Half-Life and Clearance of Cardiac Troponin I and Troponin T in Humans

医学 四分位间距 心肌梗塞 心脏病学 内科学 血浆置换术 肌钙蛋白I 肌钙蛋白 麻醉 抗体 免疫学
作者
Jonas Henrik Kristensen,Rasmus Bo Hasselbalch,Nina Strandkjær,Nicoline Jørgensen,Morten Østergaard,Hasse Møller‐Sørensen,Jens Christian Nilsson,Shoaib Afzal,Pia R. Kamstrup,Morten Dahl,Mustafa Vakur Bor,Ruth Frikke‐Schmidt,Niklas Rye Jørgensen,Line Rode,Lene Holmvang,Jesper Kjærgaard,Lia E. Bang,Julie Lyng Forman,Kim Dalhoff,Allan S. Jaffe
出处
期刊:Circulation [Ovid Technologies (Wolters Kluwer)]
卷期号:150 (15): 1187-1198 被引量:17
标识
DOI:10.1161/circulationaha.123.066565
摘要

BACKGROUND: Cardiac troponin (cTn) is key in diagnosing myocardial infarction (MI). After MI, the clinically observed half-life of cTn has been reported to be 7 to 20 hours, but this estimate reflects the combined elimination and simultaneous release of cTn from cardiomyocytes. More precise timing of myocardial injuries necessitates separation of these 2 components. We used a novel method for determination of isolated cTn elimination kinetics in humans. METHODS: Patients with MI were included within 24 hours after revascularization and underwent plasmapheresis to obtain plasma with a high cTn concentration. After at least 3 weeks, patients returned for an autologous plasma retransfusion followed by blood sampling for 8 hours. cTn was measured with 5 different high-sensitivity cTn assays. RESULTS: Of 25 included patients, 20 participants (mean age, 64.5 years; SD, 8.2 years; 4 women [20%]) received a retransfusion after a median of 5.8 weeks (interquartile range, 5.0–6.9 weeks) after MI. After retransfusion of a median of 620 mL (range, 180–679 mL) autologous plasma, the concentration of cTn in participants’ blood increased 4 to 445 times above the upper reference level of the 5 high-sensitivity cTn assays. The median elimination half-life ranged from 134.1 minutes (95% CI, 117.8–168.0) for the Elecsys high-sensitivity cTnT assay to 239.7 minutes (95% CI, 153.7–295.1) for the Vitros high-sensitivity cTnI assay. The median clearance of cTnI ranged from 40.3 mL/min (95% CI, 32.0–44.9) to 52.7 mL/min (95% CI, 42.2–57.8). The clearance of cTnT was 77.0 mL/min (95% CI, 45.2–95.0). CONCLUSIONS: This novel method showed that the elimination half-life of cTnI and cTnT was 5 to 16 hours shorter than previously reported. This indicates a considerably longer duration of cardiomyocyte cTn release after MI than previously thought. Improved knowledge of timing of myocardial injury may call for changes in the management of MI and other disorders with myocardial injury.
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