Alan Maisel1, Christian Mueller2, Sean-Xavier Neath3, Robert H Christenson4, Nils G Morgenthaler5, James McCord6, Richard M Nowak6, Gary Vilke3, Lori B Daniels3, Judd E Hollander7, Fred S Apple8, Chad Cannon9, John T Nagurney10, Donald Schreiber11, Christopher deFilippi4, Christopher Hogan12, Deborah B Diercks13, John C Stein14, Gary Headden15, Alexander T Limkakeng16, Inder Anand17, Alan H B Wu14, Jana Papassotiriou18, Oliver Hartmann18, Stefan Ebmeyer18, Paul Clopton19, Allan S Jaffe20, W Frank Peacock21. 1. VA San Diego Healthcare System, San Diego, California; University of California, San Diego, California. Electronic address: amaisel@ucsd.edu. 2. University Hospital Basel, Basel, Switzerland. 3. University of California, San Diego, California. 4. University of Maryland School of Medicine, Baltimore, Maryland. 5. Charite, Campus Virchow-Klinikum, Berlin, Germany. 6. Henry Ford Health System, Detroit, Michigan. 7. University of Pennsylvania, Philadelphia, Pennsylvania. 8. Hennepin County Medical Center, Minneapolis, Minnesota. 9. University of Kansas Hospital, Kansas City, Kansas. 10. Massachusetts General Hospital, Boston, Massachusetts. 11. Stanford University School of Medicine, Palo Alto, California. 12. Virginia Commonwealth University, Richmond, Virginia. 13. University of California, Davis Medical Center, Sacramento, California. 14. University of California, San Francisco, California. 15. Medical University of South Carolina, Charleston, South Carolina. 16. Duke University Medical Center, Durham, North Carolina. 17. VA Minneapolis, Minnesota. 18. Thermo Scientific Biomarkers, Thermo Fisher Scientific/BRAHMS GmbH, Hennigsdorf/Berlin, Germany. 19. VA San Diego Healthcare System, San Diego, California. 20. Mayo Clinic, Rochester, Minnesota. 21. Baylor College of Medicine, Houston, Texas.
Abstract
OBJECTIVES: The goal of this study was to demonstrate that copeptin levels <14 pmol/L allow ruling out acute myocardial infarction (AMI) when used in combination with cardiac troponin I (cTnI) <99 th percentile and a nondiagnostic electrocardiogram at the time of presentation to the emergency department (ED). BACKGROUND: Copeptin is secreted from the pituitary early in the course of AMI. METHODS: This was a 16-site study in 1,967 patients with chest pain presenting to an ED within 6 hours of pain onset. Baseline demographic characteristics and clinical data were collected prospectively. Copeptin levels and a contemporary sensitive cTnI (99 th percentile 40 ng/l; 10% coefficient of variation 0.03 μg/l) were measured in a core laboratory. Patients were followed up for 180 days. The primary outcome was diagnosis of AMI. Final diagnoses were adjudicated by 2 independent cardiologists blinded to copeptin results. RESULTS: AMI was the final diagnosis in 156 patients (7.9%). A negative copeptin and cTnI at baseline ruled out AMI for 58% of patients, with a negative predictive value of 99.2% (95% confidence interval: 98.5 to 99.6). AMIs not detected by the initial cTnI alone were picked up with copeptin >14 pmol/l in 23 (72%) of 32 patients. Non-ST-segment elevation myocardial infarctions undetected by cTnI at 0 h were detected with copeptin >14 pmol/l in 10 (53%) of 19 patients. Projected average time-to-decision could be reduced by 43% (from 3.0 h to 1.8 h) by the early rule out of 58% of patients. Both abnormal copeptin and cTnI were predictors of death at 180 days (p < 0.0001 for both; c index 0.784 and 0.800, respectively). Both were independent of age and each other and provided additional predictive value (all p < 0.0001). CONCLUSIONS: Adding copeptin to cTnI allowed safe rule out of AMI with a negative predictive value >99% in patients presenting with suspected acute coronary syndromes. This combination has the potential to rule out AMI in 58% of patients without serial blood draws.
OBJECTIVES: The goal of this study was to demonstrate that copeptin levels <14 pmol/L allow ruling out acute myocardial infarction (AMI) when used in combination with cardiac troponin I (cTnI) <99 th percentile and a nondiagnostic electrocardiogram at the time of presentation to the emergency department (ED). BACKGROUND:Copeptin is secreted from the pituitary early in the course of AMI. METHODS: This was a 16-site study in 1,967 patients with chest pain presenting to an ED within 6 hours of pain onset. Baseline demographic characteristics and clinical data were collected prospectively. Copeptin levels and a contemporary sensitive cTnI (99 th percentile 40 ng/l; 10% coefficient of variation 0.03 μg/l) were measured in a core laboratory. Patients were followed up for 180 days. The primary outcome was diagnosis of AMI. Final diagnoses were adjudicated by 2 independent cardiologists blinded to copeptin results. RESULTS: AMI was the final diagnosis in 156 patients (7.9%). A negative copeptin and cTnI at baseline ruled out AMI for 58% of patients, with a negative predictive value of 99.2% (95% confidence interval: 98.5 to 99.6). AMIs not detected by the initial cTnI alone were picked up with copeptin >14 pmol/l in 23 (72%) of 32 patients. Non-ST-segment elevation myocardial infarctions undetected by cTnI at 0 h were detected with copeptin >14 pmol/l in 10 (53%) of 19 patients. Projected average time-to-decision could be reduced by 43% (from 3.0 h to 1.8 h) by the early rule out of 58% of patients. Both abnormal copeptin and cTnI were predictors of death at 180 days (p < 0.0001 for both; c index 0.784 and 0.800, respectively). Both were independent of age and each other and provided additional predictive value (all p < 0.0001). CONCLUSIONS: Adding copeptin to cTnI allowed safe rule out of AMI with a negative predictive value >99% in patients presenting with suspected acute coronary syndromes. This combination has the potential to rule out AMI in 58% of patients without serial blood draws.
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