María Rubini Giménez1, Karin Wildi2, Desiree Wussler3, Luca Koechlin4, Jasper Boeddinghaus3, Thomas Nestelberger5, Patrick Badertscher6, Raphael Sedlmayer5, Christian Puelacher3, Tobias Zimmermann5, Jeanne du Fay de Lavallaz3, Pedro Lopez-Ayala3, Kathrin Leu5, Katharina Rentsch7, Òscar Miró8, Beatriz López8, F Javier Martín-Sánchez9, José Bustamante9, Damian Kawecki10, Jiri Parenica11, Jens Lohrmann12, Wanda Kloos12, Andreas Buser13, Dagmar I Keller14, Tobias Reichlin15, Raphael Twerenbold5, Christian Mueller16. 1. Department of Cardiology and Cardiovascular Research, Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland; Department of Cardiology, Heart Center Leipzig, Leipzig, Germany. 2. Department of Cardiology and Cardiovascular Research, Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland; Critical Care Research Institute, the Prince Charles Hospital, Brisbane and University of Queensland, Brisbane, Australia. 3. Department of Cardiology and Cardiovascular Research, Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland; Department of Internal Medicine, University Hospital Basel, Basel, Switzerland. 4. Department of Cardiology and Cardiovascular Research, Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland; Department of Heart Surgery, University Hospital Basel, Basel, Switzerland. 5. Department of Cardiology and Cardiovascular Research, Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland. 6. Department of Cardiology and Cardiovascular Research, Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland; Department of Cardiology, University of Illinois at Chicago, Chicago, United States. 7. Laboratory Medicine, University Hospital Basel, Basel, Switzerland. 8. Servicio de Urgencias, Hospital Clínic, Barcelona, Spain. 9. Servicio de Urgencias, Hospital Clínico San Carlos, Madrid, Spain. 10. 2nd Department of Cardiology, Medical University of Silesia, Zabrze, Poland. 11. Department of Cardiology, University Hospital Brno, Brno, Czech Republic and Medical Faculty, Masaryk University, Brno, Czech Republic. 12. Department of Cardiology and Cardiovascular Research, Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland; Emergency Department, University Hospital Basel, Basel, Switzerland. 13. Blood Transfusion Centre, Swiss Red Cross, Basel, Switzerland and Department of Hematology, University Hospital Basel, Basel, Switzerland. 14. Emergency Department, University Hospital Zurich, Zurich, Switzerland. 15. Department of Cardiology and Cardiovascular Research, Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland; Department of Department, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. 16. Department of Cardiology and Cardiovascular Research, Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland. Electronic address: Christian.Mueller@usb.ch.
Abstract
INTRODUCTION AND OBJECTIVES: Release kinetics of high-sensitivity cardiac troponin (hs-cTn) T and I in patients with acute myocardial infarction (AMI) are incompletely understood. We aimed to assess whether hs-cTnT/I release in early AMI is near linear. METHODS: In a prospective diagnostic multicenter study the acute release of hs-cTnT and hs-cTnI within 1 and 2hours from presentation to the emergency department was quantified using 3 hs-cTnT/I assays in patients with suspected AMI. The primary endpoint was correlation between hs-cTn changes from presentation to 1 hour vs changes from presentation to 2hours, among all AMI patients and different prespecified subgroups. The final diagnosis was adjudicated by 2 independent cardiologists, based on serial hs-cTnT from the serial study blood samples and additional locally measured hs-cTn values. RESULTS: Among 2437 patients with complete hs-cTnT data, AMI was the adjudicated diagnosis in 376 patients (15%). For hs-cTnT, the correlation coefficient between 0- to 1-hour change and 0- to 2 hour change was 0.931 (95%CI, 0.916-0.944), P <.001. Similar findings were obtained with hs-cTnI (Architect) with correlation coefficients between 0- to 1-hour change and 0- to 2 hour change of 0.969 and hs-cTnI (Centaur) of 0.934 (P <.001 for both). Findings were consistent among type 1 and type 2 AMI and in the subgroup of patients presenting very early after chest pain onset. CONCLUSIONS: Patients presenting with early AMI showed a near linear release of hs-cTnT and hs-cTnI. This near linearity provides the pathophysiological basis for rapid diagnostic algorithms using 0- to 1-hour changes as surrogates for 0- to 2 hour or 0- to 3 hour changes. Registered at ClinicalTrials.gov (Identifier: NCT00470587).
INTRODUCTION AND OBJECTIVES: Release kinetics of high-sensitivity cardiac troponin (hs-cTn) T and I in patients with acute myocardial infarction (AMI) are incompletely understood. We aimed to assess whether hs-cTnT/I release in early AMI is near linear. METHODS: In a prospective diagnostic multicenter study the acute release of hs-cTnT and hs-cTnI within 1 and 2hours from presentation to the emergency department was quantified using 3 hs-cTnT/I assays in patients with suspected AMI. The primary endpoint was correlation between hs-cTn changes from presentation to 1 hour vs changes from presentation to 2hours, among all AMI patients and different prespecified subgroups. The final diagnosis was adjudicated by 2 independent cardiologists, based on serial hs-cTnT from the serial study blood samples and additional locally measured hs-cTn values. RESULTS: Among 2437 patients with complete hs-cTnT data, AMI was the adjudicated diagnosis in 376 patients (15%). For hs-cTnT, the correlation coefficient between 0- to 1-hour change and 0- to 2 hour change was 0.931 (95%CI, 0.916-0.944), P <.001. Similar findings were obtained with hs-cTnI (Architect) with correlation coefficients between 0- to 1-hour change and 0- to 2 hour change of 0.969 and hs-cTnI (Centaur) of 0.934 (P <.001 for both). Findings were consistent among type 1 and type 2 AMI and in the subgroup of patients presenting very early after chest pain onset. CONCLUSIONS:Patients presenting with early AMI showed a near linear release of hs-cTnT and hs-cTnI. This near linearity provides the pathophysiological basis for rapid diagnostic algorithms using 0- to 1-hour changes as surrogates for 0- to 2 hour or 0- to 3 hour changes. Registered at ClinicalTrials.gov (Identifier: NCT00470587).