quintiles. The study included 8722 cardiovascular disease-free participants (mean±SD age, 59.5±6.3 years; 39% women). Three vascular aging clusters were identified. Cluster 1 (n=4158; 47.4%) was characterized as healthy vascular aging with the lowest arteriosclerosis and atherosclerosis indices; cluster 2 (n=2237; 25.5%) was characterized by the highest arteriosclerosis indices, including increased pulse wave velocity, β index, and Young elastic modulus and lowest distensibility coefficient; and cluster 3 (n=2377; 27.0%) was characterized by the highest atherosclerosis indices, including more frequent plaque prevalence and greater intima-media thickness. Compared with healthy vascular aging, arteriosclerosis and atherosclerosis clusters showed a graded positive association with cardiac troponin I quintiles, independent of traditional risk factors. The adjusted odds ratio for belonging to the highest quintile (quintile 5 versus quintile 1) was 1.55 (95% CI, 1.31-1.92) for arteriosclerosis and 2.66 (95% CI, 2.18-3.23) for atherosclerosis clusters.
conclusionsVascular aging manifestations of arteriosclerosis and atherosclerosis may partly explain the release of troponin I into the bloodstream in adults without clinical cardiovascular disease. REGISTRATION: URL: https://clinicaltrials.gov; Unique identifier: NCT00741728.
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