Two patients with diffuse ST depression and reciprocal ST elevation in aVR: do either/both/neither have Occlusion MI?

Written by Jesse McLaren, with additions from Smith

Two patients presented with chest pain with ST elevation in aVR, and the same final ECG interpretation: “repolarization abnormality, severe global ischemia (LM/MVD).” Do either, both, or neither require the cath lab?

Patient 1: 75 year old, history of aortic stenosis, with recent cough accompanied by shortness of breath and chest pain, then syncopal episode.

There’s sinus tachycardia, first degree AV block, borderline right axis, and normal voltages. There’s significant ischemic STD in I/II/II/aVF and V4-6 (maximal V5-6) with reciprocal STD aVR/V1.

 

This has been called a “STEMI equivalent” but is nonspecific subendocardial ischemia, with a differential that includes demand ischemia (sepsis, severe anemia, severe AS), critical stenosis of any coronary artery or triple vessel disease, and other causes (PE, dissection). So this requires resuscitation, looking for non-cardiac causes, and angiography if a coronary (ACS) cause is likely.

 

The patient presented with cough and syncope, so pretest likelihood for acute coronary occlusion was low, while severe aortic stenosis plus pneumonia could explain subendocardial ischemia. There was a consolidation on Xray and elevated white cell count. But because of STE-aVR the patient had a stat cardiology consult and then cath lab activation, which revealed normal coronaries, with minimal troponin I elevation to 60 ng/L (normal <26 in males and <16 in females). The final diagnosis was pneumonia and critical aortic stenosis. Next day ECG showed resolution of subendocardial ischemia:

Patient 2: 60 year old with two days of fluctuating chest pain, now constant

There’s normal sinus rhythm, normal intervals/axis, and low voltages. There are hyperacute T waves in V1-3 (including deWinter T wave in V3), and precordial swirl pattern (STE or hyperacute T wave in V1-2 with reciprocal STD in V5-6). There’s also straightening of ST segment in aVL, with reciprocal inferior ST depression. Because there’s ST depression in II and V5-6, there’s reciprocal STE-aVR.

 

This indicates proximal LAD occlusion, but it doesn’t meet STEMI criteria so the cath lab was not activated. The patient had serial troponin I, which were 65ng/L and then 550ng/L two hours later. Because of ongoing chest pain and an ECG that was interpreted as nonspecific, a CT chest was also done which excluded aortic dissection, and then the patient was referred to cardiology as Non-STEMI.

 

Repeat ECG done 7 hours after arrival:

Now there’s further loss of anterior R waves. The hyperacute T waves have deflated over time, and there’s a suggestion of reperfusion in aVL, but the patient had ongoing chest pain. After repeat troponin that rose from 5000 to 9000 ng/L, with ongoing chest pain refractory to nitro and morphine, the cath lab was activated. Door to cath time was 10 hours, there was a 100% proximal LAD occlusion. Peak troponin was a massive 420,000 ng/L, and echo showed EF of 30%.

 

Post-PCI ECG showed ongoing loss of R waves, and reperfusion T wave inversion:

 

 

Subendocardial ischemia vs precordial swirl

 

The first patient had unnecessary cath lab activation while the second had delayed cath lab activation. Both had initial ECGs with the same final interpretation that focused on the ST elevation in aVR reciprocal to diffuse ST depression, but there were important differences in the patients and the ECGs which could have changed management:

 

The first patient had a low pre-test likelihood of ACS, and an ECG showing non-specific subendocardial ischemia – with the main injury pattern being ST depression in the inferior and lateral precordial leads. This is nonspecific and requires resuscitation, finding the cause, and angiography if primary cardiac cause is likely. The Queen of Hearts called this “OMI high confidence” because this assumes a pre-test likelihood of ACS, but this patient’s pretest likelihood was low. Future versions may indicate "subendocardial ischemia" to alert providers to the broader differential.

 

The second patient had chest pain and an ECG showing LAD occlusion – with the main injury pattern being anterior STE/hyperacute T waves and precordial swirl. The Queen of Hearts also called this OMI high confidence, but the patient had a higher pre-test likelihood of ACS and a more specific ECG pattern. This could have saved 10 hours of reperfusion delay and prevented a massive infarct.

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Take away

1.     ST elevation in aVR is reciprocal to diffuse ST depression, which has a broad differential.

2.     Subendocardial ischemia is non-specific: find and treat reversible causes, with angiography if cardiac cause is suspected

3.     Precordial swirl can help identify subtle LAD occlusion

4.     ECGs diagnostic of STEMI/OMI are unlikely to be secondary to aortic dissection

5.     ACS with refractory ischemia requires reperfusion, not morphine

6.     Queen of Hearts can help identify OMI on ECG, but needs to be applied in clinical context to the right patients

 

See these posts

-   precordial swirl – 20 cases of swirl and look-alikes

-    SW elevation in lead AVR, with diffuse ST depression, does not represent left main occlusion

Literature

1. 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.

2.  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.

https://www.sciencedirect.com/science/article/abs/pii/S000293431930049X
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:

Background

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 multi-lead ST depression.

Methods

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.  

Smith comment: this is a very limited population, as it only includes those with STEMI activations.  There are likely many other patients with STE-aVR who did not get a STEMI activation as they were not suspected of having ACS.

Results

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).  

Comment: Again, this does not include the many STE-aVR patients who were not activated, so even fewer would have ACS, and mortality in this group is much greater than in all STE-aVR patients.

Conclusions

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.

Why is this patient in shock?

This ECG was handed to one of my partners who was working in triage.  

The conventional algorithm stated "Nonspecific ST-T wave abnormalities."

What do you think?

My partner immediately diagnosed inferior OMI.  (Do you see: the subtle STE in III and aVF?  The terminal QRS distortion in aVF?  The ST depression in aVL?  The ST depression in V2-V4 of posterior OMI?  There is terminal T-wave inversion in III with terminal upright T-wave in aVL -- This strongly suggests reperfusion IF the patient's symptoms have subsided.  But they had not.)

He went to find the patient: Middle-aged man was working this afternoon when he developed sudden onset lightheadedness with diaphoresis, nausea, and had multiple episodes of emesis. The symptoms persisted for several hours, so his wife convinced him to come to the hospital.   He has no history of similar symptoms. 

This ECG is diagnostic regardless of whether the patient has chest pain or not.

He specifically denies chest pain or trouble breathing.  This was confirmed over and over with the patient.

All of my partners are good at recognizing OMI on the ECG.

He sent it to the Queen of Hearts:

 

And here is the Explainability:

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The patient was taken to the critical care area.  His systolic blood pressure was 80 mmHg and his lactate was 6 mEq/L.   The patient is in shock.

Why was he in shock?   ---The answer is on the ECG.

If you are not sure, maybe you will understand after seeing this ECG recorded 17 minutes later:

What do you think?

There is much more obvious STE in V1 that, especially in the context of inferior OMI, is diagnostic of right ventricular (RV) OMI (RV MI).   This implies a proximal RCA occlusion, proximal to the RV marginal branch which supplies the RV.  Not all proximal RCA OMI cause RV MI physiology (decreased RV cardiac output) and RV ECG ischemia: often the RV gets collateral circulation from the LAD which protects it from events like this.

He was taken to the cath lab and a total occlusion of the proximal RCA was found.

Angiographic findings:

1. Left main: no stenosis.

2. LAD: 40-50% ostial stenosis, otherwise luminal irregularities.

3. LCX: Large, nondominant. Supplies a large OM. Luminal irregularities,

but no stenosis.

4. RCA: proximal thrombotic or embolic occlusion with TIMI 0 flow. It

supplies an RPDA (inferior OMI) and RPLA (posterior OMI) without stenoses.

A post PCI ECG was recorded:

What do you think?

This was diagnosed as "uncertain rhythm with LBBB," but there are no P-waves, so I think it is post reperfusion accelerated idioventricular rhythm (AIVR), which because it initiates in the ventricle, has LBBB morphology.  

The OMI is still evident.  

In AIVR like this, you  can still use the Smith Modified Sgarbossa Criteria, and since there is proportionally excessively discordant STE in lead III (STE at the J-point divided by S-wave = 2.5/5.5 = 0.45; a value ＞25% in just one lead is diagnostic and＞20% all but diagnostic.)

Another similar ECG was recorded an hour later:

Also AIVR with persistent ischemia

--Normal left ventricular cavity size, wall thickness and systolic function; estimated ejection fraction is 55-60%.

--Regional wall motion abnormality in the mid to basal inferior segments.

--Moderately dilated right ventricle with moderately reduced right ventricular systolic function.

The estimated pulmonary artery systolic pressure is 17 mmHg + RA pressure.

Based on the appearance of the IVC, the RA pressure is significantly elevated. (Smith: this is because of decreased RV output, so it backs up into the RA)

So this too supports RV infarction.

Right Ventricular infarction (RV OMI)

RV infarction has very high mortality if not immediately reperfused, but the RV recovers very well if reperfused.  

Treatment of RV infarction prior to reperfusion: possibly some gentle hydration (see below) and norepinephrine to keep systolic BP high.  Unlike the LV which is perfused during diastole (because of very high chamber pressure during systole), the low pressure RV is perfused best in systole.  Keeping the systolic BP normal is very important for mitigating RV ischemia.  Even with an occluded RV marginal branch, collateral circulation can save the RV if the systolic pressure is high enough.

Gentle hydration: Caution to avoid excessive volume administration; overdistension of the ischemically dilated RV can lead to pressure on the septum and decreased LV output, similar to PE.  It can also result in the descending limb of the Starling curve, resulting in further depression of RV pump performance.  

The best single lead for RV infarction on the normal 12-lead is V1.  If there is not STD in V2, V1 has moderate sensitivity for proximal RCA occlusion.  But if there is any STD in V2, there is posterior OMI which "pulls down" the ST in V1 also, hiding the RV infarction.

We proved this: In inferior myocardial infarction, neither ST elevation in lead V1 nor ST depression in lead I are reliable findings for the diagnosis of right ventricular infarction

Such attenuation of the sensitivity in the presence of posterior OMI is also true for V4R (right sided leads) (Kosuge et al.)

More articles on danger of RV OMI:

Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction.  New Engl Journal.  You can support the diagnosis of RV MI using Right Ventricular Leads, particularly V4R, but Kosuge (above) showed that even V4R ST segment can be pulled down by the ST depression of posterior MI, leading to a false negative.

Impact of right ventricular involvement on mortality and morbidity in patients with inferior myocardial infarction.  JACC

Right ventricular dysfunction and risk of heart failure and mortality after myocardial infarction.  JACC

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MY Comment, by KEN GRAUER, MD (5/10/2024):

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The "beauty" of today's case — is that the ECGs all tell a story, even before the history of this patient is known.

• I focus my comments on this story — in which I'll add some thoughts to Dr. Smith's excellent discussion. For clarity — I've labeled the 4 serial tracings in today's case.

==================================

Looking at the Initial ECG:

Even before delving into the KEY points that enabled Dr. Smith's partner to immediately diagnose the acute OMI ...

• Did YOU Notice the rhythm in ECG #1?
• 
  
•      HINT: The rhythm in ECG #1 is not sinus!

ANSWER:

• For the rhythm to be sinus — the P wave should be upright in lead II. The only 2 exceptions to this statement are dextrocardia and lead misplacement.
• The YELLOW arrows in lead II of ECG #1 show that no P wave is present in this lead. Instead — a small, upright P wave is seen in leads I and aVL (BLUE arrows in these leads). There is no lead reversal. This pattern, in which no definite P wave is seen in lead II — but an upright P wave is seen in leads I and aVL — is consistent with a low atrial rhythm.
• 
  
• KEY Point: A low atrial rhythm is most often a common normal variant — although in today's case, it may convey similar implications as would a junctional escape rhythm. That said, while clinical management of today's patient is not altered by not having a sinus rhythm — You can simplify life (and never overlook sinus rhythm again) by routinely spending the first 2-3 seconds of your inspection of every ECG you encounter by scanning the long lead II rhythm strip with your educated "eye" to make sure that each QRS is preceded by an upright P wave.
• NOTE: ECG #2 was obtained 17 minutes later. RED arrows in ECG #2 show the return of sinus rhythm (RED arrows in the long lead II of ECG #2). Beats #9 and 10 in ECG #2 occur early, and are probably PACs (with beat #10 probably being conducted with aberration).

Figure-1: I've labeled the first 2 ECGs in today's case.

Recognizing Today's OMI within Seconds!

With experience — Recognition of today's OMI should be accomplished in less than 20 seconds (even without knowing the history).

• Once we've established that the rhythm in ECG #1 is supraventricular (ie, a low atrial rhythm, as noted above) — my "eye" was immediately drawn to lead III (within the RED rectangle), which shows a large Q wave, ST segment coving with subtle-but-definite ST elevation, and terminal T wave inversion.
• Confirmation that the subtle ST segment elevation in lead III is real and acute — is forthcoming within seconds from the 2 frontal plane leads enclosed within the BLUE rectangles: i) In lead aVF — the Q wave and ST segment straightening with slight ST elevation conveys support from this neighboring lead to lead III; and, ii) In high-lateral lead aVL — we see the precise mirror-image opposite ST-T wave picture as we see in lead III. This reciprocal change is also seen in the other high-lateral limb lead ( = lead I) — and verifies the diagnosis of acute inferior OMI until proven otherwise.
• 
  
• We've emphasized on multiple occasions that the ST-T wave in leads V2 and V3 should normally show slight, gentle-upsloping ST segment elevation. Instead, lead V2 in ECG #1 (within the RED rectangle) jumps out as manifesting a flat (straight) ST segment without any ST elevation. Given that we've already established the diagnosis of acute inferior OMI — the ST-T wave appearance within this RED rectangle establishes the diagnosis of associated posterior OMI (which is further supported by abrupt transition to a predominant R wave already by lead V2).
• Within the BLUE rectangle in neighboring lead V3 — we see ST segment flattening and slight-but-real ST depression — thus providing further evidence of acute infero-postero OMI.
• NOTE: The time it should take for an "educated eye" to appreciate the above ECG findings within the 2 RED and 3 BLUE rectangles should be less than 20 seconds.

What about Lead V1 in the Initial ECG?

Acute posterior OMI produces maximal ST depression in leads V2, V3 and/or V4. Although less marked — posterior OMI typically also produces ST straightening with some depression in lead V1. Posterior OMI should not produce ST elevation or a hyperacute T wave in lead V1 — unless there is associated RV MI.

• KEY Point: As soon as the acute infero-postero OMI was recognized in ECG #1 — our "eye" should be drawn to the disproportionately tall and "fat" T wave in lead V1 of this tracing (within the PURPLE rectangle). As per Dr. Smith — the clinical importance of appreciating that the tiny QRS complex in lead V1 should not display a disproportionate hypervoluminous T wave — is that this finding is diagnostic of acute RV MI (thereby explaining this patient's hypotension). In addition, this finding localizes the "culprit" artery to the proximal RCA.

Comparison of ECG #1 and ECG #2:

With acute posterior OMI + RV involvement — there is interplay between right-sided ST elevation (from the RV MI) — and anterior ST depression (from the posterior OMI).

• In ECG #1 — ST segment flattening with slight depression from posterior OMI was most marked in leads V2 and V3.
• 17 minutes later with the recording of ECG #2 — we see marked increase in the ST elevation from the RV MI in leads V1,V2 — such that lead V2 no longer shows ST-T wave changes of posterior OMI (within the PURPLE rectangles in ECG #2). In contrast — the limb leads in ECG #2 show no significant serial change.

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What about the Rhythm after PCI?

I found the post-PCI rhythms in ECG #3 and ECG #4 to be interesting, challenging — and clinically informative.

• I completely agree with Dr. Smith — that the "theme" of these post-PCI rhythms is the development of variations of AIVR (Accelerated IdioVentricular Rhythm) — which given the timing of this rhythm, suggests this is a reperfusion arrhythmia (that is often associated with successful reperfusion from PCI).
• AIVR is most often a transient occurrence in the post-PCI setting. Although the "atrial kick" is lost — most patientts will be hemodynamically stable (from the successful PCI), in which case no intervention is needed!

Figure-2: I've labeled the 3rd and 4th ECGs in today's case.

ECG #3 is Challenging!

The difficulties I had interpreting the first post-PCI rhythm ( = ECG #3) included: i) Finding P waves; and, ii) Determining why there were so many different QRS morphologies.

• I did not think any P waves were present in ECG #3 for the first 10 beats in the long lead II rhythm strip. I dropped a vertical RED line from the onset of the very wide QRS in lead I. This told me that the initial slurring and notching in lead II did not represent atrial activity — but instead formed the inital part of the QRS complex in this lead.
• Despite the resemblance to LBBB morphology in the first 10 beats (ie, with an all-upright R wave in lateral leads I and aVL — and a predominantly negative QRS in anterior leads V1,V2,V3) — the lack of atrial activity overwhelmingly favored a ventricular rhythm (rather than a junctional rhythm with LBBB) as the cause for QRS widening.
• 
  
• KEY Point: AIVR with LBBB-like morphology suggests that this ventricular rhythm is arising from the right ventricle — which is consistent with the acute RV MI producing shock in today's case.
• 
  
• Beats #12 and 13 — are sinus conducted (RED arrows highlighting definite sinus P waves in front of beats #12 and 13).
• Working backward — I thought the RED arrow in front of beat #11 was also a sinus P wave, albeit with a shorter PR interval than that seen before beats #12 and 13.
• The QRS complex of beat #11 is clearly wider than the QRS of sinus beats #12 and 13 — but not as wide as the 10 QRS complexes that preceed beat #11 (This is perhaps easier to appreciate by looking at the simultaneously-recorded beats in the 12-lead tracing above the long lead II rhythm strip). Therefore — beat #11 is a fusion beat! (a determination that further supports our deduction that beats #1-thru-10 are ventricular in etiology = AIVR).
• 
  
• The confusing part to me in ECG #3 — was the changing QRS morphology for beats #1-thru-10 in the long lead II rhythm strip. For clarity — I labeled the wide, equiphasic complexes with an "X" ( = beats #1-thru-7; #9) — and the wide predominantly negative complexes with a "Y" ( = beats #8 and 10).
• Whereas the R-R interval for complexes "X" were equal to each other — the 2 "Y" complexes were preceded by a slightly shorter R-R interval. 
• 
  
• MY THEORY: I suspect there are 2 ventricular sites, each producing their own version of AIVR. In support of my theory — Note that ~1 hour later, ECG #4 now shows all beats in the long lead II of this 2nd post-PCI tracing with the same QRS morphology — that is consistent with the predominantly negative morphology of complex "Y" (and with a slightly faster AIVR rate than was seen for AIVR by the "X" complexes in ECG #3). 
• The rate of AIVR with the "X" complexes is ~75/minute (an R-R interval = 4 large boxes).
• The rate of AIVR with the "Y" complexes is 85-90/minute (an R-R interval = 3.4 large boxes — and similar to the shorter coupling interval for the 2 "Y" complex beats in ECG #3).
• It is because the rate of AIVR with the "Y" complexes is slightly faster than the rate of the "X" complexes — that we see dominance of the "Y" AIVR in ECG #4.

Final Point: As per Dr. Smith — Despite the ventricular rhythm in these post-PCI tracings — We still see evidence of the OMI!

• While clearly more difficult to assess ST-T wave morphology when confronted with 2 different AIVR morphologies — the coved and markedly elevated ST segment in lead III of ECG #3 and ECG #4 simply should not be there!
• In the chest leads — Note the dramatic difference in the shape of the coved and markedly elevated ST segment in lead V1 of these 2 post-PCI tracings — compared to the upward concavity and much less elevated ST segments in lead V2 and V3. Isn't this similar to the "interplay" we saw in ECGs #1 and #2 between lead V1 ST elevation from RV MI — and lack of ST elevation in leads V2,V3 from the posterior OMI?