BACKGROUND: The release kinetics of cardiac troponin T measured with conventional vs high-sensitivity cardiac troponin T (hs-cTnT) assays in patients with acute myocardial infarction (AMI) is difficult to establish. METHODS: We analyzed the release kinetics of cTnT measured by fourth generation and high-sensitivity assays, creatine kinase-MB (CK-MB), and myoglobin in patients with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy (TASH), a model of AMI. Consecutive patients (n = 21) undergoing TASH were included. Serum and EDTA-plasma samples were collected before and at 15, 30, 45, 60, 75, 90, and 105 min, and 2, 4, 8, and 24 h after TASH. RESULTS: cTnT concentrations measured by the hs assay were significantly increased at 15 min [21.4 ng/L, interquartile range (IQR) 13.3-39.7 ng/L vs 11.3 ng/L, IQR 6.0-18.8 ng/L at baseline; P = 0.031]. In comparison, cTnT concentrations measured by the conventional fourth generation assay increased significantly at 60 min (30.0 ng/L, IQR 20.0-30.0 ng/L vs <10.0 ng/L, IQR <10.0-10.0 ng/L; P < 0.01), CK-MB at 90 min (8.4 μg/L, IQR 6.9-14.4 μg/L vs 0.9 μg/L, IQR 0.4-1.1 μg/L; P < 0.01), and myoglobin at 30 min (188.0 μg/L, IQR 154.0-233.0 μg/L vs 38.0 μg/L, IQR 28.0-56.0; P < 0.01). CONCLUSIONS: cTnT concentrations measured by the hs assay were significantly increased after TASH at all of the time points, with a doubling at 15 min after induction of AMI, confirming earlier evidence of myocardial injury compared to the fourth generation cTnT assay and CK-MB and myoglobin.
BACKGROUND: The release kinetics of cardiac troponin T measured with conventional vs high-sensitivity cardiac troponin T (hs-cTnT) assays in patients with acute myocardial infarction (AMI) is difficult to establish. METHODS: We analyzed the release kinetics of cTnT measured by fourth generation and high-sensitivity assays, creatine kinase-MB (CK-MB), and myoglobin in patients with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy (TASH), a model of AMI. Consecutive patients (n = 21) undergoing TASH were included. Serum and EDTA-plasma samples were collected before and at 15, 30, 45, 60, 75, 90, and 105 min, and 2, 4, 8, and 24 h after TASH. RESULTS:cTnT concentrations measured by the hs assay were significantly increased at 15 min [21.4 ng/L, interquartile range (IQR) 13.3-39.7 ng/L vs 11.3 ng/L, IQR 6.0-18.8 ng/L at baseline; P = 0.031]. In comparison, cTnT concentrations measured by the conventional fourth generation assay increased significantly at 60 min (30.0 ng/L, IQR 20.0-30.0 ng/L vs <10.0 ng/L, IQR <10.0-10.0 ng/L; P < 0.01), CK-MB at 90 min (8.4 μg/L, IQR 6.9-14.4 μg/L vs 0.9 μg/L, IQR 0.4-1.1 μg/L; P < 0.01), and myoglobin at 30 min (188.0 μg/L, IQR 154.0-233.0 μg/L vs 38.0 μg/L, IQR 28.0-56.0; P < 0.01). CONCLUSIONS:cTnT concentrations measured by the hs assay were significantly increased after TASH at all of the time points, with a doubling at 15 min after induction of AMI, confirming earlier evidence of myocardial injury compared to the fourth generation cTnT assay and CK-MB and myoglobin.
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