ST-segment elevation in lead aVR. Is this a STEMI equivalent?

EMS was called for a young adult male who had collapsed at home.

He had been walking through the kitchen when he complained of some chest discomfort, appeared to perhaps have trouble breathing, and then had a syncopal episode.

He had a PMHx history of trisomy 21, sleep apnea, DM type 2, and right-sided CHF due to his sleep apnea. His family also told medics that he had some congenital heart problems — a ventricular septal defect had been repaired in childhood, but he currently had an un-repaired bicuspid aortic valve, with aortic stenosis.

He was conscious by the time EMS arrived. Vital signs and exam were unremarkable.

EMS obtained a series of ECGs.



What do the ECGs show?

The first ECG shows ST segment elevation (STE) in aVR, as well as in V1. ST depression is seen in most of the inferior and lateral leads. The second ECG also shows these features, as well as a right bundle branch block.

On arrival to the ED another ECG was obtained.


Given his risk factors (including diabetes and obesity), cardiology took the patient immediately for angiography, but found no significant coronary disease. His ECG improved without any specific therapy.


His aortic stenosis, on the other hand, was found to have significantly progressed, and was likely the reason for his syncope. He underwent a surgical replacement of his bicuspid aortic valve, with good results.


Were you expecting a left-main coronary occlusion?

The STE in aVR pattern that we see here is widely understood to be practically diagnostic of an acute occlusion of the left main coronary artery. However, this pattern can be seen in many clinical scenarios (e.g., anemia, sepsis, tachycardia). In fact, a recent study found that, in patients with a pulmonary embolism, STE in aVR predicted cardiovascular collapse.

As Vince explained last year, the pattern of STE in aVR, with depression elsewhere, simply reflects a widespread ischemia in the heart, and such ischemia can have many causes. Aortic stenosis likely produces this pattern thorough a few mechanisms:

  • Stenosis causes increased pressure in the left ventricle.
  • That pressure causes hypertrophy of the LV.
  • The pressure & hypertrophy reduce subendocardial blood flow
  • Tachycardia reduces diastolic filling time
  • Severe aortic stenosis reduces coronary artery flow


This isn’t just theoretical as patients with severe aortic stenosis have elevated troponin at baseline. Not good. This combination of stressors can even provoke a VF arrest in otherwise healthy-seeming people with aortic stenosis.

Bottom Line

Don’t get carried away with aVR ST elevation. Look for provoking causes!

Further Reading

Five Primary Patterns of Ischemic ST depression, without ST elevation. Some are STEMI-equivalents.

ST Elevation in Lead aVR, with diffuse ST depression, does not represent left main occlusion

Chest pain and ST-segment elevation in lead aVR


  • Josh says:

    This is a good read, however we won’t always know if they have an underlying medical problem such as aortic stenosis. I would rather just treat the ACS and declare this a STEMI to the receiving PCI facility and let them determine the problem. If it looks like a duck and quacks like a duck, I’d say it’s a duck. There are so many cases that you think is one thing but is another. I would just stick on the safe side and go with what I saw, which is an AVR STEMI.

  • Justin says:

    To add to what Josh had said, the patient is symptomatic with significant ecg findings. It wouldn’t hurt to treat ACS provided there’s no contraindications. I would also be curious about what V7, V8, and V9 would show.

  • Zach says:

    Excellent read, but I agree with josh. We won’t always know if the patient has a history of stenosis, and we have no guarantee that the stenosis is causing the issue. STE in aVR with widespread depression can also be indicative of posterior MI. I would declare STEMI, treat for ACS, and let the receiving facility sort out the details.

  • Dave Eastman says:

    I have to agree. The patient is symptomatic. The ECG suggests possible coronary artery occlusion. Better to activate the cath lab and exclude coronary artery occlusion as the cause if that is the case. Ultimately it is the hospital’s call, but ask yourself, if it were your mother, your father, your child, what would you want to have done for them.

  • NICE case with great illustrative tracings. Missing from the presentation (I suspect Brooks intentionally left this out … ) is what auscultation of the heart sounded like. I do see “vitals and exam were unremarkable” — but was there really no heart murmur? It is true that tight AS (Aortic Stenosis) can at times be surprisingly quiet — but often it is quite obvious when/if the heart is listened to. This of course would be relevant to this case.

    As to the initial series of 2 EMS tracings that were done — the ST-T wave changes are dramatic (diffuse ST dep with ST elev in aVR,V1 as described). Note in the 2nd tracing that there is now RBBB + LAHB (with Q waves in V1,V2). So there is “progression” in terms of the already “high-risk” situation suggested by the 1st ECG.

    I completely agree with the main point that Brooks Walsh is trying to make — which is that diffuse ST dep with ST elev in aVR,V1 is NOT a “stemi-equivalent”. But I would ADD that the ECGs shown in this presentation ARE an indication for immediate review by the physician in charge (usually the ED physician on duty at the receiving hospital) — AND that one needs to: i) ensure hemodynamic stability; + ii) determine the CAUSE of these ECG findings on an emergent basis. This was done here — the patient WAS stable — the cardiologist on call was notified and cardiac catheterization revealed no significant coronary disease — and arrangements were made for aortic valve replacement. So, this is NOT a stemi-equivalent — but it IS a case that needs to be immediately attended to. THANK YOU Brooks Walsh for presenting this great discussion case!

    P.S. Many patients with severe AS will also have significant coronary disease. This will often only get sorted out at cath …

  • hatim helmy says:

    Actually last guidelines of AHA 2014 put raised st in avr with st depression in at least 6 leads as indiction for reperfusion either pci or lytic therapy,,,,but on practice many patients admitted in our hospital with chest pain ,,same ecg chang es and troponin mildly elevated or even normal

  • James says:

    Literally had this job 2 days ago, however the st depression in lateral leads I and AVL were diffinitive with minor changes in III. They weren’t just septic, They were also having a stemi. Even though the patient was pain free… Im tired of people saying “stop worrying about avr) worry about it, why in the heck would we not worry about generalised cardiac ischemia?

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