Benefits of High Sensitivity Cardiac Troponin I at Admission
July-August 2017 - Vol. 6 No. 6 - Page #20

Reader’s Note: This editorial is from an author and institution based in the United Kingdom and does not represent viable laboratory practice in the United States at this time.


Chest pain is one of the most common reasons for presentation at the emergency department (ED). In 2012, in accordance with widespread practice, all patients attending Royal Wolverhampton NHS Trust (RWT) with possible cardiac chest pain were admitted to the acute medical unit where a blood sample was collected, 12 hours post onset of pain, for cardiac troponin T testing to aid in the confirmation or exclusion of acute myocardial infarction. Pressure from the commissioners to reduce hospital admissions coupled with a need to increase patient discharge rates from the ED (which had experienced a large increase in patient numbers following the overnight closure of a neighbouring unit) led to a review of the Trust’s chest pain pathway by a consultant acute care physician.

The introduction of a high-sensitivity cardiac troponin I (hs-cTnI)1 test in April 2013 afforded clinical practitioners in the United Kingdom the opportunity to implement a novel and radically different pathway (see FIGURE 1). The new pathway uses an admission hs-cTnI of ≤1.9ng/L (the limit of detection of the assay)2,3 to discharge patients with suspected acute coronary syndrome (ACS). Discharge does not occur if the patient is assessed to be at high risk of ACS, nor if the admission hs-cTnI sample is collected within one hour after the onset of chest pain. High-risk patients are admitted to the acute medical unit and low-risk patients with an hs-cTnI >1.9ng/L are transferred to a clinical decision unit (CDU) within the ED to await the hs-cTnI result from a second sample. Initially, the second sample was collected at six hours post admission, but following the publication of National Institute for Health and Care Excellence (NICE) guidance on the use of high sensitivity troponin for the early rule out of myocardial infarction (MI) in October 2014,4 the time between samples was reduced to three hours. The inclusion criteria for transfer to the CDU are listed in TABLE 1.


The percentage of patients presenting to the ED with chest pain who were admitted to the hospital and the mean length of time between admission to ED and discharge from RWT were compared for one month both before (July 2012) and after (January 2014) the introduction of the new chest pain pathway.

To assess the safety of the pathway, consecutive patients presenting to ED at RWT with chest pain were prospectively studied over six months between July 2013 and January 2014. Patients <16 years old, from trauma calls and whom self discharged, were excluded. Patients with an admission hs-cTnI of ≤1.9ng/L were followed up at 30 days and then at nine months for major adverse cardiac events (MACE) defined as death, myocardial infarction, symptom-driven revascularization, and readmission for ACS. We also assessed cardiologist input for all patients attending ED with chest pain in October 2013.

Analytical Methods
The hs-cTnI was measured using the Abbott ARCHITECT STAT high-sensitivity cardiac troponin I two-step immunoassay on the ARCHITECT i2000 analyser. The inter-assay coefficients of variation (CV) for hs-cTnI are 10.5% at 4.2ng/L, 5.8% at 20ng/L, and 3.0% at 206ng/L.


The percentage of chest pain patients admitted to the hospital declined from 60.9% in July 2012 to 38.4% in January 2014 and the mean length of stay reduced from 23 hours and 2 minutes to 9 hours and 36 minutes (see TABLE 2).

Over the course of the six-month study period, 3,853 patients presented to ED with chest pain, ACS was ruled out clinically in 1,280 patients, and the remaining 2,573 patients had an admission hs-cTnI collected. Eight hundred and forty-nine (849) patients (32% of those with possible ACS) had an admission hs-cTnI ≤1.9ng/L and 688 (27%) were immediately discharged (see FIGURE 2). Thirty-day review of all 849 patients identified three MACE: Two deaths (one unrelated malignancy and one peri-arrest sample) and one percutaneous coronary intervention (PCI). Nine-month follow-up showed a further 11 MACE: Nine deaths (eight unrelated malignancies, one pulmonary fibrosis) and two PCIs. There were no myocardial infarctions or ACS re-presentations. One discharged patient had a MACE with elective PCI following ED referral to cardiology. The negative predictive value of hs-cTnI ≤1.9ng/L on admission for MACE at 30 days and nine months was 99.6% (95% CI; 98.9-99.9) and 98.4% (95% CI; 97.2-99.1), respectively.

Of the 529 patients admitted to ED with chest pain in October 2013, attending physicians clinically ruled out ACS in 257. The remaining 272 patients had hs-cTnI samples collected, which were interpreted by acute care physicians based on clinical findings and the algorithm shown in FIGURE 3. Forty-eight (48) patients had a final diagnosis of ACS, 35 of which required cardiology input.


We have routinely used this protocol on admission to safely discharge over 25% of low-clinical-risk patients attending ED with possible ACS. This strategy, together with the introduction of a CDU, improved patient flow in the ED and reduced hospital admissions. Cardiology input was required in <13% of patients with suspected ACS and enabling safe earlier discharge has had a positive impact on patient care, both for the individuals concerned and by releasing resources for the benefit of other patients.

Subsequently, in a retrospective study, Shah et al2 reported that a hs-cTnI of <5ng/L at presentation would identify two-thirds of patients with suspected ACS as being at low risk of cardiac events (negative predictive value of 99.6%) and who could be discharged, endorsing our findings that an admission hs-cTnI protocol may be used to safely discharge patients and providing evidence for its transferability to other organisations. It must be appreciated that cut-offs are assay specific3 and not transferable to other hs-cTn assays.


1. ARCHITECTSTAT high sensitive Troponin-I product information. Abbott Ireland Diagnostics Division, Longford, Ireland. November 2013; Ref: 3P25; B3P250; G4-5578/R04.

2. Shah ASV, Anand A, Sandoval Y, et al. High sensitivity cardiac troponin I at presentation in patients with suspected acute coronary syndrome: a cohort study. Lancet 2015; 386: 2481-8.

3. Rubini GM, Hoeller R, Reichlin T, et al. Rapid rule out of acute myocardial infarction using undetectable levels of high sensitivity cardiac troponin. Int J Cardiol 2013; 168: 3896-3901.

4. National Institute for Health and Care Excellence (2014). Myocardial infarction (acute): Early rule out using high-sensitivity troponin tests (Elecsys Troponin T high-sensitive, ARCHITECT STAT High Sensitive Troponin-I and AccuTnI+3 assays). (DG15)

Clare Ford, PhD, is a consultant clinical scientist in clinical chemistry, rotating head of department, point of care testing clinical lead, and lead scientist at Royal Wolverhampton NHS Trust in Wolverhampton, United Kingdom. She also is honorary senior lecturer at the University of Wolverhampton and vice chair of the West Midlands Association for Clinical Biochemistry and Laboratory Medicine Demand Management Forum.

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