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:
- Proximal left anterior descending artery (LAD) occlusion
- Severe triple-vessel disease (3VD)
- Diffuse subendocardial ischaemia – e.g. due to O2 supply/demand mismatch, following resuscitation from cardiac arrest
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…
- 113 patients with unstable angina, including 20 patients with LMCA stenosis and 24 patients with 3VD.
- 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.
- 100 patients with anterior STEMI.
- STE in aVR of any magnitude was 43% sensitive and 95% specific for LAD occlusion proximal to the first septal branch.
- 16 patients with acute LMCA occlusion, 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.
- 775 patients with first presentation of acute NSTEMI.
- 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.
- 150 patients with acute coronary syndromes – 46 with LMCA obstruction, 104 with occlusion of a different vessel.
- STE in aVR was twice as common in patients with LMCA occlusion as those without (69.6% vs 34.6%).
- 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.
- 950 patients with STEMI (any type).
- 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.
- 15, 315 patients with STEMI enrolled in the HERO-2 trial (heparin vs bivalirudin for acute MI).
- 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%.
- 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.
- STE of ≥ 1mm in aVR during stress testing predicted LMCA or ostial LAD stenosis with sensitivity 75%, specificity 81% and overall accuracy 80%.
- 572 patients with acute NSTEMI.
- 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.
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
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
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
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
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
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.
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
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.
- 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.
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
Example (a) — Supraventricular Tachycardia
Example (b) — Atrial Flutter with 2:1 Block
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)
Check out these other pages from the LITFL ECG library.
- Aygul N, Ozdemir K, Tokac M, Aygul MU, Duzenli MA, Abaci A et al. Value of lead aVR in predicting acute occlusion of proximal left anterior descending coronary artery and in-hospital outcome in ST-elevation myocardial infarction: an electrocardiographic predictor of poor prognosis. J Electrocardiol. 2008 Jul-Aug;41(4):335-41 [abstract].
- 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].
- Chan TC, Brady WJ, Harrigan RA, Ornato JP and Rosen PR. ECG in Emergency Medicine and Acute Care. Elsevier 2005.
- 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].
- Eskola MJ, Nikus KC, Holmvang L, et al. Value of the 12-lead electrocardiogram to define the level of obstruction in acute anterior wall myocardial infarction: Correlation to coronary angiography and clinical outcome in the DANAMI-2 trial. Int J Cardiol 2009;131:378–383 [abstract].
- Gorgels AP, Engelen DJ, Wellens HJ. Lead aVR, a mostly ignored but very valuable lead in clinical electrocardiography. J Am Coll Cardiol. 2001 Nov 1;38(5):1355-6 [full text].
- Gorgels AP, Vos MA, Mulleneers R, de Zwaan C, Bär FW, Wellens HJ. Value of the electrocardiogram in diagnosing the number of severely narrowed coronary arteries in rest angina pectoris. Am J Cardiol. 1993 Nov 1;72(14):999-1003 [abstract].
- Gul EE, Nikus KC. An unusual presentation of left anterior descending artery occlusion: significance of lead aVR and T-wave direction. J Electrocardiol. 2011 Jan-Feb;44(1):27-30 [full text].
- Hennings JR, Fesmire FM. A new electrocardiographic criteria for emergent reperfusion therapy. Am J Emerg Med. 2011 Jun 22. Epub ahead of print [abstract].
- Jong G, Ma T, Chou P, et al. Reciprocal changes in 12-lead electrocardiography can predict left main coronary artery lesion in patients with acute myocardial infarction. In Heart J 2006;47:13-20 [full text].
- Kireyev D, Arkhipov MV, Zador ST, Paris JA, Boden WE. Clinical utility of aVR-The neglected electrocardiographic lead. Ann Noninvasive Electrocardiol. 2010 Apr;15(2):175-80 [abstract].
- Kosuge M, Ebina T, Hibi K, Endo M, Komura N, Hashiba K et al. ST-segment elevation resolution in lead aVR: a strong predictor of adverse outcomes in patients with non-ST-segment elevation acute coronary syndrome. Circ J. 2008 Jul;72(7):1047-53 [full text].
- Kosuge M, Ebina T, Hibi K, Morita S, Endo M, Maejima N, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol. 2011 Feb 15;107(4):495-500 [abstract].
- Kosuge M, Kimura K, Ishikawa T, Ebina T, Shimizu T, Hibi K, et al. Predictors of left main or three-vessel disease in patients who have acute coronary syndromes with non-ST-segment elevation. Am J Cardiol 2005; 95: 1366 – 1369 [abstract].
- Kosuge M, Kimura K, Ishikawa T, Ebina T, Hibi K, Tsukahara K, et al. Combined prognostic utility of ST segment in lead aVR and troponin T on admission in non-ST-segment elevation acute coronary syndromes. Am J Cardiol 2006; 97: 334 – 339 [abstract].
- Kosuge M, Ebina T, Hibi K, Morita S, Komura N, Hashiba K et al. Early, accurate, non-invasive predictors of left main or 3-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Circ J. 2009 Jun;73(6):1105-10 [full text].
- Kühl JT, Berg RM. Utility of lead aVR for identifying the culprit lesion in acute myocardial infarction. Ann Noninvasive Electrocardiol. 2009 Jul;14(3):219-25 [abstract].
- Nikus KC, Eskola MJ. Electrocardiogram patterns in acute left main coronary artery occlusion. J Electrocardiol. 2008 Nov-Dec;41(6):626-9 [abstract].
- Ozmen N, Yiginer O, Uz O, Kardesoglu E, Aparci M, Isilak Z et al. ST elevation in the lead aVR during exercise treadmill testing may indicate left main coronary artery disease. Kardiol Pol. 2010 Oct;68(10):1107-11 [abstract].
- Pickard AS, Becker RC, Schumock GT, Frye CB. Clopidogrel-associated bleeding and related complications in patients undergoing coronary artery bypass grafting. Pharmacotherapy. 2008 Mar;28(3):376-92 [abstract].
- Rostoff P, Piwowarska W, Konduracka E, Libionka A, Bobrowska- Juszczuk M, Stopyra K, et al. Value of lead aVR in the detection of significant left main coronary artery stenosis in acute coronary syndrome. Kardiol Pol 2005;62:128-37 [abstract].
- 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].
- de Winter RJ, Verouden NJW, Wellens HJJ, Wilde AAM. A new sign of proximal LAD occlusion. N Engl J Med 2008;359:2071-3 [full text].
- Wiviott SD, Braunwald E, McCabe CH, Montalescot G, Ruzyllo W, Gottlieb S, et al. TRITON-TIMI 38 Investigators. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007 Nov 15;357(20):2001-15 [abstract].
- Williamson K, Mattu A, Plautz CU, Binder A, Brady WJ. Electrocardiographic applications of lead aVR. Am J Emerg Med. 2006 Nov;24(7):864-74 [pdf].
- Wong CK, Gao W, Stewart RA, French JK, Aylward PE, White HD; for the HERO-2 Investigators. The prognostic meaning of the full spectrum of aVR ST-segment changes in acute myocardial infarction. Eur Heart J. 2011 Aug 19 [abstract].
- Yamaji H, Iwasaki K, Kusachi S, Murakami T, Hirami R, Hamamoto H, et al. Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography. ST segment elevation in lead aVR with less ST segment elevation in lead V(1). J Am Coll Cardiol. 2001 Nov 1;38(5):1348-54 [full text].
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