Unexpectedly Elevated Cardiac Troponin I Level in the Patient without Acute Coronary Syndrome (original) (raw)
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Clinical Biochemistry, 2000
The controversy whether there is a clinically significant difference between troponin T (cTnT) and troponin I (cTnI) in regard to predictive value and cardiac specificity is still ongoing. Methods: We evaluated enzyme-linked immunosorbent assay systems for cTnI and cTnT in patients with acute coronary syndromes and multiple control groups to define threshold values for risk stratification and compare their predictive value. Results: In 312 patients with noncardiac chest pain, cTnI levels were below the detection limit of 0.2 g/L and cTnT levels were 0.011 [0.010 -0.013] g/L. In patients with end-stage renal failure (n ϭ 26) and acute (n ϭ 38) or chronic (n ϭ 16) skeletal muscle damage, median concentrations were 0.20 [0.20 -0.35], below the detection limit, and 0.20 [0.20 -0.25] for cTnI, and 0.04 [0.01-0.10], 0.011 [0.005-0.025], and 0.032 [0.009 -0.054] g/L for cTnT. In patients with acute coronary syndromes (n ϭ 1130), maximized prognostic value for 30-day outcome (death, infarction) was observed at a threshold level of 1.0 g/L for cTnI (29.0% positive) and at 0.06 g/L for cTnT (35.0% positive). Significant differences in the area-under-the-curve values were observed between cTnI and cTnT (0.685 vs. 0.802; p ϭ 0.005). For both markers, the area-under-thecurve values did not increase with the second (within 24 h after enrollment) or third (48 h) blood draw. CTnI showed a less strong association with 30-day outcome than cTnT. When cTnI was put in a logistic multiple-regression model first, cTnT did add significant information. Conclusion: By using the defined threshold values and the employed test systems, single testing for cTnI and cTnT within 12 h after symptom onset was appropriate for risk stratification. Despite the lower cardiac specificity for cTnT, it appears to have a stronger association with the patients' outcome, whereas, as previously shown, the ability to identify patients who benefit from treatment with a GP IIb/IIIa receptor antagonist is similar.
Journal of Clinical Laboratory Analysis, 2001
This study compared troponin I (cTnI) to troponin T (cTnT) in a population admitted to General Medicine Divisions in whom acute myocardial infarction (AMI) was suspected; 98 consecutive patients were included. Diagnoses were made without knowledge of troponin results: 51 patients had AMI, and 47 (including 8 with unstable angina) had no AMI. Patients were considered to be troponin positive if the marker concentration was >99th percentile value of the reference population. Both troponins were associated with an almost absolute sensitivity for AMI (100% for cTnI and 98.0% for cTnT), while the specificity was marginally higher for cTnI (78.7% vs. 68.1%). Increased cTnI and/or cTnT were observed in 15 patients out of 39 without acute coronary syndromes. Simultaneous positivity was seen in 8 patients with severe disorders and complications. Discordances were more frequent in favor of increased cTnT (n = 5) than the opposite (n = 2), even if this difference did not achieve statistical significance. cTnI and cTnT detected AMI with comparable efficiency. Cases without coronary syndrome positively concordant for troponins confirmed the ability of these biomarkers to detect myocardial injury undetectable by conventional diagnostic approaches. J. Clin. Lab. Anal. 15:210-214, 2001. Cardiac troponins [cardiac troponin I (cTnI) and cardiac troponin T (cTnT)] have recently been proposed as new biochemical standards for diagnosis of acute myocardial infarction (AMI) (1,2). These markers have several advantages over traditional serological markers of myocardial injury: they provide the necessary specificity to allow AMI diagnosis when skeletal muscle damage is also present, and their persistent rise in blood after AMI results in a wide diagnostic window, making them ideal markers for diagnosing AMI in patients who are admitted to the hospital with uncharacteristic symptoms or who present several days after onset of pain (3-5). Due to their cardiospecificity and their very low concentrations in blood of normal individuals, the cardiac troponins have also a greater sensitivity for small areas of myocardial necrosis, these elevations being clearly associated with an increase in short-term adverse cardiac events (6). However, studies on the practical impact of troponin use in unselected patients are still few, and the behavior of cTnI and cTnT compared in a practical routine setting in a common heterogeneous population have not been fully described (7). Consequently, in the present study, we compared cTnI to cTnT performance under "worst-case" conditions by studying their diagnostic value in an unselected population of patients admitted to the General Medicine Divisions of our hospital in whom AMI was suspected but for whom no standard sampling protocols or critical pathways, routinely used in our cardiological setting, were implemented.
Annals of Translational Medicine, 2016
Background: Cardiac troponin (cTn) testing has reduced the likelihood of erroneous discharge of patients with acute coronary syndrome (ACS) from the emergency department (ED), but doubts remain about optimal clinical use. This study was planned for evaluating the predictive significance of cTn values between the limit of detection of the method and the 99th percentile in ED patients evaluated for suspected ACS. Methods: In this retrospective study all hospital records of patients admitted over a 6-month period to the ED and with at least one cTnI value comprised between the limit of detection (0.01 ng/mL) and the 99th percentile of the assay (0.05 ng/mL) were analyzed. Results: A total of 4,749 patients with cTnI value between 0.01-0.05 ng/mL were identified among 57,879 ED visits throughout the study period. Overall, 2,189 patients (46.1%) were discharged from the ED, 2,529 (53.25%) were admitted to the hospital and 31 (0.65%) died during ED stay. A total number of 289 patients out of 2,189 who were discharged (i.e., 13.2%) had additional ED visits within 30 days. Among these, 6 were diagnosed with ACS, representing 0.27% of patients discharged [negative predictive value (NPV) 0.997; 95% CI, 0.994-0.999] and 2.1% of those with second admission (NPV 0.979; 95% CI, 0.955-0.992). Only one of the 2,529 patients admitted to the hospital (i.e., 0.04%) developed an ACS during hospital stay. Conclusions: The results of our retrospective study suggest that the suitability of using a contemporary-sensitive cTnI immunoassay assay in the context of an appropriate protocol represents a safe and effective strategy for ruling in and ruling out ACS in patients presenting to the ED.
Diagnostic and prognostic role of cardiac troponin I (cTnI) measured on the DPC Immulite
Clinical Biochemistry, 2006
Objective: To evaluate the diagnostic and prognostic role of the Immulite cTnI assay for the detection of acute coronary syndromes (ACS). Population: 150 males and 63 females with a median age of 63 years, range 28 to 88, and an interquartile range of 18 years were admitted within 24 h of chest pain and non-ST segment elevation ACS were studied. The median onset of symptoms was 3 h (range 0-23). Methods: Venous samples were taken on admission (t = 0) and at 24 h (t = 24). The serum samples were assayed for CK, CK-MB and cTnT on an Elecsys 1010 (Roche Diagnostics, Lewes, UK). The cTnT assay CV was 5.5% at 0.32 μg/L and 5.4% at 6.0 μg/L, and the detection limit was 0.01 μg/L with an upper limit of 25 μg/L. For cTnI using the Immulite (DPC, Gwynedd, Wales), the detection limit was 0.1 μg/L, and the upper limit was 180 μg/L. Final diagnostic categorization was performed by both WHO and European Society of Cardiology criteria using cTnT as the diagnostic cardiac biomarker. Patients were followed for the major adverse cardiac events (MACE), endpoints cardiac death, AMI or need for urgent revascularization. ROC curves were constructed using final diagnosis. Outcome prediction was assessed by ROC curves and Kaplan-Meier survival curves. Results: Both methods had equivalent diagnostic efficiency using WHO criteria for AMI. When ESC criteria were used the AUC for admission and 24 h cTnT and cTnI values were 0.945 vs. 0.910, P = 0.20 and 0.998 vs. 0.937, P = 0.005, respectively. Both methods predicted outcome as either death or MI or MACE and were not significantly different. Conclusion: The Immulite cTnI assay can be used for diagnosis and risk stratification in patients admitted with non-ST segment elevation acute coronary syndromes.
Use of cardiac troponins as strong markers for patients with acute coronary syndrome
Rangsit University, 2014
Acute myocardial infarction (AMI) is the most important cause of cardiomyocyte necrosis. Cardiac troponin (cTn) T and I are structural proteins unique to the heart and have been used as the preferred cardiac biomarkers in the universal definition of myocardial infarction. Cardiac troponins have demonstrated nearly absolute myocardial tissue specificity and high clinical sensitivity for myocardial ischemia. The recent development of high-sensitivity cardiac troponin (hs-cTn) assays allows detection of very low levels of cTn. The hs-cTn assays have improved the diagnostic accuracy and rapid detection of myocardial infarction. Undetectable hs-cTn rules out AMI with a negative predictive value > 99% on emergency department admission. The diagnosis of acute myocardial damage requires a significant change with serial hs-cTn testing. Current consensus for rapid rule-in proposed a 20% increase within 3 to 6 hours when baseline cTn levels are elevated. In addition, relative increases > 50% above the 99 th percentile upper reference limit are found to be the diagnosis of AMI, in the case of negative baseline value. Besides relative change, the absolute values of hs-cTn at emergency department presentation in patients with suspected AMI should be considered as important criteria in the differential diagnosis of the cause of cardiomyocyte damage. Cardiac troponins provide both diagnostic and prognostic information in the setting of acute coronary syndrome (ACS). Elevation of cTn in the absence of ACS should prompt an evaluation for non-thrombotic mechanism of increased cTn levels and direct management at the underlying cause.