This article is the fifth in our latest series, The 12 Leads of Christmas, where each day we examine a new finding particular to an individual electrocardiographic lead.
I have a love-hate relationship with aVR. There is one big question that always looms around it:
Is ST-elevation in aVR a STEMI-equivalent?
Like most folks, I first became aware of aVR’s role in acute coronary syndrome through Amal Mattu’s lectures. I still recall the first lecture of his I came across on the now long-abandoned EMRAP.tv site. To be fair, he has since toned down his aggressive stance, but at the time he would dramatically quote stats like:
- “LMCA stenoses are associated with 70% mortality.”
- “If you see elevation in aVR plus aVL it’s like 95% specific for left-main disease.”
- “If you see elevation in aVR and in V1 that is greater in aVR than in V1, that is extraordinarily specific for left-main disease.”
Armed with my new, privileged knowledge, I thought I was going to go out there and save the world from left-main coronary artery occlusions. It didn’t take long to encounter my first case:
A 58-year-old male presented with sudden-onset shortness of breath. He was pale and diaphoretic with a respiratory rate of 40 /min, rales up to his clavicles, and a BP of 180/110 mmHg. His initial EKG is shown below.
Slam-dunk case, right? Diffuse ST-depression with ST-elevation in aVR and V1; get this guy to the cath lab for his STEMI-equivalent! This patient has a left-main stenosis and has a 70% mortality unless he gets intervention!
At least that’s what I thought at the time. The patient was intubated (this was before high-dose nitro and non-invasive ventilation became popular) and here is his EKG once his BP settled down a bit and SpO2 improved (though he still had significant rales and wasn’t out of failure yet).
I was a bit perplexed because my dying patient with aVR elevation was showing lessening ischemia and looked better. Still, I was certain this patient had either a LMCA lesion or multi-vessel disease. Cardiology was called and elected to transfer the patient to the cath lab due to a rising troponin level.
Severe multi-vessel disease not amenable to PCI. He underwent three-vessel CABG the next day and was discharged from the hospital a week later in good health.
And that’s what I believed for a few years. I always counted that as a save and would quiz new medics and docs on the utility of aVR, citing it as a case where aVR saved the day.
…except there was a problem.
I kept seeing cases of diffuse ST-depression with elevation in aVR that didn’t go to cath, yet the patients were surviving. Some would barely even bump their troponin levels. It didn’t make sense.
The above EKG is from another patient who presented in sudden-onset acute hypertensive pulmonary edema with no history of MI or coronary artery disease. While her EKG meets voltage criteria for LVH, the ST/T abnormalities here are not typical “strain” but rather diffuse subendocardial ischemia with diffuse downsloping ST-depression and elevation in aVR and V1.
Even with suboptimal management (just topical nitro paste, furosemide, and ASA), her troponin-I peaked at only 5 ng/mL. If this patient had such a life-threatening lesion then why was her troponin bump so small, especially in light of her minimal medical therapy?
After seeing several patients with acute hypertensive pulmonary edema and similar EKG’s that didn’t proceed to emergent PCI or CABG, yet survived, I began to wonder if that first patient really benefited from his emergent cath.
Let’s look at some more cases…
This patient presented with worsening shortness of breath over the past month.
It must be cardiac, right? Time to send the patient to cath and prep for CABG.
…well it’s a good thing she got routine labs because her hemoglobin was only 4.3 g/dL. The EKG normalized with improvement of her Hb and troponin-I levels remained undetectable at < 0.01 ng/mL. This patient’s ischemia was entirely due to poor oxygen supply to the heart secondary to her anemia, and not an acute coronary event.
This patient presented in respiratory distress.
I hope you’re noticing a pattern by this point and didn’t activate the cath lab because he turned out to be septic with pneumonia. His EKG normalized to baseline with supportive care troponin-I peaked around 1.0 ng/mL (ref <= 0.04 ng/mL). The ischemia in this case was secondary to the increased metabolic demand of his sepsis state and respiratory distress. He almost certainly had longstanding chronic coronary artery disease, maybe even a significant left-main stenosis, but he did not experience an acute obstruction of one of his coronary arteries.
Here’s an asymptomatic patient sent in from the nursing home for “irregular pulse.”
Don’t you dare send this patient to cath. EKG normalized with rate and eventually rhythm control and her troponin-I peaked at 0.11 ng/mL (ref <= 0.04 ng/mL). This is another case of a patient who likely has chronic CAD. The increase in heart-rate she experienced created a situation of demand ischemia, where her heart required more oxygen delivery to maintain that increased HR but chronic stenoses of her coronary arteries limited flow. There is no reason to think this asymptomatic patient was experiencing an acute obstruction of one of her coronary arteries.
Your next patient is on dialysis and being sent from the nursing home for nausea, vomiting, and weakness. An atypical presentation of left-main obstruction?
Nope. Septic and hyperkalemia with a white-count of 29,500 /mcL and K+ of 6.8 mEq/L. Troponin-I peaked at 0.21 ng/mL (ref <= 0.04 ng/mL). Another case of demand ischemia secondary to sepsis, not an acute coronary event.
85 year old female presents with SOB x 3 wks and an SpO2 of 84% on room air and a respiratory rate of 28 /min. Dx with pneumonia 2 wks ago, hasn’t improved on antibiotics. What’s the diagnosis?
Surely this one must be multi-vessel CAD with CHF? Nope, submassive PE with RV strain. Troponin-I held steady at 0.05 ng/mL (ref <= 0.04 ng/mL). The ST-depression we see is again due to a supply/demand mismatch, with increased demand from her heart to maintain the tachycardia and increased respiratory rate but decreased supply because of the V/Q mismatch from the PE.
Here’s some more…
I hope it’s clear that there’s a problem with relying on aVR as a “STEMI equivalent.” I’m not saying none of those patients have multi-vessel CAD or maybe even a stenotic LMCAâ€”most of them probably doâ€”I’m just saying that they do not need emergent or even urgent catheterization. Except for the anemic and hypokalemic patient, they all likely had stable, longstanding coronary artery disease. While they were experiencing ischemia, it wasn’t because of an acute obstruction in one of the arteries but rather increased oxygen demand by the heart. The best move for all of them was initial stabilization and workup in the ED, with the aim of fixing the underlying problem that was causing the supply/demand mismatch, not a misguided attempt at revascularization.
It helps that all of those presentations had clues that the underlying issue wasn’t an acute MI. What happens when true primary ACSÂ patients present with classic anginal chest pain, diffuse ST-depression, and elevation in aVR? Here’s a few of those cases…
The above patient presented with typical anginal chest pain that had been coming and going for the past week. For the past hour it was constant so she presented for emergency care. She was treated with aggressive medical therapy with resolution of her symptoms and return of her EKG to baseline. Troponin-I peaked at 0.38 ng/mL (ref <= 0.04 ng/mL). The patient went for non-urgent catheterization two days later. While she likely had an acute obstruction of either the LMCA or some other single artery in the setting of chronic multi-vessel disease, because her ischemia resolved with medical therapy a rush to cath was not necessary.
The next next patient presented with typical cardiac chest pain x 30 min. She had experienced a couple of similar episodes the prior week but this time it did not subside so she came in.
She was treated with ASA, SL nitro, IV nitro, and heparin with complete resolution of her symptoms and normalization of her ECG. Troponin-I peaked at 0.05 ng/mL (ref <= 0.04 ng/mL). She went for non-urgent catherization the next day. Like the last case, this patient probably had a culprit lesions, either in the LMCA or a single-vessel in the setting of multi-vessel CAD, but because her ischemia resolved with medical therapy immediate cath was not warranted. Had she gone to cath the obstruction would have been identified sooner, but at no benefit to the patient, increased cost, and increased risk of error or morbidity in the rush to angiography.
This patient presented with waxing and waning CP x 1 wk, worse with exertion. Diagnosed with angina in the past, he had used 3â€“4 bottles of SL in the week prior. The EKG was recorded on arrival in the ED.
HeÂ received anticoagulation and sub-optimal titration of IV nitro (the patient was still mildly symptomatic with ST-depression overnight). By the next day his symptoms resolved and EKG normalized. Troponin-I peaked at 0.22 ng/mL (ref <= 0.04 ng/mL). Because he was a poor candidate for intervention he was actually discharged home two days later and survived another year before his multiple medical ailments overcame him. This patient certainly had longstanding stable coronary artery disease but it is clear that ST-elevation in aVR didn’t confer to him with the same grim prognosis that it is commonly quoted as carrying.
There is always an exception, and this final case sure is exceptional.
A 68-year-old male presented with a chief complaint of chest tightness that started 3 hrs prior to arrival. It started suddenly and had been constant at 6/10. Here is his initial EKG.
That’s a striking EKG. While we might expect at least some diffuse subendocardial ischemia to accompany rapid atrial fib (demand ischemia), in this case the magnitude of the ST-deviations far exceeds our expectations. Still, this is not a STEMI and the prior cases have taught us to be cautious, so the first step is to get the rate under control and see what happens to the ischemia.
This EKG was obtained immediately s/p cardioversion with diltiazem. There is still marked diffuse subendocardial ischemia but it could be holdover demand ischemia from the prior tachycardia. Importantly, the patient’s symptoms did not change one bit with the conversion to sinus rhythm and he still had 6/10 CP. That is very concerning…
The above EKG was obtained 30 min after the previous one. If his symptoms and ischemia were due to the rapid AF, by this point the patient should have been feeling better and the ST-deviation should have resolved. In this case neither occurred and the patient was still very ischemic. This should have been a huge red flag.
The patient was given two SL nitro and his blood pressure dropped from 108/60 mmHg to 84/48 mmHg. Here is his EKG following the second nitro, when his pain had decreased to 1/10.
There is slightly less ischemia on the ECG but it is not disappeared. At this point the patient has failed medical therapy. While his symptoms have improved (importantly though, they haven’t fully resolved), his EKG is still notably ischemic and he cannot tolerate any more nitro.
Bedside echo at the time also showed diffuse hypokinesis of the anterior, antero-septal, lateral, and apical walls of the LVâ€”consistent with a left main coronary artery or very large LAD distribution.
Failed medical therapy in the setting of an ischemic EKGâ€”especially in a patient with such a classic presentation for acute MI, such a concerning magnitude of ST-deviation on the initial EKG’s, and continued echocardiographic evidence of wall-motion abnormalityâ€”is an indication for immediate cardiac catherization. As Dr. Smith would say, this is a non-STEMI that needs the cath lab now!
In this case that did not occur due and the patient was admitted to the ICU overnight.
His troponin-I, which initially returned at 0.05 ng/mL (ref <= 0.04 ng/mL), peaked at over 200 ng/mL. Echo the next day showed continued near-global hypokinesis of the LV. Catherization the day after that showed a culprit 95% LMCA lesion with chronic 75% stenoses in both the RCA and LCx. The patient went for 3-vessel CABG.
How is this final case different from the (many) prior cases with ST-elevation in aVR?
- The patient presented with sudden-onset signs and symptoms classic for acute MI. This wasn’t the waxing and waning pain of unstable angina (it still exists!) and it certainly wasn’t one of the less specific “anginal equivalent” presentations like SOB or weakness.
- The magnitude of the ST-deviations, especially in aVR, were much greater than any of the prior cases. We often emphasize that MI’s aren’t constrained by strict millimeter criteria but, with both STEMI’s and NSTEMI’s, the more ST-deviation there is, the worse the general prognosis.
- This patient’s symptoms AND ischemia could not be controlled with nitro. While his symptoms nearly resolved with nitro his EKG remained ischemic. With NSTEMI’s like this the goal is to relieve both symptoms AND ST-depression, so if either one remains after maximizing medical therapy with nitro and anticoagulation the patient’s next stop should be the cath lab.
So, after all of that, I know you still have that one burning question about aVR. Is ST-elevation in aVR with diffuse ST-depression a STEMI-equivalent?
A STEMI is almost always a STEMI. There are conditions that may cause ST-deviation in a pattern superficially mimicking a STEMI (LBBB, LVH, pacemakers, WPW…), but they do not generate a true STEMI pattern and the practiced interpreter can differentiate them. Regardless of the patient’s chief complaint (even “toe pain”), if their EKG shows a true STEMIâ€”not a mimic or borderline tracingâ€”then they are experiencing an ST-elevation myocardial infarction.
The diffuse subendocardial ischemia that produces diffuse ST-depression with elevation in aVR is a very different matter.
First, it indicates a different form of ischemia (diffuse subendocardial, vs. the localized epicardial/transmural ischemia that produces a STEMI pattern). While subendocardial ischemia can still cause cardiac muscle death and often covers a wider territory than the typical STEMI, it is generally less severe than what we see during a STEMI. Second, the coronary lesions associated with subendocardial ischemia are different from those producing a STEMI. STEMI’s result from acute complete or near-complete occlusion of a coronary artery resulting in severe transmural ischemia downstream. While subendocardial ischemia can also result from an acute obstruction similar to what produces STEMI’s, in those cases there is typically either better flow past the lesion or better collateral circulation perfusing the ischemic myocardium.
If that wasn’t the case we’d be seeing a STEMI, not diffuse ST-depression (NSTEMI).
That is why even severe but stable chronic CAD can produce diffuse subendocardial ischemia but not a STEMI. There is enough flow getting past even highly stenotic vessels or perfusing the myocardium via collaterals that, while the tissue may become ischemic at times (especially during times of increased demand), there is at least some perfusion to the epicardium and only the subendocardium is left wanting.
That is also why unstable angina due to a chronic stenosis cannot be differentiated from an acute but incomplete thrombotic lesion still permitting some flow which cannot be differentiated from severe anemia on the EKGâ€”they all results in diffuse subendocardial ischemia. There are different causes to the ischemia but the EKG doesn’t know or care about thatâ€”all it sees is diffuse subendocardial ischemia.
The final (and most complex) reason that diffuse subendocardial ischemia is not equivalent to a STEMI is that the two are managed very differently. STEMI’s (almost) always require immediate reperfusion via thrombolysis or PCIâ€”simple as thatâ€”and the main goal of emergency care is to get them reperfused. The initial management of NSTEMI’s is much more complex and depends on the patient’s presentation, their response to therapy, the result of early investigations, and the resources available.
The definitive management of NSTEMI’s is also very different from that of STEMI’s. While most STEMI’s can be stented in the cath lab, many NSTEMI’s with diffuse ST-depression and elevation in aVR end up receiving CABG for a LMCA stenosis or multi-vessel disease. These are lengthy procedures that take time to setup and usually aren’t performed immediately after the diagnostic cath unless the patient is unstable, so rushing a stable NSTEMI patient to the cath lab isn’t likely to benefit them much.
While a true review of the emergency management management of NSTEMI’s is beyond this article, here are a few basic principles (note the lack of citations and keep it in mind that you read this on a blog, not the AHA guidelines):
- There should be signs and symptoms consistent with ACS to even consider early cath.
- Unstable patients in failure and cardiogenic shock with a good story and diffuse subendocardial ischemia need to proceed to the cath lab immediately (after other life-threats are ruled-out).
- Stable patients with a good story and diffuse subendocardial ischemia that is not relieved by maximal medical therapy need to proceed to the cath lab immediately (after other life-threats are ruled-out).
- Patients with acute hypertensive pulmonary edema need their SOB, pulmonary edema, and work of breathing managed first with nitro and on-invasive ventilation. Only once those issues are fixed should you assess for ongoing ischemia. Ischemia can trigger flash pulmonary edema, but acute pulmonary edema can also cause ischemia, so it’s up to you to be a clinician and try to figure out which is the case.
- Patients with normotensive or hypotensive pulmonary edema are a different beast. They are in shock (see the second bullet) and are much more likely to have an acute lesion. They still need medical management to start but are very likely to fail and that should be planned for aggressively.
- Titrate nitro doses to relieve both symptoms and signs of ischemia on the ECG. One of two is not good enough.
- Tachycardia should be corrected with fluids or medications (depending on the cause) to reduce the effect of demand ischemia.
- Rule-out anemia.
- Severe HTN should be corrected to reduce supply/demand mismatch.
- Patients with primary ACS (type I MI) probably benefit from aggressive antiplatelet and antithrombotic therapy.
- Caution should be used in patients with diffuse subendocardial ischemia as they are likely to need CABG and the surgeon may not appreciate a fully anticoagulated patient.
- Avoid opioid analgesics in NSTEMI patients. If a patient’s pain is refractory to aggressive nitro dosing, that warrant immediate cath and these medications can and will mask symptoms (half of our assessment of ischemia and a big sign of worsening coronary obstruction!).
One final point on why aVR continues to gain unwarranted notoriety.
There are indeed sick patients with diffuse ST-depression and elevation in aVR who need emergent angiography.
On the other hand, there are patients with similar EKG’s who may not need immediate angiography but proceed to cath anyway because the treating providers are worried about triple-vessel or LMCA disease.
The reason why these latter patients don’t necessitate immediate cath is not because they don’t have coronary artery diseaseâ€”they often doâ€”it is that they will not benefit from proceeding to cath right now. Yet, when these patients do go to cath either LMCA or multi-vessel disease will be found, the patient will proceed to CABG, and the emergency provider will get word back that their cath was positive and even that the patient required bypass surgery.
A positive cath does not equal a life saved.
That is a great example of a surrogate endpoint. For all of the reasons detailed in this article,Â these patients are expected to have positive cath. What matters more is what their clinical course would have been had they proceeded to cath and eventually surgery two days, two weeks, or two months later, and in that regard a lot of the benefits for these patients wash out. Patients live with stable CAD every day, so if their ischemia can be managed medically, that is a perfectly safe option. Most patients with multi-vessel or LMCA disease on cath do not receive an emergent CABG surgery. They are allowed to “cool off” and the surgery is done in a much more controlled manner and time-frame.
It is only when we cannot control their ischemia or the patient is doing poorly that it becomes vitally important to evaluate their coronary anatomy immediately and intervene if possible.
[I know this was a long piece but it takes a lot of work to learn how to use aVR properly. If you’re more confused and less confident than when you started that probably is a good thing. The management of diffuse subendocardial ischemia has been over-simplified for too long, wasting resources and even hurting patients by rushing them to the cath lab for a situation that usually warrants a more measured response. There are indeed patients with ST-elevation in aVR who need immediate cath but they are far outnumbered by the cases who do not. If we cry wolf and send a bunch of NSTEMI’s to the lab who do not need immediate cath then the patients who really need intervention now will be ignored. Best of luck sorting that out, but hopefully this post is a start.]
Conclusion to 83 Year Old Male: Shortness of Breath (My earlier primer on diffuse subendocardial ischemia)
Conclusion to Snapshot Case: 85yo M – Chest Pain (Where I discuss some examples of true STEMI of the LMCA)
A Non STEMI That Needs the Cath Lab Now (Post by Dr. Smith that covers the management of emergent NSTEMI’s)
Five Primary Patterns of Ischemic ST depression, without ST elevation. (Amazing post by Dr. Smith on patterns of ST-depression)
Marked ST depression refractory to maximal medical therapy (More NSTEMI goodness from Dr. Smith)
ST elevation in aVR, with widespread ST depression (Another NSTEMI that needs the cath lab)
Deep and widespread ST depression signifies high risk coronary lesion (One final NSTEMI that needs the cath lab)
I hope youâ€™re enjoying our 12 Leads of Christmas series. You can check out the rest of the posts below (updated as new posts come out):
12 Leads of Christmas: Lead I
12 Leads of Christmas: Lead II
12 Leads of Christmas: Lead III
12 Leads of Christmas: aVL
12 Leads of Christmas: aVF
12 Leads of Christmas: V1
12 Leads of Christmas: V2
12 Leads of Christmas: V3
12 Leads of Christmas: V4
12 Leads of Christmas: V5
12 Leads of Christmas: V6