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.

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.