Journal
HEART
Volume 100, Issue 21, Pages 1708-+Publisher
BMJ PUBLISHING GROUP
DOI: 10.1136/heartjnl-2014-305583
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Funding
- Swiss Heart Foundation
- University of Basel
- Department of Internal Medicine of the University Hospital Basel
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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.
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