EDACS, emergency department assessment of chest pain

Clinical background

EDACS was developed to address one of the emergency department's commonest diagnostic dilemmas: the patient with chest pain that could be cardiac but probably is not. Approximately 15 per cent of those presenting with chest pain have an acute coronary syndrome [4], but missing cases carries high morbidity and mortality. The consequence is a tendency to over-investigate, with admission and stress testing of patients who do not need it. EDACS aims to identify the large proportion of low-risk patients who can go home after a short observation with serial troponins, rather than being admitted to hospital.

The score is designed to give high sensitivity for major adverse cardiac events (MACE), where the accepted rate of a missed event among low-risk patients is usually set below 1 per cent [2].

Calculating EDACS, the emergency department assessment of chest pain score

EDACS is calculated as:

$$\text{EDACS} = A + 6 \cdot [\text{male}] + 4 \cdot [\text{coronary artery disease}] + 3 \cdot [\text{diaphoresis}] + 5 \cdot [\text{radiation}] - 4 \cdot [\text{pleuritic}] - 6 \cdot [\text{palpation}]$$

where $A$ is the age score:

$$A = \min\left(2 + 2 \cdot \left\lceil \frac{\max(\text{age} - 45, 0)}{5} \right\rceil, ; 20\right)$$

All the variables are binary (1 if the criterion is met, otherwise 0). [coronary artery disease] scores for known coronary artery disease or for age 18–50 years with at least three risk factors (family history, dyslipidaemia, hypertension, diabetes, current smoking). [pleuritic] denotes pain that arose or worsened on inspiration. [palpation] denotes pain reproducible on palpation of the chest wall. [radiation] denotes pain radiating to the arm, shoulder, neck or jaw. Diaphoresis is assessed clinically as a sign of sympathetic activation during the episode of pain in question.

Low-risk classification (EDACS-ADP) requires three conditions, all of which must be met: EDACS <16, an ECG without ischaemia, and negative troponins at 0 and 2 hours.

The derivation cohort consisted of 1,974 patients presenting to emergency departments in Australia and New Zealand with chest pain suspected to be cardiac in origin [1]. Logistic regression identified predictors of MACE, defined as cardiac death, myocardial infarction or coronary revascularisation within 30 days. The statistical coefficients were converted into integers and refined with clinician feedback. In a separate validation cohort of 608 patients, both the score and its reproducibility were tested.

Interpretation in practice

Low-risk classification means that the patient can be considered for discharge without further cardiac investigation during the index attendance. Other causes of chest pain are managed as usual. The accelerated pathway means that troponin is measured on arrival and after 2 hours, and that the patient can go home after the second sample if all the criteria are met.

Patients who do not meet the low-risk criteria must not be sent home on the basis of the score alone. EDACS is a rule-out tool: it identifies low-risk patients but must not be used on its own to risk-stratify patients in the intermediate group or above. Patients with a score ≥16, ischaemia on the ECG or rising troponins require further management whatever the score.

The negative score components are central to how the tool works: pleuritic pain and tenderness on palpation lower the score and increase the proportion of low-risk patients. A patient with atypical chest pain that is tender on palpation, a normal ECG and negative troponins may reach low risk even at an advanced age.

Validation and performance

The derivation study reported a sensitivity of 99–100 per cent and a low-risk proportion of 42–51 per cent [1][2]. The intraclass correlation coefficient for the reproducibility of low-risk classification was 0.87 [1].

A systematic review of 12 studies and 14,290 patients reported a pooled sensitivity of 0.97 (95 per cent CI 0.95–0.99) and a specificity of 0.58 (0.53–0.63), with a summary ROC-AUC of 0.83 (0.79–0.86) [5]. The MACE rate among low-risk patients was 0.89 per cent. Heterogeneity between the studies was substantial, which the authors noted as a limitation on transferability.

In a Korean prospective study of 1,304 patients using high-sensitivity troponin I, 30.6 per cent were classified as low risk [3]. Sensitivity was 98.8 per cent for MACE including unstable angina and 98.7 per cent when unstable angina was excluded. The MACE rate among low-risk patients was 1.3 per cent and 1.0 per cent respectively. When unstable angina was included in the outcome, however, the miss rate exceeded the commonly accepted limit of 1 per cent, which the authors highlighted as a problem for safe discharge.

In an Iranian comparative study of 274 patients, EDACS-ADP performed moderately, with an AUC of 0.803 for 6-week MACE [4]. EDACS-ADP was inferior to the HEART score (AUC 0.925) and TIMI (AUC 0.868) in the same cohort.

An American validation in a secondary analysis of the HEART Pathway RCT with 282 patients at an academic centre showed a sensitivity of only 88.2 per cent (95 per cent CI 63.6–98.5) [2]. Among 188 low-risk patients there were 2 MACE (1.1 per cent). The authors could not validate EDACS-ADP as sufficiently sensitive for clinical use and attributed part of the difference to the higher revascularisation rate in the American health system.

Limitations

EDACS was derived using a contemporary troponin assay, not a high-sensitivity one [1]. The Korean validation with high-sensitivity troponin I showed satisfactory sensitivity but a miss rate that, with unstable angina included, exceeded 1 per cent [3]. This indicates that the move to high-sensitivity troponins may require an adjustment of the low-risk threshold or a modified ADP.

The MACE definition includes coronary revascularisation, which varies with local practice and can drive up the proportion of "missed" events in systems with a high revascularisation rate [2]. In the American validation cohort, 41 per cent of MACE events were revascularisations, compared with 8.6 per cent in the ADAPT registries of the original studies.

EDACS does not apply to patients with ST elevation or an obvious acute coronary syndrome at presentation. The score must not be used to justify withholding further management in patients with ischaemia on the ECG or rising troponins, whatever the value of the score. The systematic review [5] notes substantial heterogeneity between studies, and EDACS-ADP has not been validated in a Swedish population in published studies.

References

1. Than M et al. Development and validation of the Emergency Department Assessment of Chest pain Score and 2 h accelerated diagnostic protocol. Emerg Med Australas 2014. PMID: 24428678
2. Stopyra JP et al. Performance of the EDACS-accelerated diagnostic pathway in a cohort of US patients with acute chest pain. Crit Pathw Cardiol 2015. PMID: 26569652
3. Yoo Y et al. Performance of the EDACS-ADP incorporating high-sensitivity troponin assay: Do components of major adverse cardiac events matter? World J Emerg Med 2024. PMID: 38855369
4. Nasr Isfahani M et al. Improving chest pain risk assessment: validation of HEART, TIMI, GRACE, EDACS-ADP, and HET for MACE prediction in the emergency department. BMC Emerg Med 2025. PMID: 40847270
5. Wang M et al. A systematic review of the applicability of emergency department assessment of chest pain score-accelerated diagnostic protocol for risk stratification of patients with chest pain. Clin Cardiol 2023. PMID: 37594309