Related Experiment Video
Updated: May 20, 2025
Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
Published on: June 3, 2019
Accelerated Vascular Aging as a Possible Mechanism of Troponin I Release in the Absence of Clinically Manifested
G A Alanis1, P Boutouyrie2, M Abouqateb1
1Integrative Epidemiology of Cardiovascular Disease Université Paris Cité, INSERM U970 Paris France.
Insights
Vascular aging, specifically arteriosclerosis and atherosclerosis, is linked to higher troponin I levels in healthy adults. These vascular changes may contribute to troponin release even without diagnosed cardiovascular disease.
Area of Science:
- Cardiology
- Vascular Biology
- Biomarkers
Background:
- Vascular aging is a spectrum of changes in arteries.
- Ultrasensitive cardiac troponin I (us-cTnI) is a biomarker for cardiac injury.
- The relationship between vascular aging patterns and us-cTnI in disease-free individuals is not fully understood.
Purpose of the Study:
- To investigate the association between distinct clusters of vascular aging manifestations and ultrasensitive cardiac troponin I levels.
- To determine if specific vascular aging patterns predict elevated troponin I in individuals without cardiovascular disease.
Main Methods:
- Cross-sectional analysis of 8722 participants from the Paris Prospective Study III.
- Vascular aging assessed using carotid artery echotracking for structural and functional parameters.
- Hierarchical clustering identified vascular aging clusters; multinomial regression analyzed associations with cardiac troponin I quintiles.
Main Results:
- Three vascular aging clusters were identified: healthy, arteriosclerosis-dominant, and atherosclerosis-dominant.
- Both arteriosclerosis and atherosclerosis clusters showed a graded positive association with cardiac troponin I levels.
- Individuals in the atherosclerosis cluster had significantly higher odds of being in the highest troponin I quintile (aOR 2.66) compared to the healthy cluster.
Conclusions:
- Arteriosclerosis and atherosclerosis represent distinct vascular aging phenotypes.
- These vascular aging manifestations may contribute to troponin I release in the absence of clinical cardiovascular disease.
- Findings suggest vascular health is a key determinant of circulating troponin levels.
Background:
We examined the association between clusters of vascular aging manifestations and ultrasensitivity cardiac troponin I in individuals without cardiovascular disease.
Methods And Results:
A 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.
Conclusions:
Vascular 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.
Related Concept Videos
01:20Blood Studies for Cardiovascular System I: Cardiac Biomarkers
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
01:28Nitric Oxide Signaling Pathway
01:25Smooth Muscle Contraction
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
01:26Cross-bridge Cycle
01:17Pathophysiology of Heart Failure
01:29Relaxation of Skeletal Muscles
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open....