1. Introduction

The Aslanger pattern is a specific 12-lead ECG configuration associated with acute inferior myocardial infarction (MI), often with critical disease in one or more additional coronary arteries. Its importance is that the ECG may not show the contiguous ST-segment elevation conventionally required for an inferior STEMI diagnosis.

The pattern was described by Aslanger and colleagues in 2020. In their retrospective cohort, it was identified in 6.3% of patients classified as non-STEMI and 0.5% of patients without MI. The authors reported larger infarct size and a higher frequency of angiographic culprit lesions and acute coronary occlusion than in the comparator NSTEMI group. The pattern should therefore prompt clinicians to consider an acute coronary occlusion rather than relying on the STEMI/NSTEMI label alone.

These are findings from the original retrospective study, not population-wide prevalence estimates or validated diagnostic-performance values.

2. Electrophysiology and Pathophysiology

The proposed explanation is the superposition of two ST-segment injury/ischemia vectors:

• Inferior-wall injury current: a relatively localized inferior injury vector may be directed inferiorly and rightward, contributing to ST elevation in lead III.
• Concomitant subendocardial ischaemia: more diffuse subendocardial ischaemia, often related to critical disease in non-culprit coronary territories, produces a widespread ST vector directed toward aVR (and away from many left-sided leads), contributing to lateral precordial ST depression.

The net ST vector can therefore produce an apparently discordant pattern: isolated inferior ST elevation in III, lateral precordial ST depression, and a higher ST level in V1 than V2. The vector model is a proposed explanatory framework, not a direct measurement of the electrical source in an individual patient.

3. Characteristic ECG Features

Assess the ST segments in the inferior and precordial leads carefully. The classic pattern is defined by three features:

Heart rate, rhythm, PR interval, QRS width, QT interval and axis are not defining criteria. Interpret these conventionally and document abnormalities when present, but do not use them to replace the three pattern criteria.

4. Systematic ECG Interpretation

1. Confirm technical quality. Check calibration, paper speed, artefact and limb-lead placement. Compare with prior ECGs if available.
2. Establish the clinical context. Ask whether symptoms are compatible with acute myocardial ischaemia, including ongoing or recurrent chest discomfort, dyspnoea, diaphoresis or haemodynamic compromise.
3. Inspect inferior leads together. Look for ST elevation in III and verify that II and aVF do not show corresponding ST elevation.
4. Inspect V4–V6. Look for ST depression with a positive or terminally positive T wave; confirm that the described depression is not simply a V2 finding.
5. Compare V1 and V2. Compare ST levels at the same reference point and confirm that V1 is higher than V2.
6. Integrate the pattern. If all three features coexist, consider an Aslanger pattern and possible acute inferior OMI with multivessel coronary disease.
7. Escalate and reassess. Review serial ECGs, biomarkers, bedside imaging and the overall ACS risk; obtain urgent senior/interventional cardiology assessment when acute occlusion is suspected.

5. Diagnostic Criteria and Limitations

The original operational definition is the presence of all three ECG features below:

The source definition does not provide a separate numerical ST-elevation threshold for lead III or a numerical V1–V2 difference. Do not add an unsupported millimetre cut-off when applying this specific pattern definition.

Limitations of the evidence

• The original study was retrospective and conducted at a single centre; the authors called for further evaluation.
• The pattern was also observed in a small proportion of patients without acute MI (0.5% in the original cohort), potentially reflecting chronic ischaemic changes.
• Previous infarction may alter the net injury vector and produce a similar appearance.
• Subsequent case reports and cohort studies broaden clinical experience but do not make the pattern a definitive stand-alone test for acute coronary occlusion.

6. Differential Diagnosis

These are practical differential considerations rather than a validated exclusion algorithm. The pattern must be interpreted in context and should not delay evaluation for other acute coronary occlusion patterns.

7. Clinical Significance and Prognostic Considerations

In the original study, patients with the pattern had larger infarct size (using 24-hour troponin as an indicator), more frequent angiographic culprit lesions and a higher frequency of the composite acute coronary occlusion endpoint than other NSTEMI patients. Their in-hospital and one-year mortality were reported as similar to the inferior STEMI comparison group.

A later small, single-centre retrospective cohort of patients with acute inferior coronary occlusion reported multivessel disease in 80% of patients with the pattern, mechanical circulatory support use in 30%, and in-hospital mortality of 20%. These figures describe that selected cohort and should not be generalized as expected rates for all patients with the pattern.

• Potential missed OMI: classification as NSTEMI based only on absence of contiguous inferior STE may delay recognition of an acute occlusion.
• Multivessel disease: concomitant critical stenoses may complicate culprit-lesion identification during angiography.
• Reperfusion priority: the pattern should raise concern for an acutely compromised inferior-wall territory; angiographic findings and clinical context determine the revascularization strategy.

8. Clinical Evaluation and Management Principles

There is no separate treatment protocol established solely by the Aslanger ECG pattern. Manage the patient as suspected acute coronary syndrome with possible acute coronary occlusion, using local ACS pathways and urgent cardiology input.

Immediate assessment

• Assess airway, breathing, circulation, perfusion and haemodynamic stability; obtain continuous rhythm monitoring in an appropriate acute-care setting.
• Clarify symptom onset, duration, recurrence, associated symptoms, cardiovascular history and contraindications to antithrombotic therapy.
• Obtain and interpret a 12-lead ECG promptly; repeat ECGs with ongoing symptoms or clinical change. Consider posterior/right-sided leads when clinically indicated.
• Measure high-sensitivity cardiac troponin using the validated local serial algorithm. A normal early value does not exclude evolving MI.
• Use focused echocardiography when it can rapidly assess regional wall-motion abnormality, LV function or alternative causes, without delaying necessary reperfusion decisions.

Escalation and invasive evaluation

• Discuss urgently with an experienced cardiologist/interventional team when the pattern is present with a compatible acute presentation, especially with ongoing symptoms or instability.
• Consider emergency coronary angiography/revascularization when the integrated clinical and ECG picture indicates ongoing acute coronary occlusion or very-high-risk ACS. Do not make the decision from the eponym alone.
• At angiography, assess the inferior-wall culprit territory while recognizing that concomitant critical lesions may be present. The ECG may help focus attention but cannot reliably identify the culprit vessel in every patient.
• Provide guideline-directed ACS care, including antithrombotic and secondary-prevention treatment as appropriate to the confirmed diagnosis, bleeding risk, anatomy and local protocol.

9. Common Interpretation Pitfalls

• Calling the tracing “NSTEMI” and stopping the ECG assessment because contiguous inferior ST elevation is absent.
• Failing to compare lead III with both II and aVF, thereby overlooking that the elevation is isolated.
• Missing subtle ST depression in V4–V6 or overlooking a positive terminal T-wave component.
• Comparing V1 and V2 inaccurately because of baseline selection, artefact or lead placement.
• Assuming that the pattern proves a specific culprit artery or guarantees acute total occlusion.
• Ignoring prior ECGs, previous infarction, serial changes and the patient's clinical stability.
• Delaying escalation while waiting for troponin results in a patient with ongoing ischaemia or haemodynamic compromise.

10. ECG Interpretation Example

The supplied PDF includes a second clinical example described as a 57-year-old woman with hypertension and chest pain, without previous heart disease reported in the source.

Interpretation task: Review the tracing and assess the three defining features in sequence. The supplied PDF does not provide a full set of measured ST amplitudes, biomarker results or angiographic findings for this case; these should not be inferred from the image.

11. ECG Pearls and Quick Reference

• Think of Aslanger pattern when ST elevation is isolated to lead III rather than present across the inferior leads.
• Always inspect V4–V6 for ST depression with a positive or terminally positive T wave.
• Compare the ST level in V1 directly with V2; V1 should be higher.
• The pattern is associated with inferior MI and concomitant critical disease in other coronary territories in the original description.
• It may signal an OMI despite failure to meet conventional contiguous-lead STEMI criteria.
• It is a high-risk clue, not a definitive diagnosis, culprit-vessel locator or treatment algorithm.

12. References