Interleukin 33 and ST2 in non–ST-elevation myocardial infarction: Comparison with Global Registry of Acute Coronary Events Risk Scoring and NT-proBNP

Background Soluble ST2 is a marker of biomechanical strain for which the natural ligand is interleukin 33 (IL-33). They have not been studied together in non–ST-elevation myocardial infarction (NSTEMI). We investigated their relationship with death, heart failure (HF) readmission, and reinfarction c...

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Bibliographic Details
Published in:The American heart journal 2011-06, Vol.161 (6), p.1163-1170
Main Authors: Dhillon, Onkar S., MBChB, Narayan, Hafid K., MBChB, Quinn, Paulene A., MPhil, Squire, Iain B., MD, FRCP, Davies, Joan E., PhD, FRCP, Ng, Leong L., MD, FRCP
Format: Article
Language:English
Subjects:
Acute coronary syndromes
Aged
Aged, 80 and over
Angina pectoris
Biological and medical sciences
Biomarkers
Biomarkers - blood
Cardiology. Vascular system
Cardiovascular
Coronary heart disease
Cytokines
Enzymes
Female
Heart
Heart attacks
Heart Failure - etiology
Hospitalization
Humans
Interleukin-1 Receptor-Like 1 Protein
Interleukin-33
Interleukins - blood
Kaplan-Meier Estimate
Male
Medical prognosis
Medical sciences
Middle Aged
Mortality
Multivariate Analysis
Myocardial Infarction - blood
Myocardial Infarction - complications
Myocardial Infarction - mortality
Myocarditis. Cardiomyopathies
Natriuretic Peptide, Brain - blood
Peptide Fragments - blood
Prognosis
Receptors, Cell Surface - blood
Risk Assessment
ROC Curve
Statistical analysis
Survival analysis
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Summary:Background Soluble ST2 is a marker of biomechanical strain for which the natural ligand is interleukin 33 (IL-33). They have not been studied together in non–ST-elevation myocardial infarction (NSTEMI). We investigated their relationship with death, heart failure (HF) readmission, and reinfarction combined (termed major adverse cardiac events [ MACE ]) and, separately, in unselected patients using Global Registry of Acute Coronary Events Risk Scoring (GRACE-RS) and n terminal pro B type natriuretic peptide (NT-proBNP) as benchmark comparators. Methods ST2 and IL-33 were measured in 577 patients 3 to 5 days after admission. Mean follow-up was 532 (150-1059) days, during which 156 patients (27%) reached the primary end point. Results ST2 was higher in those who experienced MACE when compared with event-free survivors (median 782 pg/mL vs 596, P < .001), but there was no difference in IL-33 levels across any end point. Multivariate Cox regression analysis reveals that elevated ST2 is independently associated with increased risk of MACE during the long term (hazard ratio [HR] 2.01, P = .005). This relationship continues on further adjustment for either GRACE risk score or NT-proBNP individually but not on adjustment for both. ST2 also independently predicts reinfarction (HR 2.48, P = .03) and 30-day mortality (HR 4.43, P = .02, c-statistic 0.73, P < .001). Adding ST2 to GRACE or to NT-proBNP did not lead to significant improvements in the c-statistic for MACE for long-term follow-up ( P = .27 and P = .57, respectively) or the net reclassification index. Neither IL-33 nor its ratio with ST2 was associated with study end points. Conclusions Elevated ST2 predicts adverse outcome in non–ST-elevation myocardial infarction but does not significantly improve risk stratification for established markers. Interleukin 33 was not related to adverse events.
ISSN:0002-8703
1097-6744
DOI:10.1016/j.ahj.2011.03.025