ST2 in emergency department chest pain patients with potential acute coronary syndromes.
ABSTRACT The emergency department (ED) evaluation of potential acute coronary syndrome patients is limited by the initial sensitivity of cell injury biochemical markers. Increased ST2, a protein thought to participate in the response to cardiovascular injury, has been noted to be prognostic in patients with acute myocardial infarction. We hypothesize that ST2 would be increased at presentation in ED chest pain patients with myocardial ischemia, thus allowing for the early identification of acute myocardial infarction, acute coronary syndrome, and 30-day adverse cardiovascular events, with an area under the receiver operator characteristic curve (AUC) for each outcome of greater than 0.7.
Patients aged 25 years or older and presenting to the ED with chest pain prompting an ECG were prospectively enrolled. ST2 was measured at presentation. Main outcomes were acute myocardial infarction, acute coronary syndrome, and 30-day events (death, acute myocardial infarction, or revascularization). Median ST2 values were calculated for patients with and without each outcome. The AUCs were calculated for each outcome. In a post hoc analysis, patients with outlying increased ST2 values were examined to determine possible alternative causes for ST2 expression.
There were 348 patients enrolled. The outcomes were acute myocardial infarction 17 patients (4.9%), acute coronary syndrome 39 (11.2%), and 30-day events 23 (6.6%). The AUCs for acute myocardial infarction, acute coronary syndrome, and 30-day events were 0.636, 0.630, and 0.579, respectively. ST2 did not predict acute myocardial infarction, acute coronary syndrome, or 30-day events. It was increased in a small number of patients with pulmonary disease, notably, pulmonary emboli, systemic infection or inflammation, and alcohol abuse.
ST2 was not of value in the evaluation of ED patients with potential acute coronary syndrome.
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ABSTRACT: The Presage(®) ST2 Assay (Critical Diagnostics, CA, USA) is an in vitro diagnostic device that quantitatively measures soluble suppression of tumorigenicity 2 (sST2) in serum and plasma by ELISA. This assay is US FDA approved and is indicated to be used in conjunction with clinical evaluation as an aid in assessing the prognosis of patients diagnosed with chronic heart failure. sST2 binds to IL-33 and functions as a 'decoy' receptor for IL-33, thereby attenuating the systemic effects of IL-33. Due to the role of IL-33/transmembrane isoform of suppression of tumorigenicity 2 signaling in cardiac remodeling, sST2 has emerged as a novel cardiovascular biomarker. In recent studies, it was shown that sST2 is a valuable predictor of several end points in heart failure, in acute coronary syndromes and in critically ill patients. In this review, analytical considerations and clinical applications of the Presage ST2 Assay will be discussed, as well as probable future concepts for adoption of sST2 measurements into clinical practice.Expert Review of Molecular Diagnostics 01/2013; 13(1):13-30. · 4.09 Impact Factor
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ABSTRACT: There is an ongoing search for biomarkers that can facilitate the diagnosis of subclinical or clinically manifest cardiovascular disease. One of the emerging biomarkers currently under investigation is ST2, which is the receptor of Interleukin-33 (IL-33). ST2 is a member of the Interleukin-1 receptor family and exists in a transmembrane (ST2L) and a soluble form (sST2) due to alternative splicing. Several groups have reported sST2 elevations in serum of cardiovascular disease patients. There is consisting evidence that sST2 is independently predictive for mortality in patients with heart failure or myocardial infarction. In addition to its potential as a biomarker for adverse cardiovascular events, ST2 is considered to play a causal role in chronic cardiovascular diseases such as atherosclerosis and heart failure. Signaling of IL-33 via ST2 has been shown to be cardioprotective in mouse models of myocardial infarction, heart transplantation and cardiac hypertrophy and fibrosis. Furthermore, treatment with IL-33 reduced the development of plaques in atherosclerotic mice. In this paper we will review the currently available literature on sST2 as a biomarker for adverse cardiovascular events. In addition, we will elaborate on the potential mechanistic role of the IL-33/ST2 pathway in chronic inflammatory cardiovascular diseases.Minerva medica 12/2012; 103(6):513-24. · 1.20 Impact Factor
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ABSTRACT: Serum levels of soluble ST2, a member of the interleukin-1 receptor family, predict mortality in emergency department (ED) patients with dyspnea secondary to acute heart failure and acute coronary syndrome. Elevated levels of ST2 have also been described in pulmonary disease, but it is unclear if these are associated with adverse outcomes. The hypothesis for this study was that elevated ST2 levels would be associated with 180-day mortality and 180-day return ED visits or hospital readmission in patients presenting to the ED with noncardiac causes of dyspnea. This prospective observational cohort study enrolled a convenience sample of patients presenting to a single academic tertiary care ED with a chief complaint of dyspnea. Exclusion criteria included dyspnea due to chest wall trauma, airway obstruction, and known cardiac etiology (new onset heart failure, prior heart failure with current brain natriuretic peptide > 500 pg/mL, presumed ischemic chest pain, elevated troponin, electrocardiogram changes indicating myocardial infarction or ischemia, heart transplant). ST2 levels were measured at ED presentation and compared between those with and without adverse outcomes. Staff were blinded to ST2 levels. Differences between groups were assessed using the Mann-Whitney U test. Of the 82 patients enrolled, 45 (55%) were female, 48 (59%) were African American, and 34 (42%) were hospitalized. The most frequent ED or hospital diagnosis was chronic obstructive pulmonary disease (COPD) or asthma, in 29 (35%) patients. At 180 days, 36 of 81 patients (44%) had return ED visits, 21 of 81 patients (26%) were readmitted, and five of 82 patients (6%) were deceased. Median ST2 level was 227 ng/mL in patients who died versus 32 ng/mL in those who survived (difference = 195 ng/mL, 95% confidence interval [CI] = 48 to 342 ng/mL, p = 0.006). Median ST2 level was 59 ng/mL in readmitted patients versus 31 ng/mL in nonreadmitted patients (difference = 28 ng/mL, 95% CI = -3 to 60 ng/mL, p = 0.036). Median ST2 levels were 41 ng/mL in patients with return ED visits versus 31 ng/mL in those without return visits (difference = 10 ng/mL, 95% CI = -10 to 20 ng/mL, p = 0.23). Patients with noncardiac dyspnea who died or required readmission to the hospital within 180 days had higher levels of ST2 compared with nonadmitted survivors. Further research into ST2 as a prognostic tool in pathologic processes not involving the heart, such as pulmonary disease, is warranted.Academic Emergency Medicine 10/2013; · 2.20 Impact Factor