Matthias Mueller-Hennessen1, Bertil Lindahl2, Evangelos Giannitsis3, Mehrshad Vafaie1, Moritz Biener1, Alexander C Haushofer4, Josef Seier4, Michael Christ5, Aitor Alquézar-Arbé6, Christopher R deFilippi7, James McCord8, Richard Body9, Mauro Panteghini10, Tomas Jernberg11, Mario Plebani12, Franck Verschuren13, John K French14, Robert H Christenson15, Carina Dinkel16, Hugo A Katus1, Christian Mueller17. 1. Department of Internal Medicine III, Cardiology, Angiology & Pulmonology, Heidelberg University Hospital, Heidelberg, Germany. 2. Department of Medical Sciences and Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. 3. Department of Internal Medicine III, Cardiology, Angiology & Pulmonology, Heidelberg University Hospital, Heidelberg, Germany. Electronic address: evangelos_giannitsis@med.uni-heidelberg.de. 4. Central Laboratory, Klinikum Wels-Grieskirchen, Wels, Austria. 5. Department of Emergency and Critical Care Medicine, Community Hospital and Paracelsus Medical University, Nuremberg, Germany. 6. Hospital de Sant Pau, Barcelona, Spain. 7. Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, United States of America. 8. Henry Ford Heart and Vascular Institute, Henry Ford Health System, Detroit, MI, United States of America. 9. Division of Cardiovascular Sciences, The University of Manchester, and Manchester University NHS Foundation Trust, United Kingdom. 10. Department of Biomedical and Clinical Sciences 'Luigi Sacco', University of Milan Medical School, Milano, Italy. 11. Department of Clinical Sciences, Danderyd University, Karolinska Institutet, Stockholm, Sweden. 12. Department of Laboratory Medicine, University Hospital of Padova, Padua, Italy. 13. Department of Acute Medicine, Cliniques Universitaires St-Luc and Université Catholique de Louvain, Brussels, Belgium. 14. Liverpool Hospital and University of New South Wales, Sydney, Australia. 15. Department of Pathology, University of Maryland School of Medicine, Baltimore, MD, United States of America. 16. Roche Diagnostics Germany, Penzberg, Germany. 17. Cardiology & Cardiovascular Research Institute Basel, University Hospital Basel, Switzerland.
Abstract
BACKGROUND: We aimed to directly compare the diagnostic and prognostic performance of a dual maker strategy (DMS) with combined testing of copeptin and high-sensitivity (hs) cardiac troponin T (cTnT) at time of presentation with other algorithms for rapid rule-out of acute myocardial infarction (AMI). METHODS: 922 patients presenting to the emergency department with suspected AMI and available baseline copeptin measurements qualified for the present TRAPID-AMI substudy. Diagnostic measures using the DMS (copeptin <10, <14 or < 20 pmol/L and hs-cTnT≤14 ng/L), the 1 h-algorithm (hs-cTnT<12 ng/L and change <3 ng/L at 1 h), as well as the hs-cTnT limit-of-blank (LoB, <3 ng/L) and -detection (LoD, <5 ng/L) were compared. Outcomes were assessed as combined end-points of death and myocardial re-infarction. RESULTS: True-negative rule-out using the DMS could be achieved in 50.9%-62.3% of all patients compared to 35.0%, 45.3% and 64.5% using LoB, LoD or the 1 h-algorithm, respectively. The DMS showed NPVs of 98.1%-98.3% compared to 99.2% for the 1 h-algorithm, 99.4% for the LoB and 99.3% for the LoD. Sensitivities were 93.5%-94.8%, as well as 96.8%, 98.7% and 98.1%, respectively. Addition of clinical low-risk criteria such as a HEART-score ≤ 3 to the DMS resulted in NPVs and sensitivities of 100% with a true-negative rule-out to 33.8%-41.6%. Rates of the combined end-point of death/MI within 30 days ranged between 0.2% and 0.3% for all fast-rule-out protocols. CONCLUSION: Depending on the applied copeptin cut-off and addition of clinical low-risk criteria, the DMS might be an alternative to the hs-cTn-only-based algorithms for rapid AMI rule-out with comparable diagnostic measures and outcomes.
BACKGROUND: We aimed to directly compare the diagnostic and prognostic performance of a dual maker strategy (DMS) with combined testing of copeptin and high-sensitivity (hs) cardiac troponin T (cTnT) at time of presentation with other algorithms for rapid rule-out of acute myocardial infarction (AMI). METHODS: 922 patients presenting to the emergency department with suspected AMI and available baseline copeptin measurements qualified for the present TRAPID-AMI substudy. Diagnostic measures using the DMS (copeptin <10, <14 or < 20 pmol/L and hs-cTnT≤14 ng/L), the 1 h-algorithm (hs-cTnT<12 ng/L and change <3 ng/L at 1 h), as well as the hs-cTnT limit-of-blank (LoB, <3 ng/L) and -detection (LoD, <5 ng/L) were compared. Outcomes were assessed as combined end-points of death and myocardial re-infarction. RESULTS: True-negative rule-out using the DMS could be achieved in 50.9%-62.3% of all patients compared to 35.0%, 45.3% and 64.5% using LoB, LoD or the 1 h-algorithm, respectively. The DMS showed NPVs of 98.1%-98.3% compared to 99.2% for the 1 h-algorithm, 99.4% for the LoB and 99.3% for the LoD. Sensitivities were 93.5%-94.8%, as well as 96.8%, 98.7% and 98.1%, respectively. Addition of clinical low-risk criteria such as a HEART-score ≤ 3 to the DMS resulted in NPVs and sensitivities of 100% with a true-negative rule-out to 33.8%-41.6%. Rates of the combined end-point of death/MI within 30 days ranged between 0.2% and 0.3% for all fast-rule-out protocols. CONCLUSION: Depending on the applied copeptin cut-off and addition of clinical low-risk criteria, the DMS might be an alternative to the hs-cTn-only-based algorithms for rapid AMI rule-out with comparable diagnostic measures and outcomes.
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