The management of emergency department patients with chest pain continues to evolve. There was a time when  everyone with nary but a thoracic twinge got admitted. Even many low-risk patients were admitted (either to an observation unit or an inpatient bed) for noninvasive cardiac testing. Others would get testing within 24 to 72 hours. However, this approach was and remains inefficient and costly. Most important, it has never been shown to definitively improve patient-oriented outcomes.

We tend to underestimate the risks of admitting patients to the hospital as well as the risks of overdiagnosis (ie, false positives associated with noninvasive cardiac tests). With the recent introduction and use of sixth-generation high-sensitivity (hs) troponins, validation of the HEART Pathway (a clinical decision tool with an acronym that includes physician gestalt based on History, ECG features, Age of patient, traditional Risk factors for ACS, and initial Troponin) for both diagnosis and prognostication, and an ACEP clinical policy suggesting that stress testing should not be routinely done, the emergency management of the low-risk chest pain patient is undergoing a paradigm shift—for the better.^1–3

Patients at low risk for acute coronary syndromes (ACS) are those who are hemodynamically stable, have no concerning features on history or examination, and do not have objective evidence of myocardial ischemia on initial ECGs and biomarker testing. Consensus guidelines further define the low-risk patient as having a less than 1 percent risk of a major adverse cardiac event (MACE) or death at 30 days’ follow-up, a threshold below which the harms inherent in further testing appear to outweigh any clinical benefit.^4,5

Conventional Versus hs-Troponin

Conventional troponin assays use a reference limit at or near the 99th percentile of normal value, so any elevation above the reference level is, supposedly, consistent with myocardial injury. However, because these are binary assays (a test that gives a yes-or-no answer), some clinically important myocardial injury may not be initially detected at normal levels, thus necessitating serial troponin testing over 6 to 12 hours to achieve sufficient sensitivity.

In contrast, hs-troponin assays should not be considered binary tests. In fact, by definition, 50 percent of healthy individuals have detectable hs-troponin concentrations at baseline. Hs-troponin assays detect much lower concentrations of serum troponin and with much greater precision. This means that hs-troponin assays can detect clinically significant (but also some tiny insignificant) rises and falls in troponin concentrations much sooner in an ED evaluation. Moreover, the accuracy of diagnosing myocardial injury more than merely increases with hs-troponin; the Fourth Universal Definition of Myocardial Infarction is met specifically by the presence of a value above the 99th percentile and a rise or fall in that value (in order to be considered acute).⁶ The key in utilizing the hs-troponin is both recognizing elevated values and observing a rising and falling pattern of hs-troponin (the “delta troponin”), rather than relying on a binary cutoff.

The “delta troponin” is defined as the change in troponin concentration between two assays performed a prespecified time interval apart. The National Academy of Clinical Biochemistry recommends using a dynamic change of 20 percent or more to define myocardial infarction in patients with baseline elevations in troponin.⁷ Note that this change can be an increase or a decrease, in which increasing troponin suggests an evolving myocardial infarction while decreasing troponin suggests a resolving one. However, the bulk of the literature suggests that an absolute delta (eg, 10 ng/L troponin T) rather than a relative change (eg, 20 percent) generally performs better.

Several rapid testing algorithms have been developed with very high sensitivity for ruling out myocardial infarction, in some cases with a single troponin at the time of ED arrival. A normal ECG and a single undetectable hs-troponin drawn three hours or more after the onset of symptoms rules out myocardial infarction at ED arrival in a third of patients.⁸ The ability to detect lower concentrations of troponin also enables rapid serial testing protocols that are independent of the timing of the patient’s symptoms. For example, two-hour serial testing algorithms have been derived and validated for hs-troponin T and hs-troponin I assays (which are similar molecules made by different manufacturers and with different reference ranges) that rule out myocardial infarction in 60 percent of patients and rule in myocardial infarction in 15 percent of patients, leaving only 25 percent of patients undifferentiated after a two-hour ED evaluation.⁹

Utilizing the HEART score with hs-troponins also lowers the number of patients considered low risk from 40 percent to 10 percent.¹

While theoretically the higher sensitivity of these troponin assays is expected to result in lower specificity and overdiagnosis of ACS, based on experience in Canada, where hs-troponins have been widely adapted, the use of hs-troponins compared to conventional assays decreases length of stay and admissions without missing any additional myocardial infarctions.¹⁰