Risk stratification of chest pain patients by point-of-care cardiac troponin T and myoglobin measured in the emergency department

A prospective multicenter study including 1410 chest pain patients with suspected acute coronary syndromes was carried out to examine the predictive value of biological cardiac markers for adverse events measured by a point-of-care system. Admission cardiac troponin T (cTnT) and myoglobin were measured in parallel on a point-of-care system in the emergency department and -- together with CK-MB mass -- on lab analyzers. In a one-year follow-up, cardiac and non-cardiac death, acute myocardial infarction, unstable angina pectoris and need for revascularization were registered. Median time between onset of symptoms and admission was 285 min; 172 patients (12.2%) had no event during follow-up. If the cTnT, measured either by the point-of-care system or a conventional lab analyzer, was >0.05 microg/L, then the chance of a cardiac event during the follow-up period was doubled (18% vs. 9%). Serial cTnT measurement did not add any further value to the predictive power of the admission cTnT. Myoglobin and CK-MB mass identified increasing risk with increasing concentration quartiles; cardiac event rates were 2.8- to 4.4-fold higher between the quartiles with the lowest and those with the highest analyte concentration, respectively. There was no difference in non-cardiac death rates between any concentration quartiles. In conclusion, the prediction of clinical events by cardiac troponin T and myoglobin measured with a point-of-care analyzer in the emergency department was as good as that of the same cardiac markers and CK-MB mass measured on lab analyzers

Use of a quantitative point-of-care system greatly reduces the turnaround time of cardiac marker determination

The goal of this study was to examine whether point-of-care testing of cardiac markers in emergency departments or coronary care units generates a substantial reduction of the turnaround time compared with central laboratory testing. A total of 4609 samples from patients with suspected acute coronary syndromes attending each of 5 participating hospitals were used to measure cardiac troponin Ton a point-of-care system at the bedside, and 3447 of these samples were simultaneously sent to each hospital's central laboratory for an emergency determination of total CK. The time to central laboratory result varied broadly (from 52-147 minutes) from hospital to hospital. There was little difference between the hospitals in the time to result for the point-of-care system (range, 12-22 minutes). The overall gain in time from point-of-care testing compared with central laboratory measurements was 65 minutes (range, 34-135 minutes)

Diagnostic Efficiency of a Point-of-Care System for Quantitative Determination of Troponin T and Myoglobin in the Coronary Care Unit

This study was carried out to compare the time-dependent diagnostic sensitivity and specificity for acute myocardial infarction of 2 point-of-care tests for troponin T and myoglobin measured in routine use of coronary care units with those of the respective laboratory tests. A total of 794 consecutive patients with suspected acute coronary syndromes admitted to the coronary care units of 6 hospitals were enrolled in the study. Point-of-care tests and laboratory tests were measured in parallel from samples obtained serially on admission, and at 1, 2, 4, 6 to 8, 12, 24, and 48 hours from admission. The point-of-care tests achieved maximum sensitivities of 96% (troponin T) and 72% (myoglobin); and the maximum sensitivities of the laboratory tests were 96%, 81%, and 83% for troponin T, myoglobin, and CK-MB mass respectively. The specificities varied from 90 to 94% for point-of-care troponin T, 83 to 93% for point-of-care myoglobin, 97 to 99% for laboratory troponin T, 79 to 85% for laboratory myoglobin, and 95 to 100% for laboratory CK-MB mass. The following maximum areas under receiver-operator characteristics curves were obtained (at different times): point-of-care troponin T, 0.97; point-of-care myoglobin, 0.87; laboratory troponin T, 0.99; laboratory myoglobin, 0.89; and laboratory CK-MB mass, 0.96. In conclusion the point-of-care tests had a comparable clinical performance as established cardiac markers performed in the laboratory

Effect on walking distance and atherosclerosis progression of a nitric oxide-donating agent in intermittent claudication.

BACKGROUND: Peripheral arterial disease (PAD) is almost invariably associated with a generalized atherosclerotic involvement of the arterial tree and endothelial dysfunction. Previous short-term studies showed improvement of vascular reactivity and walking capacity in PAD patients by measures aimed at restoring nitric oxide (NO) production. NO is also known to prevent the progression of atherosclerosis. We wished to assess whether the prolonged administration of an NO-donating agent (NCX 4016) improves the functional capacity of PAD patients and affects the progression of atherosclerosis as assessed by carotid intima-media thickness (IMT). METHODS: This prospective, double-blind, placebo-controlled study enrolled 442 patients with stable intermittent claudication who were randomized to NCX 4016 (800 mg, twice daily) or its placebo for 6 months. The primary study outcome was the absolute claudication distance on a constant treadmill test (10% incline, 3 km/h). The main secondary end point was the change of the mean far-wall right common carotid artery IMT. RESULTS: The increase of absolute claudication distance at 6 months compared with baseline was 126±140 meters in the placebo-treated group and 117±137 meters in the NCX 4016-treated group, with no significant differences. Carotid IMT increased in the placebo-treated group (+0.01±0.01 mm; P=.55) and decreased in the NCX 4016-treated group (-0.03±0.01 mm; P=.0306). Other secondary end points did not differ between the two treatments. CONCLUSIONS: Long-term NO donation does not improve the claudication distance but does reduce progression of atherosclerosis in patients with PAD. Further studies aimed at assessing whether long-term NO donation may prevent ischemic cardiovascular events are warranted. Copyright © 2012 Society for Vascular Surgery. Published by Mosby, Inc. All rights reserve