ST Elevation: Inferior MI or Early Repol? Ultrasound Speckle Tracking Can Help.

Rob Reardon, our ultrasound director, showed me this ECG of a 50 yo with chest pain he had seen a few days prior:
I said "Early Repolarization in Limb Leads".
He had thought there might be some reciprocal ST depression in aVL and was worried about inferior MI.
I can see what he means, but I don't think it qualifies.

But these ECGs can be difficult.

As our ultrasound fellowship director, his solution was to do bedside ultrasound with Speckle Tracking Strain Echocardiography on our sophisticated Toshiba ultrasound machine.

We reported on Speckle Tracking recently in the American Journal of Emergency Medicine, where you can read about it in detail:

Diagnosis of acute coronary occlusion in patients with non–ST-elevation myocardial infarction by point-of-care echocardiography with speckle tracking: a case report

With Speckle Tracking, you mark the endocardium visually on a still picture, and then the computer follows that endocardium through the cardiac cycle, both showing and plotting its wall motion.

It is the next best thing to a contrast echocardiogram.

Here is the video he obtained:

The three segments at lower left are the inferior wall (AI = inferior apical, MI = mid apical, BI = basal inferior)
Speckle Tracking makes it so you can see that all of them contract (shorten and thicken) very well.
The graph on the right shows that your visual diagnosis is correct: the deep waves to (-30) confirm perfect function of all segments of the inferior wall.

Here is a still image:
On the left, the 2 arrows point to the mid inferior and basal inferior segments.
On the left, the one arrow points to the Purple-blue line corresponding to the purple-blue basal inferior segment, confirming that it has full contractility.

This allayed his concerns of inferior MI, but only because he is a real expert at doing this.

The patient ruled out for MI by biomarkers and the ECG did not evolve.

Speckle Tracking can also be falsely re-assuring if not done right and improperly interpreted" see this very instructive example:
Low HEART score. Acute LAD occlusion. Detected only by analysis of subtle ECG.

Learning Points:

1. Speckle Tracking can be done by an experienced emergency physician.

2. Speckle Tracking can help you to recognize a STEMI mimic if there is perfect wall motion in the echocardiographic segment in question.

3.  However, you can have false negatives, especially if you are not expert in this.

4.  Fuly trust negative results only when your clinical and ECG suspicion are already low.

5.  Do not use it to definitively "rule out" coronary occlusion.  Rather, continue to evaluate with serial ECGs and possibly emergent formal contrast echo.

60-something with Chest Pain, resolved upon arrival to the ED

A 60-something male called 911 for chest pain of less than one hour duration.  He arrived in the ED pain free and had this ECG recorded:

What to you think?

There are hyperacute T-waves in V2-V4, but the patient was pain free.  I did wonder if he had had a prehospital ECG recorded, and what it showed.  

This was 10 years ago, just when we had started doing prehospital 12-lead ECGs.  I was not even certain that one had been recorded, but if it was, I wanted to see it.

I had to look around for it, and here is what I found:

Pretty amazing, huh?

Here I have circled the computer algorithm interpretation, just so you don't miss it:

Early Repolarization???
Notice STE is both precordial and in I/aVL.

He was taken to the cath lab and there was a fresh thrombus in the proximal LAD with 80% stenosis.  

Serial troponins were all undetectable (these are less sensitive than today, but as I pointed out in my last post, the initial troponin in STEMI, even with high sensitivity troponin, can be below the level of detection.

Here is another case where the physicians did not seek out the prehospital ECG and it led to loss of myocardium, but in this case for missing the evolution.  The initial troponin was below the level of detection.

Learning Points:

1.  In spontaneously reperfused "Transient STEMI," hyperacute T-waves may still be present after resolution of pain and resolution of ST segments.

I say: "you get hyperacute T-waves on the way up (as ST segments are on the way up, shortly after occlusion) and on the way down (after ST segments have normalized, shortly after reperfusion)

2.  The Initial troponin is often undetectable in STEMI

3.  Serial troponins may be all negative in transient STEMI

4.  Always look for and examine the prehospital ECG.

Abnormal ST-T in V1-V3. What is it? Many interesting and informative twists to this case.

A middle-aged woman with a history of CAD and stents, but also a history of several subsequent visits for non-cardiac chest pain, called 911 for chest pain of 5+ hours duration.

The medics recorded this ECG at time zero:
Note the downsloping ST depression in V1-V3, with down-up T-waves in V2 and V3.

Down-up T-waves in right precordial leads during chest pain is likely posterior MI.

When I showed this to a resident, she asked if these are Wellens' waves.  I pointed out that Wellens waves are 1) up-down and 2) after resolution of pain.  And they indicated, of course, LAD thrombus with a reperfused artery (good flow), whereas this is indicative of no or low flow to the posterior wall.  I did add that subendocardial ischemia is also possible.

The medics gave NTG, and the chest pain resolved. This was recorded at time 12 minutes:
Now V2 and V3 have a long flat ST segment with a tiny upright T-wave.  This is also highly suspicious for posterior MI, probably resolving.
V5 and V6 appear to have smaller T-waves now as well.

The patient was brought to the ED, at which time she had pain again, and this ECG was recorded at time 30 minutes (nearly 6 hours after onset of pain):
New but subtle downsloping ST depression with down-up T-waves in V2 and V3.
Interestingly, limb leads are not very helpful here.

The patient's chest was quite tender, and the initial contemporary troponin was below the level of detection (0.010 ng/mL).

I activated our "Pathway B."  Pathway B is intermediate between "admit for serial troponins" and "activate the cath lab (Pathway A)".  That means I call the cardiologist on call, and he/she gets further evaluation going immediately.

The interventionalist came down immediately and talked to the patient, looked at the ECG, and decided to take her to the cath lab.


100% In-stent Occlusion of a large circumflex, easy to cross with wire.  There was no collateral filling.  A stent was placed.

However, it is very puzzling:

All serial troponins remained below the LoD!

But to the angiographer the lesion was not a chronic total occlusion.

The echocardiogram showed a new inferolateral wall motion abnormality, but it was only hypokinesis, not akinesis, and the EF was 60%.  One cardiologist did not initially see the WMA.  This suggests either ischemia with stunning (unstable angina) or small infarct.

Here is the post procedure ECG, 5 hours after PCI:
ST segments and T-waves are mostly normalized, supporting acute ischemia on the previous ECGs

The patient had no more of what she describes as her "heart attack" type chest pain.

This was recorded the next day:
Fairly normal

Coronary thrombosis is a Dynamic process!

The artery opens and closes spontaneously.  Thrombus propagates and lyses (remember there is endogenous tPA).  If the occlusion is brief, then there is no infarct and troponins are negative.  There might still be stunning from ischemia with a WMA.  Then if it occludes again just prior to the angiogram, the angiogram shows 100% occlusion, even if it has only been brief.

This appears to be a case of unstable angina due to coronary occlusion that was complete at the time of the angiogram, though opening and closing prior to the angiogram.

Alternatively (and I think less likely), it could be that she had her MI more than 2 weeks prior and all troponins are now negative.  The lesion might still be easy to cross with the wire.  She would have a wall motion abnormality.  However, with no collateral circulation and a total occlusion, there should be a dense wall motion abnormality (but it was not dense).  If this hypothesis is correct, then she was having post-infarct angina (but that begs the question of why?  Where was the new angina/ischemia originating from?)

Unstable angina still exists.  And it may have an occluded artery at angiogram.

My next post will show another example of unstable angina due to occlusion, with all negative troponins.

In our UTropIA study (see here at of about 2000 consecutive ED patients who had troponin ordered, we measured both contemporary and high sensitivity troponins (Abbott Architect Troponin I) and found that one of 9 STEMI patients (there were quite a few more patients who had ECGs diagnostic of occlusion but that did not meet STEMI criteria) had an initially undetectable high sensitivity troponin.  About half had an initial hs trop below the 99% reference value.

Resuscitated from ventricular fibrillation: what is the ECG Diagnosis?

A reader (someone in training) sent me this ECG, and asked for my interpretation.

Clinical info:  "The patient was found down in cardiac arrest, defibrillated with ROSC in the field, was unconscious on arrival. Attached is the initial ED ECG."

"I will provide details and outcome to come after your impression." 

Here is the EKG: 

Here is my interpretation: Sinus at a rate of about 80, RBBB, LAFB, ST Elevation in aVL, reciprocal ST Depression in II, III, aVF.  No precordial ST Elevation, but STE often does not show in precordial leads when there is LAD occlusion with RBBB and LAFB.  Proximal LAD occlusion.

When confronted with RBBB and LAFB in a patient with cardiac arrest or typical chest pain or cardiogenic shock, one should assume acute LAD occlusion.  Any occlusion can fail to show in ECGs with normal conduction, with LBBB, and with RBBB.  But in my experience, huge myocardial infarctions are particularly difficult to discern in the presence of RBBB and LAFB.  This is not well described, but I have seen it very often.

See this paper by Widimsky et al., which shows the high association of RBBB, especially with LAFB, with LAD occlusion.  Furthermore, among 35 patients with acute left main coronary artery occlusion, 9 presented with RBBB (mostly with LAFB) on the admission ECG.

How do you assess ST elevation on these ECGs?  First, find the lead which you believe most clearly manifests the end of the QRS.  I believe that in this ECG it is lead V4.  Then draw a line down to the lead II rhythm strip at the bottom.  Then, using the same point on the complex under leads (I, II, III), (aVR, aVL, aVF), (V1, V2, V3), you can draw a line up and see the end of the QRS in all leads.  In this way, one can see the subtle, downsloping ST elevation in aVL, with reciprocal ST depression in II, III, and aVF.

Here it is:

His response:


This was an interesting case, especially when you red the providers' interpretations of the ECGs.  After the 2nd ECG the diagnosis should be clear, but for some reason they call it "NSTEMI".   No cath done initially, and on day 3 they decided to avoid cath because they thought she was neurologically unrecoverable.

On autopsy on day seven, "99% LAD stenosis".

Here is more detail:

Old ECG on file:
Sinus.  Normal conduction (no BBB).  Baseline Q-waves in V2, V3. Nonspecific ST-T abnormalities.

ECG #2 at 19 minutes:
Smith: RBBB/LAFB persist, but the STEMI is quite obvious here

ECG #3 at 63 minutes
The right bundle branch block has resolved, suggesting that perhaps the artery has opened, but the ST elevation persists, especially in aVL.  [aVL II, III, aVF are diagnostic of high lateral STEMI with reciprocal ST depression. Note that there is NOT 1 mm STE in 2 consecutive leads, but in one lead only (aVL)]
There is some STE in V1-V3 and STD in V6 also.

ED Physician Assessment:
“Initially wide complex PEA. Responded best to bicarb and calcium. Had VT and VF and torsade in field as well…ECG shows wide complex rhythm in 80s. Suspected hyperK given wide complex and response to calcium and bicarb…On repeat ECG rate 77, sinus, now more of an incomplete LBBB pattern with STD in inferior leads and 2mm STE in aVL only. Concerning but technically does not meet STEMI criteria. Resident discussed with CCU fellow and cath lab. Not STEMI criteria.”

Initial potassium: 5.8 mmol/L

Smith comment: Although it is possible that such an ECG represents hyperkalemia, it is a very atypical ECG for hyperkalemia.  

More importantly, such an ECG would only be seen with a potassium greater than 7.0 mEq/L.


Here are some typical pseudoSTEMI patterns for hyperkalemia (multiple examples at this post):

Cardiac Arrest and ST Elevation: You Should Learn to Recognize This!

Here are some cases of RBBB and LAFB

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

don't miss this one!

Chest Pain and Right Bundle Branch Block


Clinical Course

Pt was admitted to MICU with cardiology following.

Troponin T (normal is less than 0.10 ng/mL): 1.19 ng/mL → 7.67 ng/mL → 19.53 ng/mL <0 .10="" 1.19="" 19.53.="" 7.67="" b="" nbsp="">(Smith comment: remember that, as far as one can correlate troponin levels with infarct size, troponin T levels are only 1/10th as high as troponin I levels.  So this may correspond to a troponin I level of about 200 ng/mL.)

ECG #4, next morning
There is some persistent STE in V1-V3 and aVL (and reciprocal STD), different from patient's baseline ECG.

Cardiology consult note on day 2:
“Inciting cause is unknown although there is evidence supporting coronary ischemia and metabolic derangements including hyperkalemia and acidosis.  Prognosis is tenuous and neurologic function cannot be assessed while the patient is sedated. The incremental benefits of an early invasive approach in management of this ACS may outweigh the risks as long as cognition improves and metabolic derangements are corrected. The clinical approach for ACS in ESRD is usually individualized; effectiveness data is limited and treatment related morbidity is not uncommon.”

“Assessment: “Cardiac arrest…..Non-ST elevation acute coronary syndrome”
“ECG 1: Sinus rhythm, rate 90, QRS duration ~190ms, left axis deviation with late terminal forces moving rightwards and anterior.
ECG 2: SR, rate 80; QRS 120ms with late terminal left/anterior, left axis deviation, ST elevation (~1mm in I, 1-1.5mm aVL, <1mm 1.1.5mm="" avf="" depressions="" font="" iii="" st="" v2="" v3="" v5="" v6="">

ECG 3: SR, rate ~75. ST elevation (1-2mm aVL, 1mm V2/3), ST depression (II, III, aVF, V4-6).”

Cardiology consult day 3:
“59 yo patient with ESRD on HD, DMII, who is currently in cardiogenic shock in the wake of cardiac arrest after NSTEMI. The pressing issue is whether this patient should undergo left heart catheterization today. I think this hinges on neurologic status, which at this time is largely unknown. Pt was reported to have 1 hour down time prior to being resuscitated. She has been without sedation for several hours and has no corneal or gag reflexes per the primary team. There is enough evidence to call into question her neurological viability at this time, thus a left heart catheterization would be of questionable utility.”

Autopsy, day 7:
Anoxic brain injury with total cerebral necrosis 99% stenosis of the proximal LAD, with acute transmural infarct of the anterior and anterolateral walls of the LV 75% stenosis LCx, 50% RCA, 25% LM

10 Cases of Inferior Hyperacute T-waves

In the last post, I showed: 

Ten (10) Examples of Hyperacute T-waves in Lead V2 (a few in V3), due to acute LAD occlusion

Today, 10 examples of inferior hyperacute T-waves.

Details in every case make it even better, so click on the link!!

Case 1.  

Chest Pain in a 61 year old male. Inferior STEMI without inferior ST elevation.

In this case, the followup ECG is diagnostic because of lead V1

Case 2.

Inferior Hyperacute T-waves

Case 3.

Chest Pain in a Male in his 20's; Inferior ST elevation: Inferior lead "early repol" diagnosed. Is it?

This case was missed.  Read about it.

Case 4.

Series of Prehospital ECGs Showing Reperfusion

This has an incredible sequence of ECGs!

Case 5.

The development of an inferior-posterior STEMI, from prehospital to hospital

Case 6. 

Friday's post produced skeptics.....

This case made a lot of readers angry, denying that these are hyperacute Ts

Case 7.

A Case of Clinical Unstable Angina in the ED

This case shows how hyperacute is only relative to the baseline T-waves.  Also, the critical role of reciprocal ST depression and T-wave inversion in aVL.

Case 8.

Is this STEMI? Pattern Recognition is Key 

Go to the link, and this case shows an inferior pseudoSTEMI for contrast

Case 9.

Inferior hyperacute T-waves. The clue is T-wave inversion in aVL. Serial ECGs evolve to ST Elevation.

Case 10.

Subtle Inferoposterolateral STEMI