scholarly journals Assessment of the 2016 National Institute for Health and Care Excellence high-sensitivity troponin rule-out strategy

Heart ◽  
2017 ◽  
pp. heartjnl-2017-311983 ◽  
Author(s):  
Edward Watts Carlton ◽  
John William Pickering ◽  
Jaimi Greenslade ◽  
Louise Cullen ◽  
Martin Than ◽  
...  
2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
I Restan ◽  
O.T Steiro ◽  
H.L Tjora ◽  
J Langoergen ◽  
T Omland ◽  
...  

Abstract Background NSTEMI may be ruled out in patients presenting with acute chest pain based on low baseline high sensitivity troponin (cTn) at admission. This procedure is limited by a low expected frequency of ruled out non-cardiac chest pain (NCCP) patients. Purpose To investigate if stress-induced biomarkers (glucose or copeptin) combined with cTn can increase the rate of NCCP ruled out without an unacceptable increase in incorrectly ruled out NSTEMI. Method 971 patients with suspected NSTE-ACS were included. Final diagnosis was adjudicated by two independent cardiologists using clinical data including routine cTnT. Additionally, baseline cTnI, cTnI from Singulex Clarity System (cTnI(sgx)), copeptin and glucose were measured. Diagnostic performance to rule out NSTEMI was compared between the ESC rule out algorithms for cTnT and cTnI(Abbott), a local cTnI(sgx) algorithm and different combinations of cTn with copeptin or glucose Results Median age 61 years, 60% male. 13% had NSTEMI, 12% had UAP and 60% NCCP. Distribution of copeptin and glucose concentrations (NSTEMI and NCCP) is shown in figure 1. Copeptin and cTnT produces an algorithm with lower miss rate for NSTEMI, increased rule out rate for NCCP and significantly higher AUC (DeLong test, p value <0.001) compared to the ESC algorithm (Table 1). cTnI(sgx) and copeptin showed higher rule out for NCCP and higher AUC (p value <0.001), however an increased rule out rate for NSTEMIs. Combining cTnI(Abbott) and glucose gave a similar miss rate for NSTEMI as ESC, but increased rule out rate for NCCP and higher AUC (p value <0.001). Conclusion Combining cTnT or cTnI(sgx) with copeptin; or cTnI with glucose, improves diagnostic precision and efficacy of rule out protocols for NSTEMI in patients presenting with acute chest pain. Figure 1 Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): Western Norway Regional Health Authority; Haukeland and Stavanger University Hospitals


BMJ Open ◽  
2018 ◽  
Vol 8 (10) ◽  
pp. e025339 ◽  
Author(s):  
Edward Carlton ◽  
Sarah Campbell ◽  
Jenny Ingram ◽  
Rebecca Kandiyali ◽  
Hazel Taylor ◽  
...  

IntroductionObservational data suggest a single high-sensitivity troponin blood test taken at emergency department (ED) presentation could be used to rule out major adverse cardiac events (MACE) in 10%–60% of ED patients with chest pain. This is done using an ‘undetectable’ cut-off (the Limit of Detection: LoD). We combined the LoD cut-off with ECG findings to create the LoDED strategy. We aim to establish whether the LoDED strategy works under real-life conditions, when compared with existing strategies, in a way that is cost-effective and acceptable to patients.Methods and analysisThis is a parallel-group pragmatic randomised controlled trial across UK EDs. Adults presenting to ED with suspected cardiac chest pain will be randomised 1:1. Existing rule-out strategies in current use across study centres, using serial high-sensitivity troponin testing, will be compared with the LoDED strategy. The primary outcome is successful early discharge (discharge from hospital within 4 hours of arrival) without MACE occurring within 30 days. Secondary outcomes include initial length of hospital stay; comparative costs; patient satisfaction and acceptability to patients. To detect a 9% difference between the early discharge rates (assuming an 8% rate in the standard care group) with 90% power, 594 patients need to be recruited, assuming a 95% follow-up rate.Ethics and disseminationThe study has been approved by the Frenchay Research Ethics Committee (reference 18/SW/0038). Results will be published in an international peer-reviewed journal. Lay summaries will be made available to patients.Trial registration numberISRCTN86184521; Pre-results.


2017 ◽  
Vol 63 (1) ◽  
pp. 394-402 ◽  
Author(s):  
Johannes Tobias Neumann ◽  
Nils Arne Sörensen ◽  
Francisco Ojeda ◽  
Tjark Schwemer ◽  
Jonas Lehmacher ◽  
...  

Abstract AIMS Serial measurements of high-sensitivity troponin are used to rule out acute myocardial infarction (AMI) with an assay specific cutoff at the 99th percentile. Here, we evaluated the performance of a single admission troponin with a lower cutoff combined with a low risk electrocardiogram (ECG) to rule out AMI. METHODS Troponin I measured with a high-sensitivity assay (hs-TnI) was determined at admission in 1040 patients presenting with suspected AMI (BACC study). To rule out AMI we calculated the negative predictive value (NPV) utilizing the optimal hs-TnI cutoff combined with a low risk ECG. The results were validated in 3566 patients with suspected AMI [2-h Accelerated Diagnostic Protocol to Assess Patients With Chest Pain Symptoms Using Contemporary Troponins as the Only Biomarker (ADAPT) studies]. Patients were followed for 6 or 12 months. RESULTS 184 of all patients were diagnosed with AMI. An hs-TnI cutoff of 3 ng/L resulted in a NPV of 99.3% (CI 97.3–100.0), ruling out 35% of all non-AMI patients. Adding the information of a low risk ECG resulted in a 100% (CI 97.5–100.0) NPV (28% ruled out). The 2 validation cohorts replicated the high NPV of this approach. The follow-up mortality in the ruled out population was low (0 deaths in BACC and Stenocardia, 1 death in ADAPT). CONCLUSIONS A single hs-TnI measurement on admission combined with a low risk ECG appears to rule out AMI safely without need for serial troponin testing. Trial Registration: www.clinicaltrials.gov (NCT02355457).


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
D A Psyrakis ◽  
J Bormann ◽  
B Von Jeinsen ◽  
J S Wolter ◽  
M Weferling ◽  
...  

Abstract Background Acute myocardial infarction (MI) is associated with high morbidity and mortality. A robust differentiation between type 1 and type 2 MI (T1/T2MI) has prognostic and therapeutic implications. We investigated whether serial high-sensitivity cardiac troponin I measurements could reliably discriminate T1MI from T2MI in patients presenting with a non-ST elevation myocardial infarction (NSTEMI). Methods We used data from a prospective acute coronary syndrome biomarker registry of patients with suspected MI that presented at or were transferred to one of two study centres. Here, we analysed an unselected group of 265 NSTEMI patients (67.2% males). Blood was drawn on admission and after 3 hours. High-sensitivity troponin I (hs-cTnI) was measured in frozen samples by a technician blinded to patient characteristics. T1MI or T2MI was defined as the gold-standard study diagnosis by two independent cardiologists based on all available data according to the Third Universal Definition of MI. Results A diagnosis of T2MI was made in 55 patients (20.8%) in the NSTEMI cohort. T2MI patients did not differ from T1MI patients regarding age, gender, traditional risk factors, or percentage of those with a history of coronary artery disease. Median baseline hs-cTnI levels were higher in T1MI (436.25; IQR 63.7–1918.8 ng/L) than in T2MI patients (48.4; IQR 11.7–305.9 ng/L; p<0.001). Absolute change in hs-cTnI concentration between 0 and 3 h was greater in T1MI than in T2MI patients with Dhs-cTnI 93.6 ng/L (IQR 13.5–815.3 ng/L) vs. 20.4 ng/L (IQR 2.5–106.5 ng/L) (p<0.001). hs-cTnI yielded an area under the receiver operator characteristics (AUROC) curve for identifying T2MI at baseline of 0.71 (IQR 0.64–0.79) and after 3 h of 0.7 (IQR 0.61–0.78).Dhs-cTnI was associated with an AUROC of 0.68 (IQR 0.6–0.76). Regarding a rule-out approach, Youden-optimized cut-offs for hs-cTnI at baseline as well as for the absolute change in hs-cTnI concentration were calculated (186.5 ng/L; 154.4 ng/L). Use of these two criteria yielded a sensitivity of 89% (78–96%) and a negative predictive value of 95% (89–98%) to exclude T2MI. 49 of 55 T2MI patients would have been ruled out using this algorithm. Conclusion Our data show that hs-cTnI concentrations differ between patients presenting with T1 and T2MI. The concentration of hs-cTnI and its change over time has the potential to rule out T2MI and therefore to identify patients who might benefit from an early invasive management. The differentiation between T1MI and T2MI by using hs-cTnI is nevertheless challenging, and further research on specific algorithms is needed. Acknowledgement/Funding 3German Center for Cardiovascular Research (DZHK), Partnersite Rhein Main, Bad Nauheim, Germany


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