ST elevation in aVR with co-existent multi-lead ST depression indicates subendocardial ischaemia due to O2 supply/demand mismatch.
Clinical causes include:
- Left main coronary artery (LMCA) stenosis
- Proximal left anterior descending artery (LAD) stenosis
- Severe triple vessel disease
- Hypoxia or hypotension, for example following resuscitation from cardiac arrest
ST elevation in aVR can also be seen in the context of anterior STEMI due to LAD occlusion proximal to the first septal branch, causing infarction of the basal septum. Such cases will have associated ST elevation in anteroseptal leads.
Mechanism of ST elevation (STE) in aVR
- Lead aVR is electrically opposite to the left-sided leads I, II, aVL and V4-6. In the case of subendocardial ischaemia, ST elevation in aVR is simply a reciprocal change to ST depression in these leads
- 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
Cause of ST elevation (STE) in AVR
Two possible mechanisms:
- Diffuse subendocardial ischaemia, with ST depression in the lateral leads producing reciprocal change in aVR (most common)
- 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.
LMCA “occlusion”: a misnomer
ST elevation in aVR with coexistent multi-lead ST depression can be a sign of Non-Occlusion Myocardial Infarction (NOMI) due to severe single or multi-vessel disease, but does not usually represent acute LMCA occlusion as once thought. Such acute occlusion most often causes sudden cardiac death due to simultaneous anterior, lateral and posterior STEMI.
More recent publications recognise this ECG pattern as consistent with left main coronary artery subocclusion or complete occlusion with well-developed collateral circulation. A 2019 single-centre retrospective analysis identified patients presenting with STE-aVR with multilead ST depression. Coronary occlusion was found only in 10% of patients, and none of these lesions were involving the LAD or left main coronary artery
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 stenosis or severe 3VD
- STE in aVR ≥ 1mm predicts the need for CABG
- 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%
Deep Dive into the literature of aVR
In-depth review of relevant literature
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…
- 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
- 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
- Population: 16 patients with severe LMCA stenosis, 46 patients with acute LAD occlusion and 24 patients with acute RCA occlusion.
- 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
- Population: 775 patients with first presentation of acute NSTEMI
- Two-thirds of patients with STE in aVR ≥ 1 mm had either LMCA stenosis 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
- Population: 150 patients with acute coronary syndromes – 46 with LMCA stenosis, 104 with occlusion of a different vessel
- Findings: STE in aVR was twice as common in patients with LMCA stenosis as those without (69.6% vs 34.6%)
- Population: 310 patients with non-ST-elevation acute coronary syndromes
- 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
- Population: 950 patients with STEMI (any type)
- STE in aVR ≥ 0.5 mm predicted proximal LAD 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.
- 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%.
- Population: 572 patients with acute NSTEMI
- Degree of STE in aVR was the strongest independent predictor of severe LMCA stenosis / 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 stenosis /3VD with 80% sensitivity, 93% specificity, 56% PPV, and 98% NPV.
LMCA sub-total occlusion
- 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 sub-total ostial occlusion of his left main coronary artery.
- 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 sub-occlusion.
Proximal LAD occlusion
- 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 “Head On Motor Vehicle Collision. ST depression. Myocardial Contusion?”
Proximal LAD Occlusion
- 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.
Severe Multi-Vessel Disease
- 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.
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 more highly informative blog posts on LMCA occlusion
LMCA/3VD which demonstrates:
- ST horizontal / downsloping ST depression in multiple leads (V3-6, I, II, aVL)
- ST elevation in aVR > V1
Diffuse Subendocardial Ischaemia secondary To Acute Blood Loss
- 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.
View Baseline ECG
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
LMCA / 3VD
- 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.
- 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 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.
So…is this 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:
- 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!
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
The differential diagnosis of lateral ST depression includes:
Learn from the FOAM
- Dr Smith’s ECG Blog – STE in aVR
- Dr Smith’s ECG Blog – Left Main Disease
- Salim Rezaie – aVR: The Forgotten 12th Lead
- ECG Guru.com – LMCA case
References…there are a lot of them
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- Wiesbauer F, Kühn P. ECG Yellow Belt online course: Become an ECG expert. Medmastery
- Wiesbauer F, Kühn P. ECG Blue Belt online course: Learn to diagnose any rhythm problem. Medmastery
- Rawshani A. Clinical ECG Interpretation ECG Waves
- Smith SW. Dr Smith’s ECG blog.
- Mattu A, Tabas JA, Brady WJ. Electrocardiography in Emergency, Acute, and Critical Care. 2e, 2019
- Brady WJ, Lipinski MJ et al. Electrocardiogram in Clinical Medicine. 1e, 2020
- Straus DG, Schocken DD. Marriott’s Practical Electrocardiography 13e, 2021
- Hampton J. The ECG Made Practical 7e, 2019
- Grauer K. ECG Pocket Brain (Expanded) 6e, 2014
- Brady WJ, Truwit JD. Critical Decisions in Emergency and Acute Care Electrocardiography 1e, 2009
- Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric 6e, 2008
- Mattu A, Brady W. ECG’s for the Emergency Physician Part I 1e, 2003 and Part II
- Chan TC. ECG in Emergency Medicine and Acute Care 1e, 2004
LITFL Further Reading
- ECG Library Basics – Waves, Intervals, Segments and Clinical Interpretation
- ECG A to Z by diagnosis – ECG interpretation in clinical context
- ECG Exigency and Cardiovascular Curveball – ECG Clinical Cases
- 100 ECG Quiz – Self-assessment tool for examination practice
- ECG Reference SITES and BOOKS – the best of the rest