scholarly journals Misclassification of Myocardial Injury by a High-Sensitivity Cardiac Troponin I Assay

Author(s):  
Peter A. Kavsak ◽  
Shawn Mondoux ◽  
Andrew Worster ◽  
Janet Martin ◽  
Vikas Tandon ◽  
...  
2016 ◽  
Vol 67 (13) ◽  
pp. 2354 ◽  
Author(s):  
Yader Sandoval ◽  
Stephen Smith ◽  
Sara A. Love ◽  
Karen Schulz ◽  
Jing Cao ◽  
...  

2017 ◽  
Vol 130 (12) ◽  
pp. 1431-1439.e4 ◽  
Author(s):  
Yader Sandoval ◽  
Stephen W. Smith ◽  
Anne Sexter ◽  
Sarah E. Thordsen ◽  
Charles A. Bruen ◽  
...  

2017 ◽  
Vol 63 (1) ◽  
pp. 369-376 ◽  
Author(s):  
Yader Sandoval ◽  
Stephen W Smith ◽  
Anoop S V Shah ◽  
Atul Anand ◽  
Andrew R Chapman ◽  
...  

Abstract BACKGROUND Rapid rule-out strategies using high-sensitivity cardiac troponin assays are largely supported by studies performed outside the US in selected cohorts of patients with chest pain that are atypical of US practice, and focused exclusively on ruling out acute myocardial infarction (AMI), rather than acute myocardial injury, which is more common and associated with a poor prognosis. METHODS Prospective, observational study of consecutive patients presenting to emergency departments [derivation (n = 1647) and validation (n = 2198) cohorts], where high-sensitivity cardiac troponin I (hs-cTnI) was measured on clinical indication. The negative predictive value (NPV) and diagnostic sensitivity of an hs-cTnI concentration <limit of detection (LoD) at presentation was determined for acute myocardial injury and for AMI or cardiac death at 30 days. RESULTS In patients with hs-cTnI concentrations <99th percentile at presentation, acute myocardial injury occurred in 8.3% and 11.0% in the derivation and validation cohorts, respectively. In the derivation cohort, 27% had hs-cTnI < LoD, with NPV and diagnostic sensitivity for acute myocardial injury of 99.1% (95% CI, 97.7–99.8) and 99.0% (97.5–99.7) and an NPV for AMI or cardiac death at 30 days of 99.6% (98.4–100). In the validation cohort, 22% had hs-cTnI <LoD, with an NPV and diagnostic sensitivity for acute myocardial injury of 98.8% (97.9–99.7) and 99.3% (98.7–99.8) and an NPV for AMI or cardiac death at 30 days of 99.1% (98.2–99.8). CONCLUSIONS A single hs-cTnI concentration <LoD rules out acute myocardial injury, regardless of etiology, with an excellent NPV and diagnostic sensitivity, and identifies patients at minimal risk of AMI or cardiac death at 30 days. ClinicalTrials.gov Identifier: NCT02060760


2019 ◽  
Vol 47 (7) ◽  
pp. 3234-3242 ◽  
Author(s):  
Li Jiang ◽  
Yuning Li ◽  
Zhi Zhang ◽  
Lixing Lin ◽  
Xiaoli Liu

Objective Low-cost diagnostic and prognostic biomarkers could help guide clinical management of neonates with myocardial injury after asphyxia. This study aimed to assess the utility of creatine kinase (CK)-MB, high-sensitivity cardiac troponin I (hs-cTnI), brain natriuretic peptide (BNP), and myoglobin in the early diagnosis of myocardial injury following neonatal asphyxia. Methods Eighteen neonates with asphyxia and myocardial injury, 22 neonates with asphyxia and no myocardial injury, and 19 neonates without asphyxia (controls) were enrolled consecutively at the Neonatology Department, First Hospital of Lanzhou University (August 2013 to December 2014). Serum CK-MB, hs-cTnI, BNP, and myoglobin levels were evaluated at 12 hours and 7 days after birth. Their diagnostic value for myocardial injury was assessed by receiver operating characteristic (ROC) curve analysis. Results Levels of all four markers were higher in neonates with asphyxia and myocardial injury than in neonates with asphyxia and no myocardial injury or controls 12 hours after birth. The marker hs-cTnI had the highest diagnostic value. Using a cutoff value of 0.087 µg/L for hs-cTnI, the sensitivity, specificity, and diagnostic accuracy for asphyxia-induced myocardial injury were 55.6%, 95.5%, and 77.5%, respectively. Conclusions Serum hs-cTnI levels can predict myocardial injury caused by neonatal asphyxia at an early stage.


2021 ◽  
Vol 9 ◽  
Author(s):  
Jing Li ◽  
Shenwei Zhang ◽  
Li Zhang ◽  
Yu Zhang ◽  
Hua Zhang ◽  
...  

Acute myocardial infarction has a high clinical mortality rate. The initial exclusion or diagnosis is important for the timely treatment of patients with acute myocardial infarction. As a marker, cardiac troponin I (cTnI) has a high specificity, high sensitivity to myocardial injury and a long diagnostic window. Therefore, its diagnostic value is better than previous markers of myocardial injury. In this work, we propose a novel aptamer electrochemical sensor. This sensor consists of silver nanoparticles/MoS2/reduced graphene oxide. The combination of these three materials can provide a synergistic effect for the stable immobilization of aptamer. Our proposed aptamer electrochemical sensor can detect cTnl with high sensitivity. After optimizing the parameters, the sensor can provide linear detection of cTnl in the range of 0.3 pg/ml to 0.2 ng/ml. In addition, the sensor is resistant to multiple interferents including urea, glucose, myoglobin, dopamine and hemoglobin.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A Moss ◽  
M R Dweck ◽  
M K Doris ◽  
J P M Andrews ◽  
R Bing ◽  
...  

Abstract Background High-risk coronary atherosclerotic plaque is associated with higher plasma troponin concentrations suggesting ongoing myocardial injury that may be a target for dual antiplatelet therapy. Purpose To determine whether ticagrelor reduces high-sensitivity troponin I concentrations in patients with established coronary artery disease and high-risk coronary plaque with 18F-fluoride uptake. Methods In a randomized double-blind placebo-controlled trial, patients with multivessel coronary artery disease underwent coronary 18F-fluoride positron emission tomography-computed tomography and measurement of high-sensitivity cardiac troponin I and were randomized (1:1) to ticagrelor 90 mg twice daily or matched placebo. The primary endpoint was troponin I concentration at 30 days in patients with increased coronary 18F-fluoride uptake. Results In total, 202 patients were randomized and 191 met the pre-specified criteria for inclusion in the primary analysis. In patients with increased coronary 18F-fluoride uptake (n=120/191) there was no evidence that ticagrelor had an effect on plasma troponin concentrationsat 30 days (ratio of geometric means for ticagrelor versusplacebo, 1.11, [95% confidence interval 0.90 to 1.36], p=0.32) (Table 1). Over 1 year, ticagrelor had no effect on troponin concentrations in patients with increased coronary 18F-fluoride uptake (ratio of geometric means, 0.86, 95% confidence interval 0.63 to 1.17, p=0.33). Table 1 Adjusted Geometric Mean (GSE) Ratio of Geometric Means p-value Ticagrelor Placebo (95% CI) Cardiac troponin I, ng/L (18F-fluoride activity) 3.8 (1.1) 3.4 (1.1) 1.11 (0.90 to 1.36) 0.32 Cardiac Troponin I, ng/L (No 18F-fluoride activity) 2.4 (1.1) 2.3 (1.1) 1.02 (0.80 to 1.31) 0.87 Plasma high-sensitivity cardiac troponin I concentration (ng/L) at 30 days for the per-protocol population.Estimates are back transformed estimates from analysis of log transformed values at 30 days adjusting for age, sex and log transformed baseline troponin. Ratio of geometric means is Ticagrelor divided by Placebo. GSE, geometric standard error. Conclusions Dual antiplatelet therapy with ticagrelor does not reduce plasma troponin concentrations in patients with coronary 18F-fluoride uptake. This suggests that subclinical plaque thrombosis does not contribute to ongoing myocardial injury in this setting. Clinical Trials Study ID: NCT02110303Study ID: NCT02110303 Acknowledgement/Funding Wellcome Trust Senior Investigator Award WT103782AIA


Sign in / Sign up

Export Citation Format

Share Document