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Published on: May 10, 2021
Leakage of cardiac troponin I in aortic valve stenosis
M Kupari1, S Eriksson, H Turto
1Division of Cardiology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland. markku.kupari@hus.fi
Insights
Detectable cardiac troponin I (cTnI) in aortic valve stenosis (AS) patients is common and linked to heart failure (HF). Measuring cTnI may help detect early signs of deterioration in AS patients.
Area of Science:
- Cardiology
- Biomarkers
- Heart Failure Research
Background:
- Aortic valve stenosis (AS) leads to cardiomyocyte degeneration and heart failure (HF).
- Ongoing myocyte damage in AS is a key factor in HF development.
- Detecting myocyte damage through circulating biomarkers is crucial for managing AS.
Purpose of the Study:
- To investigate if circulating cardiac troponin I (cTnI) concentrations can detect ongoing myocyte damage in patients with AS.
- To assess the association between detectable cTnI levels and the presence of HF in AS patients.
- To determine if transcardiac gradients of cTnI correlate with left ventricular (LV) systolic function.
Main Methods:
- A cross-sectional cohort study involving 131 adult patients with isolated AS undergoing echocardiography and cardiac catheterization.
- Blood samples were collected from the aortic root and, in a subset of 49 patients, from the coronary sinus.
- Sensitive immunoassays were used to determine cTnI concentrations.
Main Results:
- 56% of AS patients had detectable aortic cTnI, with 23% exceeding the reference limit for healthy individuals.
- Detectable cTnI was associated with a higher prevalence of HF (42% vs. 19%, P = 0.004).
- A transcardiac cTnI gradient (> or =5 ng L(-1)) was observed in 27% of AS patients, correlating with lower LV ejection fractions (P = 0.011).
Conclusions:
- Detectable circulating cTnI is frequent in AS and moderately associated with HF.
- Leakage of cTnI into the coronary sinus is linked to impaired LV systolic function.
- Monitoring cTnI levels may offer a method to identify early clinical deterioration in AS.
Objective:
Degeneration and death of cardiomyocytes contribute to the genesis of heart failure (HF) in aortic valve stenosis (AS). We studied whether the ongoing myocyte damage in AS can be detected from circulating cardiac troponin I (cTnI) concentrations.
Design And Setting:
A cross-sectional cohort study in a university hospital.
Subjects And Methods:
We examined 131 adult patients undergoing echocardiography and cardiac catheterization for isolated AS. Blood was sampled from the aortic root and, in a subset of 49 patients, also from the coronary sinus for the determination of cTnI using a sensitive immunoanalysis.
Results:
Seventy-three patients (56%) had detectable aortic cTnI (> or =5 ng L(-1)) with 30 of them (23% of the total group) having cTnI above the reference limit in healthy subjects (>14 ng L(-1)). Patients with detectable cTnI had a higher prevalence of HF than those with undetectable cTnI (42% vs. 19%, P = 0.004). Plasma cTnI rose from the aorta to the coronary sinus by > or =5 ng L(-1) in 13 of 49 patients with AS (27%) versus in none of 12 control patients free of structural heart disease (P = 0.044). AS patients with transcardiac cTnI gradients > or =5 ng L(-1) had lower left ventricular (LV) ejection fractions than AS patients with gradients <5 ng L(-1) (mean +/- SD, 52 +/- 14% vs. 61 +/- 11%; P = 0.011).
Conclusions:
Detectable circulating cTnI is not uncommon in AS and shows a moderate association with the presence of HF. Leakage of cTnI into the coronary sinus associates with impairment of LV systolic function. Monitoring cTnI could provide a means to expose incipient clinical deterioration in AS.
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