Circumflex Artery Myocardial Infarction: When Acute Coronary Occlusion Does Not Meet STEMI Criteria on ECG

Acute occlusion of the left circumflex coronary artery (LCx) frequently causes transmural myocardial infarction without meeting classic STEMI criteria on the standard 12-lead ECG. This article explains why LCx infarctions are often misclassified as NSTEMI, illustrates a typical ECG pattern, and highlights key anatomical and electrophysiological principles that can prevent delayed revascularization.

Prehospital ECG - standard leads

Prehospital ECG - precordial leads

Circumflex Artery Myocardial Infarction

When the ECG Does Not Show Classic STEMI

Acute occlusion of the left circumflex coronary artery (LCx or CX) is a well-known diagnostic challenge. Even in cases of transmural myocardial infarction, only about half of LCx infarctions fulfill standard STEMI criteria on the 12-lead ECG.

As a result, LCx infarction is a common cause of delayed or missed reperfusion therapy, particularly when ECG interpretation is rigid and disconnected from coronary anatomy and electrophysiology.

This case illustrates a classic, yet frequently overlooked, LCx infarction pattern.

Case Presentation

A man in his 50s presents with acute chest pain.

Admission ECG findings:

• ST depression in leads II, III, and aVF

• ST depression in V2–V3, with subtle involvement of V4

• Discrete ST elevation in aVL, not meeting formal STEMI criteria

  
  

The ECG is classified as non-STEMI. However, based on clinical presentation and ECG pattern recognition, the patient is taken directly to the catheterization laboratory.

Coronary angiography:

• Critical stenosis in a marginal branch of the left circumflex artery

• Successful treatment with percutaneous coronary intervention (PCI)

LCx Anatomy – Why ECG Patterns Vary

The left circumflex artery typically supplies:

• The lateral wall of the left ventricle

• The posterior wall

• Parts of the inferior wall in left-dominant circulation

  
  

There is substantial anatomical variability, including:

• Obtuse marginal branches (OM1, OM2)

• Ramus intermedius

• Variation in coronary dominance

  
  

These factors contribute to greater heterogeneity and lower ECG sensitivity for LCx infarction compared with LAD or RCA occlusion.

Coronary anatomy

Why LCx Infarction Produces This ECG Pattern

Posterior Wall: ST Elevation That Looks Like ST Depression

The standard 12-lead ECG has no direct posterior leads. In transmural posterior myocardial infarction, ST elevation is therefore recorded as reciprocal ST depression, most prominently in leads V1–V3.

This pattern is often misinterpreted as subendocardial ischemia, when it actually represents a posterior STEMI equivalent.

Lateral Wall and Lead aVL: Small Changes, Major Significance

ST elevation in aVL during LCx infarction is often subtle and rarely exceeds formal STEMI thresholds. This does not make the finding insignificant.

A likely explanation is that lead aVL views the lateral wall at an unfavorable angle, resulting in a low-amplitude ST vector. While this is a vector-based hypothesis rather than a fully proven mechanism, it aligns well with repeatedly observed clinical patterns in LCx occlusion.

Inferior ST Depression: Prominent but Potentially Misleading

ST depression in leads II, III, and aVF is often more pronounced than ST elevation in aVL. These inferior leads are more parallel to the heart’s electrical axis, producing larger voltage changes.

The diagnostic error occurs when these inferior ST depressions are interpreted in isolation, without recognizing the combined pattern of posterior and lateral transmural ischemia.

Why LCx Infarction Is Often Misclassified as NSTEMI

LCx myocardial infarction is frequently misdiagnosed because:

• STEMI criteria are not met

• ST depressions attract more attention than subtle ST elevations

• Minor changes in aVL are underestimated

• The posterior wall is not actively evaluated

  
  

The result is delayed or absent revascularization, despite ongoing transmural myocardial injury.

Key Clinical Learning Points

• LCx infarction is often transmural myocardial infarction without STEMI criteria

• ST depression in V1–V3 may represent posterior STEMI

• Discrete ST elevation in aVL with reciprocal inferior changes is a critical warning sign

• ECG interpretation should be pattern-based and anatomically informed

• Clinical suspicion must outweigh rigid ECG thresholds

• A low threshold for urgent coronary angiography is warranted when LCx infarction is suspected

  
  

FAQ – LCx Myocardial Infarction in Clinical Practice

How often does LCx infarction meet STEMI criteria?

Approximately 50% of cases.

Is ST depression in V2–V3 always NSTEMI?

No. In LCx infarction, this may represent reciprocal ST elevation from posterior wall transmural infarction.

Why is ST elevation in aVL often minimal?

Likely due to the angle between the infarction vector and lead aVL, although the mechanism is not fully established.

Should posterior leads be recorded?

Yes. Leads V7–V9 may reveal diagnostic ST elevation and strengthen the decision for emergent PCI.

Conclusion

LCx myocardial infarction highlights the limitations of ECG criteria-based diagnosis. Recognition of ECG patterns, understanding of coronary anatomy, and clinical judgment are essential to identify patients who require urgent reperfusion therapy — even when the ECG does not show classic STEMI.