Diagnosing total left main obstruction on ECG, is the role of lead avR "overhyped" ?

ST-segment elevation in aVR has traditionally been used for ECG diagnosis of left main coronary artery (LM) myocardial infarction. But when lead avR lacks STE, are there any other alternative clues on ECG to suggest an acute LM occlusion? A recent JACC case report highlights two such cases and reviews different ECG discriminators of LM STEMI in absence of STE in lead avR.

Unprotected left main coronary artery (LM) ST-segment elevation myocardial infarction (STEMI) is the most lethal type of acute myocardial infarction (60% to 90% mortality) often resulting in cardiogenic shock or sudden cardiac death.

The case report discusses two patients who presented with an acute presentation of MI with hemodynamic compromise. Both their ECGs lacked the classical ST elevation in lead avR(Figure), but complete acute LM occlusion was confirmed on angiography (TIMI 0 flow).

First patient's ECG showed left axis deviation (LADEV) and left anterior fascicular block (LAFB), plus STEs in leads V2 to V6, I and aVL, with reciprocal inferior ST-segment depressions (STDs), which are consistent with anterolateral STEMI. The second patient's ECG showed a new right bundle branch block (RBBB), LADEV, LAFB, plus STEs in V2 to V4, I, and aVL, with reciprocal STDs in V5, V6 and the inferior leads, again compelling for anterolateral STEMI.

LM infarctions have two distinct ECG features:

1. Subtotal LM occlusion and NSTE acute coronary syndrome (TIMI flow >1): Manifests as diffuse STDs (≥8 leads) involving the inferior and precordial leads plus a reciprocal STE in aVR that denotes global left ventricular subendocardial ischemia.

2. STEMI due to acute total occlusion (TIMI flow grade 0): the more common and more deadly variant causing transmural ischemia: As in both cases reviewed these patients will show:

a. STEs in the anterior (V2 to V5) and high-lateral leads (aVL, I) with

b. reciprocal inferior STDs,

c. plus they may or may not have aVR elevation as well as LADEV and RBBB.

Conduction abnormalities can often arise as ischemia of the basal septum occurs. In fact, coexistence of LADEV (>−30°) and LAFB, as in the above cases has shown to predict LM occlusion with 95% specificity, and 88% positive (PPV) and negative predictive value (NPV).

STE in lead avR alone has limited sensitivity and specificity. It may still be absent in 20% to 38% of cases and may occur in almost 25% of LAD infarctions if occlusion is prior to the first septal branch.

Besides the above features, following clues in surface ECG may also be of great utility in diagnosing complete acute occlusion in an unprotected LM:

1. Larger STDs in lead II when compared with the magnitude of the STE in V2 (PPV = 90% to 100%; NPV = 94% to 95%).

2. The presence of STDs in V5 and/or V6 (PPV = 46% to 62%; NPV = 96% to 96.2%).

3. A larger absolute magnitude of STD in V6 over ST-segment deviation in V1 (V6/V1 ≥1).

With regard to STE in avR; STE aVR/V1 ≥1 suggests LM involvement while aVR/V1 <1 means that STE in V1 is unopposed by posterior infarct changes (LCx territory) and thus suggest proximal LAD occlusion.

Most studies till date evaluating ECG changes in LM STEMI have not discriminated between acute total and subtotal involvement of LM that may account for limited diagnostic utility of STE in lead avR. Infact, a case series of 7 STEMI patients with unprotected LM ATO and TIMI flow grade 0 revealed that 100% had no STE in leads aVR and V1.

This is possibly caused by the fact that when large anterior (LAD territory) and posterior (LCx territory) walls are subjected to infarction, the ST elevation in leads avR and V1 tend to cancel each other and thus the classical STE in avR is absent from the ECG. This calls for application of multiple alternative criteria to diagnose this lethal condition.

Source: JACC case reports: J Am Coll Cardiol Case Rep. Apr 28, 2021. Epublished DOI: 10.1016/j.jaccas.2021.02.014