ST Elevation in aVR – LMCA occlusion?

This ECG demonstrates the classical pattern of left main coronary artery (LMCA) occlusion:

  • Widespread horizontal ST depression, most prominent in leads I, II and V4-6
  • ST elevation in aVR ≥ 1mm
  • ST elevation in aVR ≥ V1

This ECG was initially posted by Johnson Francis at Cardiophile.org

However, ST elevation in aVR is not entirely specific to LMCA occlusion. It may also be seen with:

NB. Some authors argue that using the term “LMCA occlusion” is inaccurate, as most of these patients have at least some flow in their LMCA (i.e. incomplete LMCA occlusion); whereas a complete LMCA occlusion would rapidly lead to STEMI, cardiogenic shock and death. 

 

Mechanism of STE in aVR

  • Lead aVR is electrically opposite to the left-sided leads I, II, aVL and V4-6; therefore ST depression in these leads will produce reciprocal ST elevation in aVR.
  • Lead aVR also directly records electrical activity from the right upper portion of the heart, including the right ventricular outflow tract and the basal portion of the interventricular septum. Infarction in this area could theoretically produce ST elevation in aVR.

ST elevation is aVR is therefore postulated to result from two possible mechanisms:

  • Diffuse subendocardial ischaemia, with ST depression in the lateral leads producing reciprocal change n aVR (= most likely).
  • Infarction of the basal septum, i.e. a STEMI involving aVR.

The basal septum is supplied by the first septal perforator artery (a very proximal branch of the LAD), so ischaemia / infarction of the basal septum would imply involvement of the proximal LAD or LMCA.

 

Predictive Value of STE in aVR

In the context of widespread ST depression + symptoms of myocardial ischaemia:

  • STE in aVR ≥ 1mm indicates proximal LAD / LMCA occlusion or severe 3VD
  • STE in aVR ≥ 1mm predicts the need for CABG
  • STE in aVR ≥ V1 differentiates LMCA from proximal LAD occlusion
  • Absence of ST elevation in aVR almost entirely excludes a significant LMCA lesion

In the context of anterior STEMI:

  • STE in aVR ≥ 1mm is highly specific for LAD occlusion proximal to the first septal branch

In patients undergoing exercise stress testing:

  • STE of ≥ 1mm in aVR during exercise stress testing predicts LMCA or ostial LAD stenosis

Magnitude of ST elevation in aVR is correlated with mortality in patients with acute coronary syndromes:

  • STE in aVR ≥ 0.5mm was associated with a 4-fold increase in mortality
  • STE in aVR ≥ 1mm was associated with a 6- to 7-fold increase in mortality
  • STE in aVR ≥ 1.5mm has been associated with mortalities ranging from 20-75%

A Brief Review of the Literature

Over the past 18 years, multiple studies have examined the utility of ST elevation in aVR for predicting severe coronary artery disease (proximal LAD/LMCA/3VD) and mortality in patients with acute coronary syndromes and those undergoing exercise stress testing. Some of the important studies are summarised below…

Gorgels et al. (1993)

Population:

  • 113 patients with unstable angina, including 20 patients with LMCA stenosis and 24 patients with 3VD.

Findings:

  • Patients with LMCA or 3VD frequently demonstrated ST-segment depression in multiple leads (typically I, II and V4-V6) plus ST-segment elevation in lead aVR during attacks of angina.

Engelen et al. (1999)

Population:

  • 100 patients with anterior STEMI.

Findings:

  • STE in aVR of any magnitude was 43% sensitive and 95% specific for LAD occlusion proximal to the first septal branch.

Yamaji et al. (2001)

Population:

  • 16 patients with acute LMCA occlusion, 46 patients with acute LAD occlusion and 24 patients with acute RCA occlusion.

Findings:

  • STE in aVR (≥ 0.5mm) occurred with a significantly higher incidence in the LMCA group (88%) than in the LAD (43%) or RCA (8%) groups.
  • Magnitude of STE in aVR was significantly greater in the LMCA group (1.6 ± 1.3 mm) than the LAD group (0.4 ± 1.0 mm).
  • In contrast, magnitude of STE in V1 was less in the LMCA group (0.0 ± 2.1 mm) than in the LAD group (1.4 ± 1.1 mm).
  • STE in aVR ≥ V1 distinguished the LMCA group from the LAD group with 81% sensitivity, 80% specificity and 81% accuracy.

Barrabes et al. (2003) 

Population:

  • 775 patients with first presentation of acute NSTEMI.

Findings:

  • Two-thirds of patients with STE in aVR ≥ 1 mm had either LMCA occlusion or severe 3VD.
  • Degree of STE in aVR was an independent predictor of mortality: STE of ≥ 1 mm was associated with a six- to seven-fold increase in in-hospital mortality (odds ratio of death = 6.6).
  • Magnitude of STE in aVR was also closely associated with rates of recurrent ischemic events and heart failure.
  • STE in aVR predicted the need for CABG – coronary grafting was required in 22% of patients with aVR STE > 1mm compared to 5% of those without.

Rostoff et al. (2005)

Population:

  • 150 patients with acute coronary syndromes – 46 with LMCA obstruction, 104 with occlusion of a different vessel.

Findings:

  • STE in aVR was twice as common in patients with LMCA occlusion as those without (69.6% vs 34.6%).

Kosuge et al. (2005) 

Population:

  • 310 patients with non-ST-elevation acute coronary syndromes.

Findings:

  • STE in aVR  ≥ 0.5 mm was the strongest predictor of LMCA or 3VD (78% sensitivity, 86% specificity, 57% PPV and 95% NPV).
  • STE in aVR was superior to the presence of ST depression in other leads for predicting LMCA/3VD.

Aygul et al. (2008)

Population:

  • 950 patients with STEMI (any type).

Findings:

  • STE in aVR ≥ 0.5 mm predicted proximal LAD or LMCA occlusion (with 50% sensitivity, 91% specificity, 55% PPV, 89% NPV).
  • STE in aVR ≥ 0.5 mm was also an independent predictor of mortality (in-hospital mortality was 19% in those with ≥ 0.5 mm STE in aVR compared to only 5% in those without).
  • Patients with STE in aVR also had higher heart rates, lower systolic BPs, lower ejection fractions and worse Killip class at the time of admission.

Wong et al. (2011)

Population:

  • 15, 315 patients with STEMI enrolled in the HERO-2 trial (heparin vs bivalirudin for acute MI).

Findings:

  • STE ≥1.5 mm in aVR was associated with a two-fold increase in 30-day mortality for both inferior and anterior STEMI, compared to the baseline mortality rate of 10.8%.

Population:

  • 454 patients undergoing both exercise stress testing (standard Bruce protocol) and cardiac catheterization within 6 months, including 75 patients with LMCA or ostial LAD stenosis.

Findings:

  • STE of ≥ 1mm in aVR during stress testing predicted LMCA or ostial LAD stenosis with sensitivity 75%, specificity 81% and overall accuracy 80%.

Kosuge et al. (2011)

Population:

  • 572 patients with acute NSTEMI.

Findings:

  • Degree of STE in aVR was the strongest independent predictor of severe LMCA occlusion / 3VD requiring CABG (odds ratio 29.1), followed by positive troponin T level (odds ratio 1.27).
  • STE ≥ 1.0 mm in aVR identified severe LMCA occlusion /3VD with 80% sensitivity, 93% specificity, 56% PPV, and 98% NPV.

ECG Examples

Example 1 – LMCA occlusion

The ECG shows:

  • Marked ST elevation in aVR >> V1
  • ST depression in mulitple leads (V2-6, I, II, aVL, aVF), to some extent masked by a non-specific interventricular conduction delay

This patient presented to our ED recently with severe ischaemic chest pain, vomiting, syncope  (due to runs of VT) and cardiogenic shock. He was taken for emergent angiography and found to have a complete ostial occlusion of his left main coronary artery

 

Example 2 – LMCA Occlusion

lmca 1-1

The ECG shows:

  • Sinus tachycardia
  • Widespread ST depression (V4-6, I, II, aVL)
  • ST elevation in aVR > V1

This patient was an elderly gentleman presenting with chest pain and cardiogenic shock (hence the tachycardia). He had a brief episode of VF whilst being transferred onto the cath lab table. Angiography revealed a LMCA occlusion. 

 

Example 3 – Proximal LAD occlusion

 This ECG shows:

  • ST elevation in aVR and V1 of similar magnitude.
  • Widespread ST depression (V3-6, I, II, III, aVF)

This patient had a severe ostial LAD thrombus that was close to the left main. This ECG is reproduced from Dr Smith’s ECG Blog – click here to see the ECG in its original context.

 

Example 4 – Proximal LAD Occlusion

Proximal LAD septal STEMI

The ECG shows:

  • A septal STEMI, with ST elevation and Q wave formation in V1-2
  • ST elevation in aVR
  • Widespread ST depression, most prominent in leads I, II and V5-6

Given the signs of septal STEMI, this ECG most likely represents a proximal LAD occlusion. 

 

Example 5 – Severe Multi-Vessel Disease

This ECG shows:

  • ST elevation in aVR and V1, of similar magnitude
  • ST depression in multiple leads (V5-6, I, II, aVL, aVF)
  • Evidence of anteroseptal STEMI – ST elevation with Q wave formation in V1-3

It would be reasonable to suspect a proximal LAD occlusion based on this ECG. However, this patient actually had severe multi-vessel disease. Angiography demonstrated a chronic total occlusion of his circumflex artery, with critical stenoses of his proximal LAD, RCA and ramus intermedius. Surprisingly, in this case the culprit vessel was thought to be the RCA, which had been collateralising his chronically occluded circumflex. 

 

Example 6 – LMCA/3VD

LMCA Steve Smith

Another classic example of the LMCA / 3VD ECG pattern:

  • Deep horizontal ST depression in multiple leads (V4-6, I, II and aVL)
  • ST elevation in aVR + V1

This ECG was contributed by Dr Steve Smith. Read his highly informative blog posts on LMCA occlusion here.

 

Example 7 – LMCA / 3VD

LMCA FACEM

This ECG originally appeared in the 2012.2 FACEM Exam as an example of LMCA/3VD. It demonstrates:

  • ST horizontal / downsloping ST depression in multiple leads (V3-6, I, II, aVL)
  • ST elevation in aVR > V1

View the ECG in the context of the exam question here.

 

Example 8 – Diffuse Subendocardial Ischaemia Due To Acute Blood Loss

LMCA dz GI bleed repeat

The ECG shows:

  • Sinus tachycardia + RBBB.
  • ST depression in a distribution typical of subendocardial ischaemia (leads V4-6, I, II), with ST elevation in aVR > 1mm.
  • The ST depression in V1-3 is an expected finding in RBBB, and is therefore more difficult to attribute to ischaemia.

This ECG was taken from an elderly man who presented with an acute GI bleed plus chest pain on the background of coronary artery disease. His ischaemic symptoms and ECG improved with blood transfusion. In this case the subendocardial ischaemia was likely due to cellular hypoxia (O2 supply < demand) from his acute anaemia, exacerbated by poor coronary blood flow. 

LMCA dz GI bleed baseline

This is the patient’s ECG following blood transfusion and resolution of symptoms. Note:

  • Resolving ST depression in V4-6, I, II
  • Improved ST depression in V2-3 (initial STD perhaps not entirely due to RBBB then!)
  • Resolving ST elevation in aVR

 

Example 9 – LMCA / 3VD

?LMCA2

The ECG shows:

  • Widespread deep ST depression involving V2-6, I, II, aVL
  • ST elevation in aVR > V1

The depth and extent of the ST depression indicates severe subendocardial ischaemia.

 

Implications for therapy in acute coronary syndromes

Given the ability of STE in aVR to predict critical coronary lesions and death, this ECG pattern is increasingly being recognised as a “STEMI equivalent” that requires emergent reperfusion therapy to prevent cardiogenic shock and death.

Furthermore, the presence or absence of STE in aVR may potentially inform the decision to give thienopyridine platelet inhibitors (e.g. clopidogrelprasugrel) during an acute coronary syndrome:

  • Clopidogrel treatment ≤ 7 days before CABG is associated with an increase in major bleeding, haemorrhage-related complications, and transfusion requirements.
  • Prasugrel is associated with even more bleeding than clopidogrel.
  • If urgent CABG (within 7 days) is likely, then there is an argument for omitting thienopyridines during the initial management of an acute coronary syndrome (or at least using clopidogrel instead of prasugrel).

In the recent study by Kosuge et al. (2011)

  • STE in aVR ≥ 1 mm was a strong predictor of severe LMCA / 3VD requiring CABG.
  • Conversely, patients with < 1mm ST elevation in aVR had a negligible risk of severe LMCA / 3VD requiring CABG.

Based on this data:

  • Patients with < 1mm STE in aVR may safely receive clopidogrel/prasugrel during the initial treatment of their ACS as they are unlikely to proceed to urgent CABG.
  • Patients with ≥ 1 mm STE in aVR may potentially require early CABG; therefore these patients should ideally be discussed with the interventional cardiologist (± cardiac surgeon) before thienopyridines are given.

 

LMCA Occlusion?

This ECG below was originally posted as an example of LMCA occlusion. What do you think?

There are some features on this ECG that suggest LMCA/3VD:

  • Widespread ST depression, most prominent in the lateral leads (V4-6, I, aVL)
  • ST elevation > 1mm in aVR

However, note also:

  • Tachycardia
  • Flutter waves in V2 — indicating that this patient has atrial flutter with 2:1 block

In this case the ST changes may be due to atrial flutter rather than ischaemia (see below).

Thanks to Christopher Watford of EMS 12-lead.com for spotting this one!

 

LMCA Mimics

Tachycardia-Related ST Depression

Widespread ST depression (with reciprocal STE in aVR) is a common finding in patients with supraventricular tachycardias such as AVNRT or atrial flutter. The significance of this finding in individual patients is unclear, and may be due to:

  • Rate-related ischaemia (O2 demand > supply)
  • Unmasking of underlying coronary artery disease (i.e. tachycardia as a “stress test”)
  • A pure electrical phenomenon (e.g. the young patient with SVT who is relatively asymptomatic and has normal coronary arteries)

ECGs taken following reversion to sinus rhythm will usually show resolution of the ST depression. I would be concerned about underlying coronary artery disease in the following situations:

  • ST depression that persists after reversion to sinus rhythm
  • Signs of clinical instability – severe chest pain with diaphoresis, hypotension, syncope
  • Elevated cardiac biomarkers, with delta troponin rise (NB. a small troponin leak with SVT is common and probably not significant)
  • Older patient, multiple cardiac risk factors

Example (a) — Supraventricular Tachycardia

SVT ST depression

 

Example (b) — Atrial Flutter with 2:1 Block

aflutter RVR 160bpm

 

Differential Diagnosis

The differential diagnosis of lateral ST depression includes:

More Cases of LMCA

Check out these additional examples of LMCA/3VD from the wonderful world of FOAM!

Learn from the Experts!

Consolidate your learning with lessons from the masters of ECG interpretation. Follow the links below for expert commentary, video lessons, case-based discussion and detailed explanations to take your learning to the next level.

  • Amal Mattu’s Emergency ECG Video of the Week — STE in aVR 1 (video lesson)
  • Amal Mattu’s Emergency ECG Video of the Week — STE in aVR 2 (video lesson)
  • Dr Smith’s ECG Blog — STE in aVR (case discussions + analysis)
  • Dr Smith’s ECG Blog — Left Main Disease (case discussion + analysis)
  • John Larkin’s ECG of the Week – LMCA (case discussion)
  • Salim Rezaie – aVR: The Forgotten 12th Lead (blog post)

Related Topics

Check out these other pages from the LITFL ECG library.

References

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  • Barrabes JA, Figueras J, Moure C, Cortadellas J, Soler-Soler J. Prognostic value of lead aVR in patients with a first non-ST-segment ele- vation acute myocardial infarction. Circulation 2003; 108: 814 – 819 [full text].
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  • Engelen DJ, Gorgels AP, Cheriex EC, De Muinck ED, Ophuis AJ, Dassen WR et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol. 1999 Aug;34(2):389-95 [full text].
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  • Uthamalingam S, Zheng H, Leavitt M, Pomerantsev E, Ahmado I, Gurm GS, Gewirtz H. Exercise-induced ST-segment elevation in ECG lead aVR is a useful indicator of significant left main or ostial LAD coronary artery stenosis. JACC Cardiovasc Imaging. 2011 Feb;4(2):176-86 [abstract].
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