Sensitive Troponin Assay and the Classification of Myocardial Infarction (original) (raw)
Related papers
JAMA, 2011
Context Although troponin assays have become increasingly more sensitive, it is unclear whether further reductions in the threshold of detection for plasma troponin concentrations will improve clinical outcomes in patients with suspected acute coronary syndrome (ACS). Objective To determine whether lowering the diagnostic threshold for myocardial infarction (MI) with a sensitive troponin assay could improve clinical outcomes. Design, Setting, and Patients All consecutive patients admitted with suspected ACS to the Royal Infirmary of Edinburgh, Edinburgh, Scotland, before (n=1038; February 1-July 31, 2008, during the validation phase) and after (n=1054; February 1-July 31, 2009, during the implementation phase) lowering the threshold of detection for myocardial necrosis from 0.20 to 0.05 ng/mL with a sensitive troponin I assay were stratified into 3 groups (Ͻ0.05 ng/mL, 0.05-0.19 ng/mL, and Ն0.20 ng/mL). During the validation phase, only concentrations above the original diagnostic threshold of 0.20 ng/mL were reported to clinicians. Main Outcome Measure Event-free survival (recurrent MI and death) at 1 year in patients grouped by plasma troponin concentrations. Results Plasma troponin concentrations were less than 0.05 ng/mL in 1340 patients (64%), 0.05 to 0.19 ng/mL in 170 patients (8%), and 0.20 ng/mL or more in 582 patients (28%). During the validation phase, 39% of patients with plasma troponin concentrations of 0.05 to 0.19 ng/mL were dead or had recurrent MI at 1 year compared with 7% and 24% of those patients with troponin concentrations of less than 0.05 ng/mL (PϽ.001) or 0.20 ng/ mL or more (P=.007), respectively. During the implementation phase, lowering the diagnostic threshold to 0.05 ng/mL was associated with a lower risk of death and recurrent MI (from 39% to 21%) in patients with troponin concentrations of 0.05 to 0.19 ng/mL (odds ratio, 0.42; 95% confidence interval, 0.24-0.84; P=.01). Conclusions In patients with suspected ACS, implementation of a sensitive troponin assay increased the diagnosis of MI and identified patients at high risk of recurrent MI and death. Lowering the diagnostic threshold of plasma troponin was associated with major reductions in morbidity and mortality.
Application of High-Sensitivity Troponin in Suspected Myocardial Infarction
New England Journal of Medicine, 2019
BACKGROUND Data regarding high-sensitivity troponin concentrations in patients presenting to the emergency department with symptoms suggestive of myocardial infarction may be useful in determining the probability of myocardial infarction and subsequent 30-day outcomes. METHODS In 15 international cohorts of patients presenting to the emergency department with symptoms suggestive of myocardial infarction, we determined the concentrations of highsensitivity troponin I or high-sensitivity troponin T at presentation and after early or late serial sampling. The diagnostic and prognostic performance of multiple high-sensitivity troponin cutoff combinations was assessed with the use of a derivation-validation design. A risk-assessment tool that was based on these data was developed to estimate the risk of index myocardial infarction and of subsequent myocardial infarction or death at 30 days. RESULTS Among 22,651 patients (9604 in the derivation data set and 13,047 in the validation data set), the prevalence of myocardial infarction was 15.3%. Lower high-sensitivity troponin concentrations at presentation and smaller absolute changes during serial sampling were associated with a lower likelihood of myocardial infarction and a lower short-term risk of cardiovascular events. For example, high-sensitivity troponin I concentrations of less than 6 ng per liter and an absolute change of less than 4 ng per liter after 45 to 120 minutes (early serial sampling) resulted in a negative predictive value of 99.5% for myocardial infarction, with an associated 30-day risk of subsequent myocardial infarction or death of 0.2%; a total of 56.5% of the patients would be classified as being at low risk. These findings were confirmed in an external validation data set. CONCLUSIONS A risk-assessment tool, which we developed to integrate the high-sensitivity troponin I or troponin T concentration at emergency department presentation, its dynamic change during serial sampling, and the time between the obtaining of samples, was used to estimate the probability of myocardial infarction on emergency department presentation and 30-day outcomes.
BMJ (Clinical research ed.), 2017
Objective To evaluate how selection of patients for high sensitivity cardiac troponin testing affects the diagnosis of myocardial infarction across different healthcare settings.Design Prospective study of three independent consecutive patient populations presenting to emergency departments.Setting Secondary and tertiary care hospitals in the United Kingdom and United States.Participants High sensitivity cardiac troponin I concentrations were measured in 8500 consecutive patients presenting to emergency departments: unselected patients in the UK (n=1054) and two selected populations of patients in whom troponin testing was requested by the attending clinician in the UK (n=5815) and the US (n=1631). The final diagnosis of type 1 or type 2 myocardial infarction or myocardial injury was independently adjudicated.Main outcome measures Positive predictive value of an elevated cardiac troponin concentration for a diagnosis of type 1 myocardial infarction.Results Cardiac troponin concentra...
High-Sensitivity Cardiac Troponin and the Universal Definition of Myocardial Infarction
Circulation
Background: The introduction of more sensitive cardiac troponin assays has led to increased recognition of myocardial injury in acute illnesses other than acute coronary syndrome. The Universal Definition of Myocardial Infarction recommends high-sensitivity cardiac troponin testing and classification of patients with myocardial injury based on pathogenesis, but the clinical implications of implementing this guideline are not well understood. Methods: In a stepped-wedge cluster randomized, controlled trial, we implemented a high-sensitivity cardiac troponin assay and the recommendations of the Universal Definition in 48 282 consecutive patients with suspected acute coronary syndrome. In a prespecified secondary analysis, we compared the primary outcome of myocardial infarction or cardiovascular death and secondary outcome of noncardiovascular death at 1 year across diagnostic categories. Results: Implementation increased the diagnosis of type 1 myocardial infarction by 11% (510/4471)...
Heart (British Cardiac Society), 2016
International guidelines to rule-in acute myocardial infarction (AMI) in patients presenting with chest pain to the emergency department (ED) recommend an algorithm using high-sensitivity cardiac troponin (hs-cTn) sampling on presentation and 3 h following presentation. We tested the diagnostic accuracy of this algorithm by pooling data from five distinct cohorts from three countries of prospectively recruited patients with independently adjudicated outcomes. We measured high-sensitivity cardiac troponin I (hs-cTnI) and high-sensitivity cardiac troponin T (hs-cTnT) on presentation (0 h) and 3 h post-presentation samples in adult patients attending an ED with possible AMI to validate the European Society of Cardiology (ESC) Working Group on Acute Cardiac Care rule-in algorithm (ESC-rule-in). Specifically, (i) in patients with a 0 h hs-cTn concentration ≤99th percentile and a 3 h hs-cTn >99th percentile, positive patients are those with an absolute change in troponin ≥50% of the 99...
Clinical chemistry, 2018
Low concentrations of cardiac troponin (cTn) have been recommended for rapid rule-out of acute myocardial infarction (AMI). We examined the Beckman Coulter Access high-sensitivity cardiac troponin I (hs-cTnI) assay to identify a single test threshold that can safely rule out AMI. This analysis used stored samples collected in 2 prospective observational studies. In all, 1871 patients presenting to a tertiary emergency department with symptoms of acute coronary syndrome had blood taken for measurement of cTnI on presentation. The endpoint was type 1 myocardial infarction (T1MI). Sensitivity and negative predictive value (NPV) were calculated for hs-cTnI values below the 99th percentile. Ninety-eight patients had T1MI (5.2%), and 638 (34.1%) patients had an hs-cTnI <2 ng/L (limit of detection), with sensitivity of 99.0% (95% CI, 94.4%-100%) and NPV of 99.8% (95% CI, 99.1%-100%). No hs-cTnI value above a concentration of 2 ng/L achieved sensitivity of 99%. However, an NPV of 99.5% w...
European Heart Journal: Acute Cardiovascular Care, 2014
Background: Myonecrosis provoked by illness unrelated to unstable coronary plaque is common, but uncertainty about a cause-effect relationship with future events challenges the appropriateness of initiating therapies known to be effective in cardiac conditions. We examined the causal relationship between troponin elevation in non-coronary diagnoses and late cardiac events using the Bradford Hills criteria for causality. Methods and results: Patients presenting acutely to South Australian public hospitals receiving at least one troponin between September 2011-September 2012 were included. Diagnoses were classified as coronary, non-coronary cardiac and non-cardiac using the International Classification of Diseases, version 10 Australian Modified, codes. The relationship between peak in-hospital troponin, using a high-sensitivity troponin T assay and adjudicated cardiac and non-cardiac mortality, and subsequent myocardial infarction (MI) was assessed using competing-risk flexible parametric survival models. Troponin results were available for 38,161 patients of whom, 12,645 (33.6%), 3237 (8.5%), and 22,079 (57.9%) patients were discharged with coronary, non-coronary cardiac and non-cardiac diagnoses, respectively. Troponin >14 ng/l was observed in 43.6%. The relationship between troponin and cardiac mortality was stronger among the non-coronary diagnosis group (troponin 1000 ng/l: coronary hazard ratio: 5.1 (95% confidence interval (CI) 4.0-6.6) vs non-coronary hazard ratio: 16.3 (95% CI 12.6-22.4)). The temporal hazard for cardiac death was marked within 30 days in both groups. Among non-coronary diagnoses, the hazard for recurrent MI was higher but did not vary with time. Conclusions: Consistency with causal criteria between secondary myonecrosis and cardiac events suggest the potential benefit for extending cardiac specific interventions to this population if supported in trials appropriately designed to address competing risks. Troponin elevation precipitated by non-coronary events is common and demonstrates an associations with late mortality that are analogous to spontaneous MI resulting from unstable coronary plaque. These observations help inform the design of randomized clinical trials exploring the benefits and risk of therapies with established benefits in other cardiac conditions. Such studies will need to appropriately account for competing risks in this population of patients.
International journal of health sciences
Introduction: Coronary Artery disease is one of the major causes of Mortatlity I the world that included Myocardial ischemia and infarction. Cardiac toponins are (troponin- I and Troponin -T) the markers of myocardial ischemia and they are the sign of Myocardial damage. They can provide important diagnostic and prognostic information. Aim : In the present study the correlation of clinical presentation, complication and outcome with reference of different level (mild, moderate and severe) of elevated troponin enzyme level was studied. Material and method: 100 patientspresented with acute myocardial infarct ion were studied for clinical presentation (hemodynamics, heart failure, mechanical complication, angina, shock) and ICCU stay and total hospital stay, recurrent angina, heart failure, re-infarct, morbidity and mortality was recorded. Their cardiac troponin- I level was measured and corelated accordingly in group 1 (mild elevation: cTnIlevel baseline (0.004) totentimes), group 2 (m...
CMAJ Open, 2014
H igh-sensitivity troponin assays have greatly improved the analytical performance of conventional cardiac troponin T and I testing. 1-3 These assays permit the measurement of cardiac troponin concentrations that are about one-tenth of those measurable with conventional assays. 4 The detection level is close to the physiologic concentrations of these biomarkers; 5 therefore, there is interest in using high-sensitivity assays to diagnose acute myocardial infarction (MI) accurately, possibly within 3 hours of admission. The ability to use the rate of change in troponin level to diagnose acute MI is also being investigated. Many institutions throughout Europe and North America have transitioned from using the conventional troponin T assay to the high-sensitivity troponin T assay with no technical issues; both assays are run using the same analyzer. 6 However, the US Food and Drug Administration has yet to approve the use of the high-sensitivity assays. This is partly because of the need for more information about their diagnostic accuracy and risk stratification. 7 One of the main challenges is the potential for overdiagnosis of acute coronary syndromes because of the increased sensitivity of the high-sensitivity troponin test. Our aim was to assess the use of this test as a diagnostic tool. The early and accurate detection of myocardial injury leads to potentially earlier diagnosis
International Journal of Cardiology
Objectives The aim of this study is to compare a new improved point of care cardiac troponin assay (new POC-cTnI) with 1. its predecessor (old POC-cTnI) and 2. a high sensitivity assay (hs-cTnI) for the diagnosis of acute myocardial infarction (AMI) and for major adverse cardiac events (MACE) by 30 days. Methods This is a single centre observational study, set in Christchurch Hospital, New Zealand. Patients presenting to the emergency department with non-traumatic chest pain underwent blood sampling at 0 h and 2 h post presentation for analysis with the 3 cTnI assays for the outcome of AMI and for analysis using an accelerated diagnostic protocol (ADP-normal 2 h troponins, normal electrocardiograms and Thrombolysis In Myocardial Infarction (TIMI) score of 0 or ≤ 1) for 30 day MACE. Results Of 962 patients, 220 (22.9%) had AMI. Old POC-cTnI was least sensitive at 70.0% (65.4–73.9%) by 2 h (p < 0.001). New POC-cTnI, sensitivity 93.6% (89.9–96.2%) had similar sensitivity to hs-cTnI,...