Background:The American Heart Association (AHA) case definition for acute myocardial infarction (AMI) requires an "adequate set" of biomarkers: 2 measurements of the same marker at least 6 h apart. A sensitive troponin assay might detect significant changes in concentration earlier. We determined AMI prevalence, using protocols with shorter intervals between measurements, with and without incorporating the time from onset of symptoms. Methods: The AHA case definition was used to retrospectively assign a diagnosis in 258 patients presenting to the emergency department with symptoms of cardiac ischemia. AMI was diagnosed if either specimen in an adequate set had a cardiac troponin I (cTnI) above the 99th percentile (AccuTnI

BACKGROUND: Improvements in cardiac troponin (cTn) assays have increased the rapidity with which clinicians can identify patients with changing cTn concentrations (rise or fall) indicative of acute myocardial injury. The aim of the present study was to characterize a new, high-sensitivity cTnI (hs-cTnI) assay and examine whether increased sensitivity can result in still earlier detection of evolving injury. METHODS:We determined the limit of detection, precision profiles, and preliminary estimates of the 99th percentile for the Beckman Coulter hs-cTnI assay in 125 healthy individuals (age Ͻ55 years, 54% male). We compared AccuTnI and hs-cTnI to assess whether change criteria for early concentration changes (i.e., Ն3SD for low concentrations and 20% difference for concentrations Ͼ0.10 g/L) were exceeded in the first 2 specimens (median time between specimens, 1 h; 25th-75th percentile, 1-3 h) from subjects with symptoms suggestive of cardiac ischemia (n ϭ 290). RESULTS:The limit of detection for the hs-cTnI assay was 2.06 ng/L, and the 20% CV and 10% CV concentrations were 2.95 and 8.66 ng/L, respectively. The preliminary 99th percentile estimates in lithium heparin, serum, and EDTA plasma were 9.20, 8.00, and 8.60 ng/L, respectively. In 108 patients with myocardial injury based on the peak AccuTnI concentration, applying the change criteria on the 2 earliest specimens identified 81% (95% CI 73%-88%) of patients using the hs-cTnI assay compared to 62% (53%-71%) using the AccuTnI assay (P Ͻ 0.001). CONCLUSIONS:Although more extensive validation studies are required, this Beckman Coulter hs-cTnI assay appears to detect patients with evolving myocardial injury earlier.Guidelines from laboratory and cardiology groups (1, 2 ) have adopted the 99th percentile as the cutoff for cardiac troponin (cTn) 5 for the diagnosis of myocardial infarction (MI). Recent data document that chronic heart disease may cause persistent elevations above the 99th percentile (3 ). Thus, using a changing pattern of cTn values for the diagnosis of acute disease has been advocated (4 ). More sensitive assays would facilitate these recommendations and reduce the time required to evaluate patients with acute coronary syndromes (ACS) (5,6 ). This study examines the analytical and clinical characteristics of a highly sensitive cTn assay for identifying evolving myocardial injury earlier. Materials and MethodsThe high-sensitivity cardiac troponin I (hs-cTnI) assay from Beckman Coulter employs the same antibodies (i.e., recognizes the same epitopes) as the current AccuTnI assay. Increased sensitivity and precision is achieved by the use of an increased sample volume (100 L compared to 40 L for the current assay), increased incubation time, and changes in the microparticle capture bead. Specifically, the capture antibody is biotinylated and coated to a streptavidin-bound paramagnetic particle. The concentration units for the hs-cTnI assay are ng/L (or pg/mL); the present AccuTnI assay uses g/L (or ng/mL). The analytical range for the hscTnI assay i...

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Background: Inflammation in acute coronary syndrome (ACS) can identify those at greater long-term risks for heart failure (HF) and death. The present study assessed the performance of interleukin (IL)-6, IL-8, and monocyte chemoattractant protein-1 (MCP-1) (cytokines involved in the activation and recruitment of leukocytes) in addition to known biomarkers [e.g., N-terminal probrain natriuretic peptide (NT-proBNP)] for predicting HF and death in an ACS population. Methods: In a cohort of 216 ACS patients, NT-proBNP (Elecsys ® ; Roche) and IL-6, IL-8, and MCP-1 (evidence investigator™; Randox) were measured in serial specimens collected early after symptom onset (n ‫؍‬ 723). We collected at least 2 specimens from each participant: an early specimen (median 2 h; interquartile range 2-4 h) and a later specimen (9 h; 9 -9 h), and used the later specimens' biomarker concentrations for risk stratification. Results: An increase in both IL-6 and NT-proBNP was observed but not for IL-8 or MCP-1 early after pain