Monday, March 9, 2020

Does ST Elevation in lead aVR indicate acute coronary occlusion?

A paper out last January shows what I've been saying for years, that ST Elevation in aVR, with diffuse ST depression, is NOT a sign of left main occlusion, or of any acute coronary occlusion (It is not OMI).

ST Elevation in aVR with diffuse ST depression

In the right clinical context
, it is a sign of ACS with subendocardial ischemia.
  It may also be due to LVH or to subendocardial ischemia from any cause of supply/demand mismatch (hypovolemia with coronary disease, severe tachycardia, GI bleeding with anemia, aortic stenosis, etc.).  If due to ACS, the culprit is usually Left Main, LAD, or any artery in the context of severe 3-vessel disease (although in this new study, none were due to left main or LAD!).  The ST Elevation in aVR is reciprocal to the diffuse ST depression.  It is not, unlike STEMI, due to subepicardial ischemia of the myocardium underlying the lead -- there is no ventricular myocardium under aVR; rather, there are only atria.

If due to ACS, it can sometimes be managed medically with nitro, heparin, and antiplatelet agents, with angiogram later if all ischemia resolves.  Usually, (again, only if due to ACS), it is indeed better to go emergently to the cath lab.

The ACC/AHA guidelines, as of 2013 and for the first time, recommends thrombolytics for ACS with this ECG pattern if PCI is not available.  (This recommendation is, however, due to the idea that the ECG finding is one of occlusion).  I agree that thrombolytics should be used if the ischemia is refractory to medical management and the patient is a long way from a PCI center.

It is important to know that with this pattern of ischemia, there is often no wall motion abnormality, as there is no one wall with full thickness ischemia.

Here is a post from 2014:

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

Now there is a paper published in 2019 that proves the point beyond doubt, though makes it clear that this pattern is associated with very high mortality.
Harhash AA et al. aVR ST Segment Elevation: Acute STEMI or Not? Incidence of an Acute Coronary Occlusion.  American Journal of Medicine 132(5):622-630; May 2019.

Here is the abstract:

Identification of ST elevation myocardial infarction (STEMI) is critical because early reperfusion can save myocardium and increase survival. ST elevation (STE) in lead augmented vector right (aVR), coexistent with multilead ST depression, was endorsed as a sign of acute occlusion of the left main or proximal left anterior descending coronary artery in the 2013 STEMI guidelines. We investigated the incidence of an acutely occluded coronary in patients presenting with STE-aVR with multilead ST depression.


STEMI activations between January 2014 and April 2018 at the University of Arizona Medical Center were identified. All electrocardiograms (ECGs) and coronary angiograms were blindly analyzed by experienced cardiologists. Among 847 STEMI activations, 99 patients (12%) were identified with STE-aVR with multi-lead ST depression.


Emergent angiography was performed in 80% (79/99) of patients. Thirty-six patients (36%) presented with cardiac arrest, and 78% (28/36) underwent emergent angiography. Coronary occlusion, thought to be culprit, was identified in only 8 patients (10%), and none of those lesions were left main or left anterior descending occlusions. A total of 47 patients (59%) were found to have severe coronary disease, but most had intact distal flow. Thirty-two patients (40%) had mild to moderate or no significant disease. However, STE-aVR with multilead ST depression was associated with 31% in-hospital mortality compared with only 6.2% in a subgroup of 190 patients with STEMI without STE-aVR (p less than 0.00001).


STE-aVR with multilead ST depression was associated with acutely thrombotic coronary occlusion in only 10% of patients. Routine STEMI activation in STE-aVR for emergent revascularization is not warranted, although urgent, rather than emergent, catheterization appears to be important.

Previously, Knotts et al. had published different, but also convincing, data:
Knotts et al. found that such ECG findings (STE in aVR) only represented left main ACS in 14% of such ECGs: 
Only 23% of patients with the aVR STE pattern had any LM disease (fewer if defined as ≥ 50% stenosis). Only 28% of patients had ACS of any vessel, and, of those patients, the LM was the culprit in just 49% (14% of all cases).  It was a baseline finding in 62% of patients, usually due to LVH.

Reference: Knotts RJ, Wilson JM, Kim E, Huang HD, Birnbaum Y. Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? J Electrocardiol 2013;46:240-8.

MY Comment by KEN GRAUER, MD (3/9/2020):
Important paper highlighted in this post by Dr. Smith (above) — in support of the concept that diffuse ST depression with ST elevation in lead aVR is not a sign of acute coronary occlusion. Instead it suggests diffuse Subendocardial Ischemia — which as per Dr. Smith, may be due to:
  • Severe Coronary Disease (due to LMain, proximal LAD, or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
  • Subendocardial ischemia from another Cause (ie, sustained tachyarrhythmia; shock/profound hypotension; GI bleeding; anemia; etc.).

I thought it would be of interest to present a case (sent to me by Dr. Ong of Taiwan) that illustrates the above concepts.

The CASE: The patient is a previously healthy 60-something man, who presented to the ED with palpitations and chest pain. His BP at the time ECG #1 was obtained was ~70 mm Hg systolic (Figure-1).
  • QUESTION #1: DOES this patient have severe coronary disease?
  • QUESTION #2: WHAT are your thoughts about this case?

Figure-1: The initial ECG seen in the ED (See text).

My THOUGHTS on ECG #1: Hopefully YOU did not answer Question #1 before systematically assessing this tracing!
  • The rhythm is rapid (ie, ~170-180/minute) and regular. The QRS is narrow. BUT — No P waves are seen. Therefore — this is a regular SVT rhythm without clear sign of atrial activity. The usual Differential Diagnosis for a regular SVT without clear sign of P waves includes: i) Sinus Tachycardiaii) Atrial Flutteriii) A Reentry SVT (ie, AVNRT or  orthodromic AVRT)oriv) Something Else (ie, much less commonly there could be atrial tachycardia, junctional tachycardia, sinoatrial reentrant tachycardia, etc.).
  • PEARL #1 — The heart rate of ~170-180/minute for this regular SVT without P waves strongly suggests that the rhythm most probably is a Reentry SVT because: i) Sinus Tach usually does not go faster than 170-180/minute in a supine adult (ie, someone who has not just exercised); andii) The most common ventricular response for untreated AFlutter is between ~140-160/minute (ie, the atrial rate with untreated flutter is usually ~300/minute — which with 2:1 AV conduction results in a ventricular rate between ~140-160/minute). The rate of ~175/minute in this case — would mean that if the rhythm was AFlutter with 2:1 AV conduction — then the atrial rate would be ~175 X 2 = 350/minute, which is faster than is seen in most cases of new, untreated AFlutter.
  • Otherwise — There is diffuse and marked ST depression in ECG #1 + ST elevation in lead aVR. The axis is normal. A Q wave is seen in lead III. R wave progression is normal — with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V2-V3.
  • NOTE: There is an S1Q3T3 pattern in ECG #1! That said — this patient did not have acute Pulmonary Embolism.
  • PEARL #2 — As helpful as recognition of an S1Q3T3 pattern can be in the ECG diagnosis of acute PE when a suggestive clinical history and other ECG findings of acute hypoxemia and acute RV “strain” are present — the specificity of an S1Q3T3 pattern for acute PE is poor in the absence of other ECG findings.

ANSWER to Question #1: This patient may or may not have severe coronary disease. More important than answering this question is treating the patient!
  • Tachyarrhythmias may cause chest pain. They may also produce an ECG picture of diffuse subendocardial ischemia from supply/demand mismatch.
  • Regardless of whether the cause of this patient’s chest pain is the fast rate of the SVT — severe underlying coronary disease (possibly with ACS) — and/or a combination of these 2 entities — the 1st Priority is to Treat the SVT!

FOLLOW-UP: This patient was treated with Adenosine. The result of this treatment is shown in ECG #2 (which I have placed under ECG #1 in Figure-2).
  • NOTE: The decision was made by the providers on-the-scene to treat medically with Adenosine, rather than with immediate synchronized cardioversion. While one can debate whether it was optimal to use medical therapy in this hemodynamically compromised patient (ie, with chest pain, hypotension, and an ECG suggesting marked subendocardial ischemia) — this is what was done.

Figure-2: Both ECGs in this case. Note — ECG #2 was obtained ~30 minutes after Adenosine was given! (See text).

My THOUGHTS on ECG #2: To emphasize — ECG #2 was obtained ~30 minutes after Adenosine was given.
  • ECG #2 shows that this patient has converted to sinus rhythm! Of note — this conversion to sinus rhythm occurred promptly after giving the 2nd dose of Adenosine (12 mg) — with resolution of this patient’s palpitations and chest pain as soon as sinus rhythm was established!
  • Despite resolution of symptoms with conversion to sinus rhythm — ECG #2 shows that significant diffuse ST depression persists (ie, not as much ST depression as was seen in ECG #1 — but still 2-3 mm in most leads, with a comparable amount of ST elevation still present in lead aVR).

I probably would have opted for immediate synchronized cardioversion instead of Adenosine in this patient — given apparent hemodynamic compromise (at least on paper!). That said — since this patient promptly converted to sinus rhythm after the 2nd dose of Adenosine, with complete resolution of symptoms — giving Adenosine was also a “right Answer”. Sometimes — Yjust gotta bthere”.
  • Because significant ST depression persisted a good 30 minutes after conversion to sinus rhythm (as seen in ECG #2) — cardiac cath was performed. The surprising result was no more than minimal coronary disease!

PEARL #3 — Treat the patientECG #1 clearly suggested marked diffuse subendocardial ischemia. But the tachyarrhythmia needed to be treated 1st — and in this case, despite persistence of marked ST depression for at least 30 minutes after conversion to sinus rhythm — We see how an ECG as worrisome as that shown in ECG #1 can sometimes be the result of a sustained tachyarrhythmia without there necessarily being severe underlying coronary disease.

Our THANKS to Dr. Smith for updating us on the entity of diffuse ST depression with ST elevation in lead aVR.


  1. thank you for sharing this valuable information

    1. Our pleasure! THANK YOU for your interest — :)

  2. Sir , what is the treatment of choice for SVT if BP is less than 90mmHg systolic?

    1. @ Ahammed — As ALWAYS, the treatment of choice for a tachyarrhythmia (SVT or VT!) depends on the clinical setting in which it occurs! For example — at BP of 89 mmHg (which is less than your “90 mmHg”) may or may NOT necessarily be hemodynamically stable. “Ya gotta be there” (ie, sometimes a BP of 80 mmHg or less might not necessarily mandate immediate cardioversion, depending on the patient’s “normal” BP, and how the patient is tolerating the arrhythmia). As to the treatment of choice of an “SVT” rhythm (as you ask) — the term “SVT” is a generic one, including ANY arrhythmia originating from at-or-above the AV node. If the rhythm turns out to be (or most probably is — if uncertain about the etiology) a SINUS tachycardia — and IF (despite somewhat low BP) the patient is tolerating the arrhythmia — measures such as fluid infusion might be all that is needed. Alternatively — valsalva maneuver or some medication vs cardioversion might be all that is needed, DEPENDING on the circumstances of the case at hand. BOTTOM Line: Impossible to answer your question without knowing specifics of the case at hand — :)


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