Subtle ECG Findings in ACS: Part I Left Main Coronary Artery Disease
Authors: Jamie Santistevan, MD (EM Resident Physician, University of Wisconsin, @Jamie_Rae_EMDoc) // Edited by: Alex Koyfman, MD (EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital, @EMHighAK) & Justin Bright, MD (EM Attending, Henry Ford Hospital, @JBright2021)
A patient with a history of hypertension and hyperlipidemia presents to the emergency department with crushing, substernal chest pain. He is diaphoretic and has this ECG:
It is quite obvious that this patient is having an anterior STEMI. But acute coronary syndrome (ACS) is not always so obvious, in fact sometimes it is very subtle.
One hallmark of our profession is being able to delicately discriminate the sick from the not sick. It is only through careful refinement of our clinical skills that we can develop the ability to pick up a very subtle diagnosis. Unfortunately, it is the subtle cases that are at risk of being missed; and it is through the subtle presentations that we can be made a fool by disease processes.
When it comes to ACS, some ECGs are obvious. This article is not about those ECGs. This article will be the first in a series of blog posts related to subtle ECG findings in ACS. In this post we will look at ECG findings associated with left main coronary artery disease and explore the significance of ST-segment elevation in the “forgotten lead”. In the next post, we will review the appearance and significance of hyperacute T-waves, which may be the first, subtle sign of coronary vessel occlusion. Finally, we will discuss a mimicker: the subtle anterior STEMI, which may be mistaken for benign early repolarization.
Left main coronary artery disease
Early identification of left main coronary artery (LMCA) disease is critical because acute occlusion can cause rapid hemodynamic and electrical deterioration [1, 2]. LMCA insufficiency due to critical stenosis of the left main artery is important to recognize because these patients can progress to complete occlusion and are likely to require surgical intervention (such as CABG). Below, we will discuss the significance of ST elevation in lead aVR and review difference between LMCA occlusion and insufficiency.
Classic findings on ECG that are taught to represent LMCA “occlusion” are:
- ST depression in leads I, II, aVL and V4-6 
- ST elevation in aVR ≥ 1mm 
- ST elevation in aVR ≥ V1 
Lead aVR has often been called the “forgotten lead”, but it is worth paying attention to because ST-segment elevation in aVR portents a worse prognosis in ACS [1, 2, 3, 6]. ST elevation in aVR ≥ 1mm is the strongest independent predictor of either severe LMCA or triple-vessel disease requiring CABG in patients with NSTEMI [3, 7]. Elevation in aVR of ≥ 0.5 mm is an independent predictor of mortality in patients with STEMI .
ST-elevation in aVR occurs by the following mechanisms:
- Critical narrowing of the LMCA causing subendocardial ischemia due to insufficient blood flow.
- Transmural infarction of the basal septum due to a very proximal LAD occlusion or complete LMCA occlusion.
- Severe multi-vessel coronary artery disease.
- Diffuse subendocardial ischemia from oxygen supply/demand mismatch.
Understanding these mechanisms first requires visualization of the anatomic location of aVR. Lead aVR is an augmented limb lead, with its vector pointing toward the right shoulder. Therefore, it is recording activity from the right upper portion of the heart. This includes the basal (upper) portion of the interventricular septum, which is perfused by the first septal perforator, a branch of the proximal LAD.
In mechanism 1, critical narrowing of the LMCA produces subendocardial ischemia due to insufficient blood flow through a tight left main artery. This causes widespread ST-segment depression in nearly all leads, but it is often most pronounced in the left-sided leads (I, II, aVL and V4-6). Because aVR is anatomically opposite from the left-sided leads, ST depression due to ischemia is met with reciprocal ST elevation in aVR (also often in V1, which is a right-sided lead). This produces the classic findings on ECG described above. Remember, in this mechanism, there is still some flow through the tight LMCA, but it is not enough to match the demand. This is known as LMCA insufficiency.
Critical stenosis of the LMCA is quite dangerous. The entire artery can become occluded if the thrombus propagates. In addition, a large portion of the myocardium is ischemic due to lack of sufficient blood flow. Therefore, these patients require prompt recognition, and most experts agree that they should go to the cath lab immediately for revascularization.
This ECG demonstrates critical LMCA stenosis:
Notice the diffuse ST depression in multiple leads (I, II, aVF, aVL, V2-V6) with reciprocal elevation in aVR. This pattern represents diffuse subendocardial ischemia due to flow limitation through the LMCA. This patient presented in cardiogenic shock and was found to have critical stenosis of the LMCA on angiography.
In Mechanism 2, ST elevation in AVR is produced by transmural infarct to the basal septum. Remember, the LMCA gives rise to the LAD and the left circumflex. The first septal perforator arising from the proximal LAD supplies the basal septum. Infarct of the basal septum occurs secondary to either complete occlusion of the proximal LAD (before the takeoff of the first septal perforator) or complete occlusion of the LMCA. When either occurs, the patient will have STEMI in all areas of the heart supplied by these vessels. This can include the anterior wall (supplied by the LAD), the lateral wall (supplied by the left circumflex), and occasionally the posterior wall (if the left circumflex gives rise to the posterior descending artery).
Therefore, complete left main occlusion causes at least two syndromes to occur simultaneously: a proximal anterior STEMI producing ST elevation in aVR and V1-4 in addition to a lateral STEMI producing ST elevation in I, aVL and V5-6. If the posterior wall is involved, then posterior STEMI will produce ST depression in the anterior leads, which may be superimposed or even hidden within the ST elevation from the anterior STEMI. The bottom line is that a complete, very proximal LAD occlusion or a complete LMCA occlusion will produce STEMI in the locations supplied by those arteries.
This case demonstrates a very proximal LAD occlusion:
Notice that there is RBBB, a septal STEMI (ST elevation in V1-V3) plus ST elevation in aVR. This suggests an LAD occlusion proximal to the first septal perforator. This patient presented post-VF arrest and was found to have 100% occlusion of the proximal LAD on angiography.
An ECG demonstrating acute, complete occlusion of the LMCA is difficult to find, because patients with complete LMCA occlusion often have rapid electrical-mechanical dissociation and death [1,2]. This probably explains why only a very small percentage (0.19-1.3%) of patients with STEMI are found to have complete LMCA occlusion in the cath lab [1,8]. The need for cath lab activation in patients with complete LMCA occlusion is typically apparent based on their clinical picture (they often are in cardiogenic shock), as opposed to relying on their ECG findings alone .
Here is an excellent case of STEMI in more than one territory due to LMCA occlusion of a patient who presented in cardiogenic shock after VF arrest:
In mechanism 3, ST elevation in aVR is caused by multi-vessel coronary artery disease. In this mechanism, diffuse subendocardial ischemia produces widespread ST depression and therefore reciprocal ST elevation in aVR. This is similar to patients with critical stenosis of the LMCA. Here is an ECG of a patient who was found to have triple-vessel coronary artery disease.
Severe multi-vessel disease and LMCA disease appear similar on ECG and, coincidentally, both entities are likely to require CABG. Because they are often treated the same, the fact that they cannot be differentiated on ECG is not so important. Many authors agree that Clopidogrel should be avoided in patients found to have NSTEMI and STE in aVR ≥ 1mm due to likelihood of requiring CABG [2, 3, 7, 9].
In Mechanism 4, diffuse subendocardial ischemia due to oxygen supply/demand mismatch produces widespread ST depression and reciprocal ST elevation in aVR. This is similar to the other mechanisms whereby diffuse subendocardial ischemia produces ST depression most pronounced in the lateral leads with reciprocal elevation in AVR.
Differentiating the ECG of mechanism 4 from the other three requires analysis of axis of the ST segment elevation. For a detailed explanation of the ST-segment elevation axis please visit Dr. Smith’s ECG blog and read this post at http://hqmeded-ecg.blogspot.com/2012/02/five-primary-patterns-of-ischemic-st.html
TAKE HOME POINTS:
- ST-segment elevation in lead aVR portends a worse prognosis in ACS and often predicts the need for CABG.
- ST-segment elevation in aVR can be caused by any of the following 4 mechanisms:
- LMCA insufficiency
- Very proximal LAD occlusion or complete LMCA occlusion
- Multi-vessel coronary artery disease
- Diffuse subendocardial ischemia
- Patients with complete occlusion of the LMCA often present in cardiogenic shock and require immediate revascularization.
- Patients with NSTEMI and ST elevation ≥ 1mm in aVR are likely to have multi-vessel or LMCA disease and are likely to require CABG, therefore withholding Clopidogrel may be prudent.
Well, that concludes this post on LMCA disease. Please stay tuned for the next installment on subtle ECG findings: Hyperacute T-waves!
References / Further Reading
- Baek JY et al. Clinical outcomes and predictors of unprotected left main stem culprit lesions in patients with acute ST segment elevation myocardial infarction. Catheter Cardiovasc Interv. 2014 Jun 1;83(7):E243-50.
- Smith, SW. Updates on the Electrocardiogram in Acute Coronary Syndromes Curr Emerg Hosp Med Rep (2013) 1:43–52.
- Barrabes, JA et al. Prognostic value of lead aVR in patients with a first non-ST-segment elevation acute myocardial infarction. Circulation. 2003 Aug 19;108(7):814-9.
- Gorgels, AP et al. 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.
- Yamaji, 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.
- Aygul N 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;41(4):335–41.
- Kosuge, M 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.
- Zoghbi GJ et al. ST elevation myocardial infarction due to left main culprit lesions: percutaneous coronary intervention outcomes free. J Am Coll Cardiol. 2010;55(10s1): E1712.
- “Anterior Myocardial Infarction” Life in the Fast Lane Medical Blog. 19 Oct. 2015. Web. http://lifeinthefastlane.com/ecg-library/anterior-stemi/
- “MI Localisation” Life in the Fast Lane Medical Blog. 19 Oct. 2015. Web. http://lifeinthefastlane.com/ecg-library/basics/ecg-anatomy/
- “Five primary patterns of ischemic ST depression, without ST elevation. Some STEMI equivalents” Dr. Smith’s ECG Blog. 19. Oct. 2015. Web. http://hqmeded-ecg.blogspot.com/2012/02/five-primary-patterns-of-ischemic-st.html
- “Head on motor vehicle collision. ST depression. Myocardial contusion?” Dr. Smith’s ECG Blog. 19 Oct. 2015. Web. http://hqmeded-ecg.blogspot.com/2014/07/head-on-motor-vehicle-collision-st.html
- “The difference between left main occlusion and left main insufficiency” Dr. Smith’s ECG Blog. Web. 19 Oct. 2015. Web. http://hqmeded-ecg.blogspot.com/2014/08/the-difference-between-left-main.html