Document Detail

ST2 and mortality in non-ST-segment elevation acute coronary syndrome.
MedLine Citation:
PMID:  20435187     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: ST2 is a member of the interleukin-1 receptor family that is up-regulated in conditions associated with increased myocardial strain. ST2 has been shown to be independently predictive of adverse outcome in heart failure and ST-segment elevation myocardial infarction, but its prognostic value in non-ST-elevation acute coronary syndrome (NSTE-ACS) has not been established. METHODS: We measured ST2 at randomization and after 24, 48, and 72 hours in 403 NSTE-ACS patients from the GUSTO IV study, and studied its kinetics and its associations to clinical baseline factors and 1-year mortality. RESULTS: Median ST2 levels decreased from 28.4 U/mL at randomization to 21.8 U/mL at 72 hours (P < .001). Peak levels were noted 6 to 17 hours after symptom onset. Randomization ST2 levels were independently associated to N-terminal pro-B-type natriuretic peptide but otherwise exhibited only weak relations to cardiovascular risk factors and comorbidities, and biomarkers of myocardial necrosis or inflammation. ST2 was related to 1-year mortality independently of clinical risk indicators (odds ratio 2.3 [95% CI 1.1-4.6], P = .03) but lost its predictive value after additional adjustment for prognostic biomarkers, in particular N-terminal pro-B-type natriuretic peptide. CONCLUSIONS: ST2 levels are elevated early in NSTE-ACS and predict 1-year mortality. Our data indicate that ST2 represents an interesting novel pathophysiologic pathway in the setting of ischemia-related myocardial dysfunction. However, future prospective evaluations in larger populations are needed before the clinical utility of ST2 can be determined.
Kai M Eggers; Paul W Armstrong; Robert M Califf; Maarten L Simoons; Per Venge; Lars Wallentin; Stefan K James
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Publication Detail:
Type:  Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American heart journal     Volume:  159     ISSN:  1097-6744     ISO Abbreviation:  Am. Heart J.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-05-03     Completed Date:  2010-05-24     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370465     Medline TA:  Am Heart J     Country:  United States    
Other Details:
Languages:  eng     Pagination:  788-94     Citation Subset:  AIM; IM    
Copyright Information:
2010 Mosby, Inc. All rights reserved.
Department of Medical Sciences, Uppsala University, Sweden.
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MeSH Terms
Acute Coronary Syndrome / blood*,  mortality,  physiopathology
Middle Aged
Receptors, Cell Surface / blood*
Reg. No./Substance:
0/IL1RL1 protein, human; 0/Receptors, Cell Surface

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