ECGs showing ST elevation in lead aVR are often interpreted as resulting from left main occlusion. But that is a misunderstanding of the literature and physiology.
There are many publications stating that ST elevation in lead aVR, with diffuse ST depression elsewhere, is due to left main (LM) occlusion. This is even stated in the latest 2013 ACC/AHA STEMI guidelines (O’Gara PT et al. JACC 61(4):e83; January 29, 2013). However, the guidelines use as evidence an article by Jong et al. (Int Ht J 2006; 47(1):13-20) that misleadingly defines “occlusion” as any stenosis greater than 50%, when it should rather be defined as 100%, or nearly so. All of the articles that claim ST elevation in aVR is a sign of left main occlusion confuse LM occlusion with LM insufficiency.
The truth is, ischemic ST elevation in aVR fits into one of two broad categories:
- Patients with recognized STEMI (due to coronary occlusion, usually of the LAD – a situation with high mortality)
- Patients without ischemic ST elevation, but rather diffuse ST depression of subendocardial ischemia (due to either supply-demand mismatch, or ACS).
If you’re seeing diffuse ST depressions due to ACS, this STE in aVR is associated not only with acute LM insufficiency, but alternatively with three vessel disease, or with LAD insufficiency.
Got it? Let’s apply this knowledge. Take a look at the ECG in figure 1 in a patient with acute chest pain, then look at the angiogram in figure 2 below.
(Figure 1) There is diffuse ST depression, with ST elevation in aVR. This is diffuse subendocardial ischemia. The ST elevation in aVR is reciprocal to the ST depression vector that is directed anterior, lateral, and inferior (towards leads II and V5). STE in aVR is thus reciprocal ST Elevation!
(Figure 2) There is a very tight stenosis that limits the blood flow, but there is clearly flow in all the arteries supplied by the left main. This limitation causes subendocardial ischemia with ST depression, but not transmural ischemia with ST elevation. It is not left main occlusion.
Interestingly, these cases frequently have no wall motion abnormality because the epicardium is working well and contracting.
Of course, this is a very dangerous situation: the myocardium is ischemic, and if it is due to thrombus (due to ACS), then the thrombus can and often does propagate to occlude the entire artery and then results in STEMI.
Must you activate the cath lab?
Rokos et al. call this a “STEMI-equivalent” and suggest that the patient should go immediately to the cath lab (Rokos IC et al. Catheterization and Cardiovasc Interventions 79:1092-1098; 2012). However, in the Rokos paper, there were 11 patients with true left main occlusion; five of them had ST elevation in lead aVR. You’ve got to read the fine print to realize that all 11 patients with the left main as the culprit vessel were enrolled in the study based upon the standard STEMI criteria on index ECG: 8 anterior, 1 inferior, 1 LBBB, and 1 without an ECG submitted to the core laboratory. In other words, these were STEMI that were already diagnosed as STEMI who also had ST elevation in lead aVR; one did not need lead aVR in order to make the diagnosis of STEMI.
The conundrum arises when there is STE in aVR and ST depression in all the other leads, and thus it is not a classic STEMI. Is this situation a STEMI-equivalent?
No. Recall, ST depressions with STE in aVR signifies diffuse subendocardial ischemia and is just as common in non-ACS etiologies of ischemia (supply-demand mismatch) as in ACS etiologies. You’ll see this in patients with GI bleed, sepsis, respiratory failure, severe anemia, tachydysrhythmias, severe hypertension, and more.
For instance, see this case of carbon monoxide poisoning, with a CO level of 28% displayed in figure 3.
(Figure 3) Diffuse ST depression with STE in aVR. There was no ACS – all these EKG changes resolved after hyperbaric therapy.
Cath lab activation should only be done for ACS. For non-ACS etiologies of diffuse ST depression, treat the underlying illness!
Of course, it is not always easy to determine which came first, ACS or other underlying illness:
- Did ACS initiate the ischemia, which then resulted in cardiogenic shock, which then resulted in pulmonary edema with hypoxia, respiratory failure, and tachycardia?
- Or was the inciting factor bleeding, hypoxia, or severe hypertension with pulmonary edema and subsequent ischemia?
This requires careful patient evaluation of volume status, laboratory values, presence of pulmonary edema and of course much more. One must evaluate the patient, with help from the ECG.
The patient who has ST elevation in lead aVR that is not due to ACS will have appropriate treatment delayed and will undergo harm with cath lab activation.
Furthermore, as stated above, even if STE in aVR with diffuse ST depression is indeed due to ACS, it implies an open artery, not a 100% occluded one. There are institutions in which cath lab activation is a major use of resources, and if cath lab activation at night is not absolutely necessary, then it may be okay to avoid it. When there is diffuse subendocardial ischemia (which may or may not be left main insufficiency, but could also be LAD insufficiency, or three vessel insufficiency), it is reasonable to treat medically with nitroglycerine, aspirin, antithrombotics, and dual or triple antiplatelet therapy, and to re-assess. Often, the thrombus will cool off and the chest pain and ECG findings will resolve. If the symptoms resolve and the ST depression greatly improves, then the patient can wait until the morning to go to the cath lab as long as there is very close monitoring, preferably with continuous 12-lead ST segment monitoring. Ischemia due to ACS that is refractory to medical therapy (persistent symptoms or persistent ECG findings) requires emergent cath.
A Few Words on Left Main Occlusion
The majority of 100% left main occlusions do not make it alive to the ED, or arrive in arrest. At cath, only 0.19%-1.3% of STEMI patients have LMCA occlusion (or 0.42% – 3% of anterior STEMI).
(Figure 4) Both the rhythm and QRST are difficult to interpret, but there is clearly a wide QRS with ST elevation in I, aVL and V1, and little if any STE in aVR (and who knows what in other precordial leads)
The Prehospital ECG in Fig 4 is the ECG of a patient who collapsed in v fib, underwent prolonged resuscitation and had return of spontaneous circulation, but was in cardiogenic shock. Now EMS has dropped off this same patient in your ED. Your ECG looks like figure 5 below. What’s going on? It helps to draw some lines – using lead II across the bottom as the best place to see the end of the QRS (use slider on figure 5 below).
This ECG is typical of a patient with left main occlusion. (In fact, this case was not exactly LM occlusion, but rather simultaneous LAD and circumflex occlusion, which is in effect the same problem.) The rhythm in this case is difficult to interpret. There appear to be non-conducted P-waves, so it may be supraventricular or nodal, or it could be idioventricular. We do know there is a wide QRS complex. So, if the rhythm is supraventricular, this is RBBB + LAFB (often seen in massive MI). If it’s idioventricular, then it is originating near the left posterior fascicle, which mimics RBBB + LAFB. In any case, there is ST elevation in I and aVL (high lateral MI) with reciprocal ST depressions in inferior leads. There is also ST elevation in V2 and V4-V6.
The lesson from Figures 5 and 6 and similar ECGs is this: Left Main occlusion results in an ECG with overlapping syndromes of proximal LAD occlusion (STE in V1-V6, I, aVL) and circumflex occlusion (lateral STE and posterior STEMI, which has ST depression in V1-V4), which may diminish the ST elevation of the anterior STEMI.