Rasmus Bo Hasselbalch, Selma Salonen, Jonas Henrik Kristensen, Tuulia Tuominen, Nina Strandkjær, Morten Østergaard, Hasse Møller-Sørensen, Jens Christian Nilsson, Morten Dahl, Mustafa Vakur Bor, Ruth Frikke-Schmidt, Niklas Rye Jørgensen, Line Rode, Lene Holmvang, Jesper Kjærgaard, Lia E Bang, Julie Forman, Kim P Dalhoff, Allan S Jaffe, Kristian Thygesen, Henning Bundgaard, Saara Wittfooth, Kasper Karmark Iversen
{"title":"长型心肌肌钙蛋白T的半衰期。","authors":"Rasmus Bo Hasselbalch, Selma Salonen, Jonas Henrik Kristensen, Tuulia Tuominen, Nina Strandkjær, Morten Østergaard, Hasse Møller-Sørensen, Jens Christian Nilsson, Morten Dahl, Mustafa Vakur Bor, Ruth Frikke-Schmidt, Niklas Rye Jørgensen, Line Rode, Lene Holmvang, Jesper Kjærgaard, Lia E Bang, Julie Forman, Kim P Dalhoff, Allan S Jaffe, Kristian Thygesen, Henning Bundgaard, Saara Wittfooth, Kasper Karmark Iversen","doi":"10.1093/jalm/jfag142","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Long forms of cardiac troponin T (cTnT) are promising markers that may differentiate myocardial infarction from other causes of acute and chronic myocardial injury. However, to understand the clinical utility of long cTnT, knowledge of the half-life (T½) is key. By using auto-transfusion in humans we determined the T½ of long forms of cTnT and compared long cTnT to a commercial high-sensitivity total cTnT assay.</p><p><strong>Methods: </strong>Patients with ST-segment-elevation-myocardial infarction were included within 24 h after revascularization and underwent plasmapheresis to obtain plasma with a high cTnT concentration. After at least 3 weeks, patients returned for an autologous plasma re-transfusion followed by repeated blood sampling. A novel assay measured long cTnT and a commercially available assay measured total cTnT.</p><p><strong>Results: </strong>We included 17 patients with median age 63 years (25th-75th percentiles 59-70), and 4 (24%) were female. The median concentrations after transfusion were 99 ng/L (54-125) for long cTnT vs 252 ng/L (233-322) for total cTnT. The median ratio of long cTnT to total cTnT was 0.39 (0.26-0.55) after transfusion and declined to 0.30 (0.20-0.44) after 60 min. Long cTnT displayed a 2-phase exponential decay, similar to what was observed for total cTnT but with shorter T½ both for the distribution phase [16 min (11-18) vs 22 min (20-24), P < 0.001] and the elimination phase [103 min (78-125) vs 133 min (114-168), P < 0.001].</p><p><strong>Conclusion: </strong>The elimination of long forms of cTnT was faster than for total cTnT following re-transfusion. This understanding could aid in differentiating myocardial infarction from other causes of acute and chronic myocardial injury.</p>","PeriodicalId":46361,"journal":{"name":"Journal of Applied Laboratory Medicine","volume":" ","pages":""},"PeriodicalIF":2.3000,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The Half-Life of Long Forms of Cardiac Troponin T.\",\"authors\":\"Rasmus Bo Hasselbalch, Selma Salonen, Jonas Henrik Kristensen, Tuulia Tuominen, Nina Strandkjær, Morten Østergaard, Hasse Møller-Sørensen, Jens Christian Nilsson, Morten Dahl, Mustafa Vakur Bor, Ruth Frikke-Schmidt, Niklas Rye Jørgensen, Line Rode, Lene Holmvang, Jesper Kjærgaard, Lia E Bang, Julie Forman, Kim P Dalhoff, Allan S Jaffe, Kristian Thygesen, Henning Bundgaard, Saara Wittfooth, Kasper Karmark Iversen\",\"doi\":\"10.1093/jalm/jfag142\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Long forms of cardiac troponin T (cTnT) are promising markers that may differentiate myocardial infarction from other causes of acute and chronic myocardial injury. However, to understand the clinical utility of long cTnT, knowledge of the half-life (T½) is key. By using auto-transfusion in humans we determined the T½ of long forms of cTnT and compared long cTnT to a commercial high-sensitivity total cTnT assay.</p><p><strong>Methods: </strong>Patients with ST-segment-elevation-myocardial infarction were included within 24 h after revascularization and underwent plasmapheresis to obtain plasma with a high cTnT concentration. After at least 3 weeks, patients returned for an autologous plasma re-transfusion followed by repeated blood sampling. A novel assay measured long cTnT and a commercially available assay measured total cTnT.</p><p><strong>Results: </strong>We included 17 patients with median age 63 years (25th-75th percentiles 59-70), and 4 (24%) were female. The median concentrations after transfusion were 99 ng/L (54-125) for long cTnT vs 252 ng/L (233-322) for total cTnT. The median ratio of long cTnT to total cTnT was 0.39 (0.26-0.55) after transfusion and declined to 0.30 (0.20-0.44) after 60 min. Long cTnT displayed a 2-phase exponential decay, similar to what was observed for total cTnT but with shorter T½ both for the distribution phase [16 min (11-18) vs 22 min (20-24), P < 0.001] and the elimination phase [103 min (78-125) vs 133 min (114-168), P < 0.001].</p><p><strong>Conclusion: </strong>The elimination of long forms of cTnT was faster than for total cTnT following re-transfusion. This understanding could aid in differentiating myocardial infarction from other causes of acute and chronic myocardial injury.</p>\",\"PeriodicalId\":46361,\"journal\":{\"name\":\"Journal of Applied Laboratory Medicine\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":2.3000,\"publicationDate\":\"2026-09-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Applied Laboratory Medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1093/jalm/jfag142\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICAL LABORATORY TECHNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Applied Laboratory Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/jalm/jfag142","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICAL LABORATORY TECHNOLOGY","Score":null,"Total":0}
The Half-Life of Long Forms of Cardiac Troponin T.
Background: Long forms of cardiac troponin T (cTnT) are promising markers that may differentiate myocardial infarction from other causes of acute and chronic myocardial injury. However, to understand the clinical utility of long cTnT, knowledge of the half-life (T½) is key. By using auto-transfusion in humans we determined the T½ of long forms of cTnT and compared long cTnT to a commercial high-sensitivity total cTnT assay.
Methods: Patients with ST-segment-elevation-myocardial infarction were included within 24 h after revascularization and underwent plasmapheresis to obtain plasma with a high cTnT concentration. After at least 3 weeks, patients returned for an autologous plasma re-transfusion followed by repeated blood sampling. A novel assay measured long cTnT and a commercially available assay measured total cTnT.
Results: We included 17 patients with median age 63 years (25th-75th percentiles 59-70), and 4 (24%) were female. The median concentrations after transfusion were 99 ng/L (54-125) for long cTnT vs 252 ng/L (233-322) for total cTnT. The median ratio of long cTnT to total cTnT was 0.39 (0.26-0.55) after transfusion and declined to 0.30 (0.20-0.44) after 60 min. Long cTnT displayed a 2-phase exponential decay, similar to what was observed for total cTnT but with shorter T½ both for the distribution phase [16 min (11-18) vs 22 min (20-24), P < 0.001] and the elimination phase [103 min (78-125) vs 133 min (114-168), P < 0.001].
Conclusion: The elimination of long forms of cTnT was faster than for total cTnT following re-transfusion. This understanding could aid in differentiating myocardial infarction from other causes of acute and chronic myocardial injury.