Absence of chest pain is more reproducible than the broad label “atypical”, although presentations remain heterogeneous. Symptoms include dyspnoea, nausea, epigastric or back discomfort, diaphoresis, syncope, palpitations and fatigue. These are plausible manifestations of ventricular dysfunction, autonomic activation, reduced cardiac output or ischaemia-related arrhythmia.

Older age, diabetes, heart failure, cerebrovascular disease, haemodynamic instability and NSTEMI are associated with non-chest-pain presentation [3][4]. Women may report a broader symptom mix but commonly experience chest discomfort; labelling women inherently “atypical” risks stereotyping. Current guidance recommends specific symptom descriptors [5] and recognises chest, shoulder, arm, neck, back, upper-abdominal or jaw discomfort, dyspnoea and fatigue as possible anginal equivalents [6]. Subgroup information should heighten vigilance, not replace ECG and troponin assessment.

Dominant symptoms can redirect attention to a complication rather than its coronary cause. Dyspnoea may reflect ventricular dysfunction and syncope impaired output or arrhythmia. Respiratory treatment may be necessary, but immediate ECG assessment should proceed in parallel when ACS is plausible. Figure 1 illustrates how failure to recognise ACS at triage can delay ECG acquisition, diagnosis, escalation and reperfusion.

Figure 1. Diagnostic pathway model. A failure to recognise ACS at triage delays ECG and diagnosis, with downstream effects on escalation and reperfusion. ACS, acute coronary syndrome; ECG, electrocardiography.

Patient-level recognition is the first potential failure. Symptoms such as fatigue, indigestion or breathlessness may be attributed to infection, anxiety, gastrointestinal illness, chronic lung disease or ageing. In a prospective study of suspected ACS, unusual fatigue and failure to use emergency medical services were associated with prolonged prehospital delay [7]. A Danish study of 8336 patients with MI linked symptom presentation to emergency response: patients without chest pain were less likely to receive an emergency dispatch and had worse short-term survival [8]. A systematic review from low- and middle-income countries found that delay reflects interacting patient, transport and health-system barriers, underscoring the importance of measuring symptom-onset-to-first-medical-contact and first-medical-contact-to-hospital intervals separately [9].

The next failure occurs at triage. A chest-pain-dependent protocol can place a patient with dyspnoea in a respiratory stream or a patient with epigastric discomfort in a gastrointestinal stream without a concurrent 12-lead ECG. The 2025 cohort by Huang et al. provides the clearest contemporary decomposition of this delay. Among 807 patients with STEMI undergoing primary PCI, 13.5% had atypical symptoms. Atypical presentation was associated with delayed door-to-ECG time (adjusted odds ratio [aOR] 11.52, 95% CI 6.04 - 22.06), activation-to-catheter-laboratory arrival (aOR 1.71, 95% CI 1.04 - 2.80) and catheter-laboratory-arrival-to-balloon time (aOR 1.95, 95% CI 1.24 - 3.06) [10]. The magnitude and sequence of these estimates suggest that the largest inequity emerges before the diagnosis is secure, then propagates downstream. Figure 2 displays these adjusted delay estimates.

Figure 2. Adjusted odds of delay with atypical versus typical STEMI presentation in the 2025 PCI-era cohort by Huang et al. [10]. The largest association was for door-to-ECG time exceeding 10 minutes. CI, confidence interval; ECG, electrocardiography; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation myocardial infarction.

Early delay has three modifiable mechanisms. Pattern recognition fails when symptoms do not match the chest-pain script; triage templates may use chest discomfort as the ECG gateway; and a plausible alternative diagnosis can cause anchoring. Education can broaden clinical scripts, electronic rules can widen ECG eligibility, and team prompts can mandate reassessment when vital signs, troponin or the clinical course conflict with the initial diagnosis.

Other PCI-era studies support this mechanism. In a 2024 Omani cohort, atypical symptoms were associated with approximately threefold higher odds of delayed door-to-balloon time (OR 3.003, 95% CI 1.409 - 6.400) [11]. A 2021 AMI registry likewise found less timely reperfusion with atypical presentation (Figure 3) and higher 30-day mortality (hazard ratio 2.33, 95% CI 1.20 - 4.38) [12]. Despite different definitions and settings, studies show that patients who do not match the expected presentation move less rapidly through ECG acquisition, escalation and reperfusion.

Figure 3. Timely reperfusion by presentation phenotype. Door-to-balloon time within 90 minutes was achieved in 40.0% of atypical versus 66.3% of typical AMI presentations [12]. AMI, acute myocardial infarction; PCI, percutaneous coronary intervention.

A total door-to-balloon interval can conceal delay in ECG acquisition, repeat testing, cardiology review, catheter-laboratory activation, transfer or the procedure. Separating components directs intervention: triage redesign for late ECG, decision support for late escalation, and network coordination for transfer delay. Figure 1 shows how early recognition failure propagates downstream.

Treatment disparity follows recognition failure. Late ECG or diagnosis can delay or prevent antithrombotic therapy, specialist review, angiography and reperfusion. Recent syntheses report less consistent evidence-based care in non-chest-pain presentations, although many estimates derive from older registries [3][4]. Modern audits should test whether phenotype predicts treatment omission after adjustment for contraindications, frailty, haemodynamic severity and ACS subtype.

Once ACS is recognised, treatment should follow risk and ECG findings, not pain presence. Guidance recommends immediate ECG, serial high-sensitivity troponin, repeat ECG when suspicion persists, appropriate antithrombotic therapy and urgent STEMI reperfusion [1][2][13][14]. These measures require reliable pathway entry and parallel evaluation of cardiac and competing diagnoses. A symptom-inclusive trigger can include new unexplained dyspnoea; diaphoresis with nausea or vomiting; exertional epigastric, back, arm or jaw discomfort; acute pulmonary oedema; unexplained hypotension; high-risk syncope; or new arrhythmia with weakness. These findings justify early ECG and possible troponin testing.

To avoid excessive testing, triggers should incorporate age, cardiovascular risk, abnormal vital signs, clinician concern and local prevalence. Electronic prompts should recommend ECG, not diagnose ACS, and be evaluated for sensitivity, workload, crowding and unintended inequity. In haemodynamic instability, acute heart failure or diagnostic uncertainty, bedside echo can be used to aid assessment, but not delay STEMI reperfusion. ECG is not useful as a rule out test for ACS; serial troponin and repeat ECG are still valuable when there is persistent ACS symptoms or a change in clinical status.

The short bedside note should record onset of symptoms and autonomic features, vital signs and perfusion, immediate 12-lead ECG if ACS is considered, and should include troponin and tests for competing emergencies. Set a re-evaluate time point for repeat ECG, troponin review and escalation, if symptoms or instability continues. Implementation involves symptom-inclusive dispatch scripts, nurse-authorised ECG requests, rapid repeat testing, rules for access to cardiology and escalation to the catheter-lab that are not based on pain severity. Teams should review delayed cases and feedback should be provided to them on a chart indicating where delays started in the intervals.

Quality improvement requires an explicit denominator: chest discomfort present or absent, dominant symptom and mixed presentations. Report medians and interquartile ranges for onset-to-first-medical-contact, door-to-ECG, door-to-troponin, door-to-diagnosis, diagnosis-to-specialist activation and door-to-reperfusion. Also report target attainment as similar medians can mask a high-risk tail of delay. The 2026 Delphi study recommended time-limited definitions of delayed and missed coronary diagnosis such as a missed STEMI if the diagnosis had not been made 90 minutes after arrival [15]. These thresholds enable comparable audit. Validation should test associations with treatment omission, infarct size, heart failure and mortality across emergency systems.

Research should separate STEMI from NSTEMI, absence of chest pain from broad atypical classifications, prehospital from in-hospital delay, and diagnostic from procedural delay. Prospective multicentre cohorts should use time-stamped electronic data and prespecify age, sex, diabetes, renal disease, heart failure, haemodynamic severity, ambulance use and transfer status. Implementation trials should compare usual chest-pain triggers with symptom-inclusive triage rules. The primary process outcome should be door-to-ECG by phenotype, with unnecessary ECGs, false activations, length of stay and clinical outcomes as balancing measures. Report results by age, sex and diabetes.

Analyses should preserve event order by modelling door-to-ECG, diagnosis, activation and reperfusion separately. Mediation analysis can estimate how delayed recognition contributes to treatment delay. Time-to-event and quantile methods can address variable follow-up and delayed tails. Report missing timestamps and uncertain symptom onset, with sensitivity analyses for imputation. Equity analysis should cross-tabulate symptom phenotype with age, sex, diabetes, ambulance use and transfer status while suppressing unstable small-cell estimates. Interviews with patients and triage staff can explain measured gaps and guide acceptable changes to public messaging, triage questions and escalation procedures. Table 2 presents the proposed minimum audit set.

Table 2. Minimum audit set for ACS presentations without chest pain.

FMC, First Medical Contact; ECG, Electrocardiography; IQR, Interquartile Range; NSTEMI, Non-ST-Segment Elevation Myocardial Infarction; STEMI, ST-Segment Elevation Myocardial Infarction.