The impact of implementing a high sensitivity assay for cardiac troponin I on long term outcomes in patients with suspected acute coronary syndrome

In a recent study published in the journal BMJ, a team of researchers from the United Kingdom evaluated the use of a high-sensitivity assay to measure cardiac troponin I and its impact on myocardial infarction (MI) risk or other long-term outcomes such as death at five years in individuals with suspected acute coronary syndrome.

Background

Cardiac troponin assays with high sensitivity are used to detect very low levels of troponin, which can improve the risk stratification and diagnosis in patients suspected of having acute coronary syndrome.

Furthermore, the recommendations that are followed worldwide include the use of high-sensitivity assays with troponin levels being evaluated for sex-specific thresholds in the 99^th centile for diagnosing MI and injury.

However, despite the global application of these guidelines, the impact of implementing these high-sensitivity cardiac troponin assays on long-term outcomes remains unclear.

About the study

In the present study, the researchers reported the results of a randomized controlled trial that was carried out to assess the impact of evaluating troponin levels according to the Universal Definition of Myocardial Infarction guidelines using high-sensitivity troponin assays.

Previous studies have reported that the use of high-sensitivity troponin I assay with a diagnostic threshold of sex-specific 99^th centile resulted in the identification of more cases of MI or injury and provided better opportunities for evidence-based treatments but had no impact on reducing the number of cardiac events in a year.

Given that the impact of the implementation of such recommendations often shows results over the long term, the researchers hypothesized that the implementation of high-sensitivity cardiac troponin I assay, and subsequent improvements in early care could influence long-term outcomes such as MI risk and death beyond a year. Therefore, they conducted a secondary observational analysis of the results of the High-Sensitivity Troponin in the Evaluation of patients with suspected Acute Coronary Syndrome (High-STEACS) trial.

The trial was conducted in a stepped wedge manner across ten hospitals in Scotland that were either secondary or tertiary care centers. Patients who presented with symptoms of suspected acute coronary syndrome at the emergency department of these hospitals were screened using a cardiac troponin testing electronic form.

The study included all patients whose cardiac troponin I levels were tested using standard care or the high sensitivity trial assays. Nonresidents of Scotland, as well as patients already hospitalized during the trial, were excluded.

The hospital sites were cluster-randomized to circumvent clinical errors that could occur from concurrent reports involving different assays and threshold levels. Troponin levels were tested using plasma samples when the patient presented with the symptoms at the emergency department and then twice again at intervals of six hours. The clinicians administering the assays were blinded to the high-sensitivity assay results. Furthermore, the doctors adjudicating the diagnoses after reviewing the results of the assays were also blinded.

Based on the troponin I level, sex-specific 99^th centile thresholds, and symptoms, diagnoses consisted of type 1 MI, type 2 MI, and non-ischemic myocardial injury. The primary outcomes of the trial were type 1 or 4b MI or death within one year.

Results

The results reported that implementation of the high-sensitivity assay for measuring cardiac troponin I levels in patients suspected of having acute coronary syndrome showed reductions in the risk of developing MI or of death at five years. Furthermore, the most significant improvements were observed in patients diagnosed with non-ischemic myocardial injury, indicating that the application of the high-sensitivity assay for measuring cardiac troponin I has other benefits than early identification of MI risk.

The study found that the administration of the high-sensitivity assay using sex-specific thresholds in the 99^th centile resulted in the reclassification of one-fifth of the patients who presented with myocardial injury and provided opportunities to implement evidence-based treatments. However, the researchers observed that out of the patients who had been reclassified based on the results of the high-sensitivity assay, most had been diagnosed with non-ischemic myocardial injury, and only a few had diagnoses of type 1 MI.

The implications of these results are significant in cases of non-ischemic myocardial injury. The differentiation of myocardial injury from MI is based on symptoms of myocardial ischemia and cardiac imaging. For patients with non-ischemic myocardial injury, many of the electrocardiographic findings and symptoms might be silent, making this high-sensitivity troponin assay a significant tool for ensuring positive outcomes. Furthermore, this assay could also be used for other conditions such as renal failure, sepsis, heart failure, pulmonary embolisms, and even in cases of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections.

Conclusions

To summarize, the study found that the implementation of a high-sensitivity assay to measure cardiac troponin I levels was effective in reducing MI risk and death in five years. Furthermore, the improvements in outcomes were notable for patients diagnosed with non-ischemic myocardial injury. These findings also highlight the potential application of the high-sensitivity assay for other non-cardiac and cardiac conditions.