Cardiac Troponin Is Elevated in Patients with Thyrotoxicosis and Decreases as Thyroid Function Improves and Brain
Natsuko Watanabe1, Jaeduk Yoshimura Noh1, Naomi Hattori1
1Department of Internal Medicine, Ito Hospital, Tokyo, Japan.
Insights
Thyrotoxicosis can elevate high-sensitive troponin I (hsTnI) in about 20% of patients, indicating subclinical myocardial injury. hsTnI levels decrease with improved thyroid function and reduced brain natriuretic peptide (BNP).
Area of Science:
- Cardiology
- Endocrinology
- Biomarker Research
Background:
- High-sensitive cardiac troponin (hsTnI) serves as a sensitive indicator of myocardial injury, even without overt myocardial infarction.
- Thyrotoxicosis, a condition of excess thyroid hormones, can impact cardiovascular function and potentially affect cardiac biomarkers.
Purpose of the Study:
- To investigate the relationship between thyrotoxicosis and elevated levels of high-sensitive troponin I (hsTnI).
- To determine how hsTnI levels change during the treatment of hyperthyroidism.
Main Methods:
- Prospective observational study conducted in Japan involving 143 untreated thyrotoxicosis patients.
- Measurements of thyroid function (free T4), hsTnI, and brain natriuretic peptide (BNP) were taken at baseline and every 3 months for one year.
- Medical treatment was initiated for hyperthyroidism during the study period.
Main Results:
- Approximately 20% of patients presented with elevated hsTnI levels at baseline (≥5.0 pg/mL).
- hsTnI levels were significantly correlated with age and BNP, while BNP was influenced by age, hemoglobin, free T4, and hsTnI.
- A decrease in hsTnI and BNP was observed within the first 3 months, correlating with improvements in thyroid function (FT4).
Conclusions:
- Elevated hsTnI is common in patients with thyrotoxicosis, suggesting potential subclinical myocardial strain.
- hsTnI levels normalize in a majority of affected patients within a year as thyroid function improves.
- The study highlights the interplay between thyroid status, cardiac biomarkers (hsTnI), and heart strain indicators (BNP).
Introduction:
High-sensitive cardiac troponin reflects micro-myocardial injury in the absence of overt myocardial infarction.
Objective:
This study aimed to clarify how thyrotoxicosis affects cardiac troponin.
Methods:
This was a prospective observational study in Japan. Untreated patients with thyrotoxicosis who visited Ito Hospital were enrolled, and medical treatment was initiated for hyperthyroidism. Thyroid function, high-sensitive troponin I (hsTnI), and brain natriuretic peptide (BNP) were measured at baseline and then every 3 months for 1 year.
Results:
Data from a total of 143 patients (median age, 42 years; 32 men and 111 women) were investigated. At baseline, median hsTnI was 1.9 pg/mL and ranged from 0 to 69.6 pg/mL. Five patients (3.5%) had a high hsTnI value that exceeded 26.2 pg/mL, which is used as the cutoff for diagnosis of myocardial infarction, and 22 patients (15.4%) had an intermediate value between 5.0 and 26.2 pg/mL. Multivariable regression analysis showed that significant predictors of the hsTnI value were age (β = 0.20, p = 0.01) and BNP (β = 0.43, p < 0.0001) (R2 = 0.27, F = 26.0, p < 0.0001), and significant predictors of the BNP value were age (β = 0.23, p = 0.001), hemoglobin (β = -0.43, p < 0.0001), free T4 (FT4) (β = 0.23, p = 0.001), and hsTnI (β = 0.27, p < 0.0001) (R2 = 0.49, F = 33.8, p < 0.0001). Correlations were found between a decrease in hsTnI and BNP in the first 3 months (ρ = 0.49, p < 0.0001). A decrease in FT4 in the first 3 months was weakly correlated with decreases in hsTnI (ρ = 0.32, p = 0.0004) and BNP (ρ = 0.32; p = 0.0003). Of the 27 patients with elevated hsTnI (≥5.0 pg/mL), the hsTnI level was normalized in 20 patients within a year.
Conclusions:
In thyrotoxicosis, the myocardial biomarker hsTnI is elevated in about 20% of patients; hsTnI levels decrease as thyroid function improves and BNP decreases.
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