Fabio Stallone1, Raphael Twerenbold2, Karin Wildi3, Tobias Reichlin1, Maria Rubini Gimenez4, Philip Haaf1, Nicole Fuechslin5, Petra Hillinger1, Cedric Jaeger1, Philipp Kreutzinger1, Christian Puelacher1, Milos Radosavac1, Zoraida Moreno Weidmann1, Berit Moehring2, Ursina Honegger1, Carmela Schumacher1, Kris Denhaerynck5, Christiane Arnold6, Roland Bingisser7, Jörn Ole Vollert8, Stefan Osswald1, Christian Mueller1. 1. Cardiovascular Research Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland Department of Cardiology, University Hospital Basel, Basel, Switzerland. 2. Cardiovascular Research Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland Department of Cardiology, University Hospital Basel, Basel, Switzerland Department of Internal Medicine, University Hospital, Basel, Switzerland. 3. Department of Cardiology, University Hospital Basel, Basel, Switzerland Department of Internal Medicine, University Hospital, Basel, Switzerland. 4. Cardiovascular Research Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland Department of Cardiology, University Hospital Basel, Basel, Switzerland Servicio de Urgencias y Pneumologia, CIBERES ISC III, Hospital del Mar-Institut Municipal d'Investigació Mèdica, Barcelona, Spain. 5. Cardiovascular Research Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland. 6. Medizinische Klinik, Kantonsspital Olten, Basel, Switzerland. 7. Cardiovascular Research Institute Basel (CRIB), University Hospital Basel, Basel, Switzerland Emergency department, University Hospital, Basel, Switzerland. 8. BRAHMS GmbH, Thermo Fisher Scientific, Henningsdorf, Germany.
Abstract
OBJECTIVE: Copeptin, a quantitative marker of endogenous stress, seems to provide incremental value in addition to cardiac troponin in the early rule-out of acute myocardial infarction (AMI). Prevalence, characteristics and outcome of acute chest pain patients with causes other than AMI and elevated copeptin are poorly understood. METHODS: A total of 984 consecutive patients with non-cardiac chest pain were selected from a prospective multicentre study of acute chest pain patients presenting to the emergency department. Levels of copeptin were determined in a blinded fashion and considered elevated if above 13 pmol/L (the 97,5th centile of healthy individuals). The final diagnosis was adjudicated by two independent cardiologists. Median duration of follow-up was 756 days. RESULTS:Elevated copeptin levels were seen in 215 patients (22%). In comparison to patients with normal copeptin levels, patients with elevated levels were older, had more pre-existing cardiac and non-cardiac disorders, more silent cardiomyocyte injury and increased haemodynamic stress as quantified by levels of high-sensitivity cardiac troponin T (9.6 ng/L (3.6-18.3) vs 5.8 ng/L (2.9-9.4)) and B-type natriuretic peptide (75 ng/L (37-187) vs 35 ng/L (15-77)) (both p<0.001), more electrocardiographic abnormalities, more often an adjudicated diagnosis of gastroesophageal reflux or bronchitis/pneumonia and higher 2- year mortality (HR 2.9, 95% CI 1.5 to 5.7). The increased mortality rate seemed to be largely explained by age and comorbidities. CONCLUSIONS: Elevated levels of copeptin are present in about one in five patients with non-cardiac chest pain and are associated with aging, cardiac and non-cardiac comorbidities as well as mortality. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
RCT Entities:
OBJECTIVE:Copeptin, a quantitative marker of endogenous stress, seems to provide incremental value in addition to cardiac troponin in the early rule-out of acute myocardial infarction (AMI). Prevalence, characteristics and outcome of acute chest painpatients with causes other than AMI and elevated copeptin are poorly understood. METHODS: A total of 984 consecutive patients with non-cardiac chest pain were selected from a prospective multicentre study of acute chest painpatients presenting to the emergency department. Levels of copeptin were determined in a blinded fashion and considered elevated if above 13 pmol/L (the 97,5th centile of healthy individuals). The final diagnosis was adjudicated by two independent cardiologists. Median duration of follow-up was 756 days. RESULTS: Elevated copeptin levels were seen in 215 patients (22%). In comparison to patients with normal copeptin levels, patients with elevated levels were older, had more pre-existing cardiac and non-cardiac disorders, more silent cardiomyocyte injury and increased haemodynamic stress as quantified by levels of high-sensitivity cardiac troponin T (9.6 ng/L (3.6-18.3) vs 5.8 ng/L (2.9-9.4)) and B-type natriuretic peptide (75 ng/L (37-187) vs 35 ng/L (15-77)) (both p<0.001), more electrocardiographic abnormalities, more often an adjudicated diagnosis of gastroesophageal reflux or bronchitis/pneumonia and higher 2- year mortality (HR 2.9, 95% CI 1.5 to 5.7). The increased mortality rate seemed to be largely explained by age and comorbidities. CONCLUSIONS: Elevated levels of copeptin are present in about one in five patients with non-cardiac chest pain and are associated with aging, cardiac and non-cardiac comorbidities as well as mortality. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
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