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.
[Show abstract] [Hide abstract]
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; 20(11). DOI:10.1111/acem.12250 · 2.20 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: OBJECTIVES: To test the diagnostic accuracy for detecting an acute myocardial infarction (AMI) using highly sensitive troponin assays and a range of new cardiac biomarkers of plaque destabilisation, myocardial ischaemia and necrosis; to test the prognostic accuracy for detecting adverse cardiac events using highly sensitive troponin assays and this range of new cardiac biomarkers; and to estimate the cost-effectiveness of using highly sensitive troponin assays or this range of new cardiac biomarkers instead of an admission and 10- to 12-hour troponin measurement. DESIGN: Substudy of the point-of-care arm of the RATPAC (Randomised Assessment of Treatment using Panel Assay of Cardiac markers) trial. SETTING: The emergency departments of six hospitals. PARTICIPANTS: Prospective admissions with chest pain and a non-diagnostic electrocardiogram randomised to point-of-care assessment or conventional management. INTERVENTIONS: Blood samples taken on admission and 90 minutes from admission for measurement of cardiac markers [cardiac troponin I (cTnI), myoglobin and creatine kinase MB isoenzyme (CK-MB)] by point-of-care testing. An additional blood sample was taken at admission and 90 minutes from admission for analysis of high-sensitivity cTnI (two methods) and cardiac troponin T (cTnT), myoglobin, heart-type fatty acid-binding protein (H-FABP), copeptin and B-type natriuretic peptide (NTproBNP). MAIN OUTCOME MEASURES: 1. Diagnostic accuracy compared with the universal definition of myocardial infarction utilising laboratory measurements of cardiac troponin performed at the participating sites together with measurements performed in a core laboratory. 2. Ability of biomarker measurements to predict major adverse cardiac events (death, non-fatal AMI, emergency revascularisation or hospitalisation for myocardial ischaemia) at 3 months' follow-up. 3. Comparison of incremental cost per quality-adjusted life-year (QALY) of different biomarker measurement strategies for the diagnosis of myocardial infarction. RESULTS: Samples were available from 850 out of 1132 patients enrolled in the study. Measurement of admission myoglobin [area under the curve (AUC) 0.76] and CK-MB (AUC 0.84) was diagnostically inferior and did not add to the diagnostic efficiency of cTnI (AUC 0.90-0.94) or cTnT (AUC 0.92) measurement on admission. Simultaneous measurement of H-FABP and cTnT or cTnI did improve admission diagnostic sensitivity to 0.78-0.92, but only to the same level as that achieved with troponin measured on admission and at 90 minutes from admission (0.78-0.95). Copeptin (AUC 0.62) and NTproBNP (AUC 0.85) measured on admission were not useful as diagnostic markers. As a prognostic marker, troponin measured on admission using a high-sensitivity assay (AUC 0.73-0.83) was equivalent to NTproBNP measurement (AUC 0.77) on admission, but superior to copeptin measurement (AUC 0.58). From modelling, 10-hour troponin measurement is likely to be cost-effective compared with rapid rule-out strategies only if a £30,000 per QALY threshold is used and patients can be discharged as soon as a negative result is available. CONCLUSIONS: The measurement of high-sensitivity cardiac troponin is the best single marker in patients presenting with chest pain. Additional measurements of myoglobin or CK-MB are not clinically effective or cost-effective. The optimal timing for measurement of cardiac troponin remains to be defined. Copeptin measurement is not recommended. H-FABP requires further investigation before it can be recommended for simultaneous measurement with high-sensitivity troponin in patients with acute chest pain. TRIAL REGISTRATION: ISRCTN37823923. FUNDING: This project was funded by the NIHR Health Technology Assessment programme and will be published in full in Health Technology Assessment; Vol. 17, No. 15. See the HTA programme website for further project information.04/2013; 17(15):1-122. DOI:10.3310/hta17150
[Show abstract] [Hide abstract]
ABSTRACT: Cardiovascular diseases (CVD) are the major cause of death worldwide. The identification of markers able to detect the early stages of such diseases and/or their progression is fundamental in order to adopt the best actions in order to reduce the worsening of clinical condition. Brain natriuretic peptide (BNP) and NT-proBNP are the best known markers of heart failure (HF), while troponins ameliorated the diagnosis of acute and chronic coronary artery diseases. Nevertheless, many limitations reduce their accuracy. Physicians have tried to develop further detectable molecules in order to improve the detection of the early moments of CVD and prevent their development. Soluble ST2 (suppression of tumorigenicity 2) is a blood protein confirmed to act as a decoy receptor for interleukin-33. It seems to be markedly induced in mechanically overloaded cardiac myocytes. Thus, HF onset or worsening of a previous chronic HF status, myocardial infarct able to induce scars that make the myocardium unable to stretch well, etc, are all conditions that could be detected by measuring blood levels of soluble ST2. The aim of this review is to explore the possible role of ST2 derived-protein as an early marker of cardiovascular diseases, above all in heart failure and ischemic heart diseases.Molecules 12/2013; 18(12):15314-15328. DOI:10.3390/molecules181215314 · 2.10 Impact Factor