Monday, January 31, 2022

Subtle ECG Signs of OMI in LBBB

A 70 yo F with no previous cardiac history, but with a h/o hypertension, hyperlipidemia, and strong family history of ACS, presented with one hour of classic chest pain and appeared uncomfortable.

Her systolic BP was 210.  The ECG is here:

Atypical LBBB (see explanation below)
As for Occlusion MI (OMI), what do you think?

A bedside echo was normal to that provider's eye (no bubble contrast).

She had a CT for dissection that was negative.

A 2nd ECG was recorded:

There is an atypical left bundle branch block (LBBB) -- atypical because the R-wave in V6 is not all upright.  
But the Smith Modified Sgarbossa criteria work in both typical and atypical LBBB.

As for presence or absence of Occlusion MI (OMI), what do you think?

Here are the 2 ECGs (leads II, III, aVF, aVL) side by side:

                                        First ECG                                                             2nd ECG

What do you think?

The first time I looked at these was on my phone, and I did not notice the change.  See how the J point in lead III has risen in the 2nd ECG (and become more reciprocally depressed in aVL).  On the first, the ST/S ratio is 2/12 = 0.167 (16.7%); on the 2nd it is 2.5/11.5 = 0.217 (21.7%).  Any value over 15% is suspicious, and a value over 20% still has 94% specificity for OMI in our validation study.  See Ken Grauer's additional points below.

Moreover, when there is a change, with increase in ratio, it is much more specific.

Also, remember that New LBBB is no more likely than old LBBB in MI, and that only about 7% of patients with chest pain and LBBB in the ED have acute MI, with only about 3% having OMI.

See this review paper that I and others wrote in Current Cardiology Reports (we recommend use of the Cai and Sgarbossa algorithm which uses the Smith Modified Sgarbossa ECG Criteria):  Diagnosis of Occlusion Myocardial Infarction in Patients with Left Bundle Branch Block and Paced Rhythms

Clinical Course:

The physician tried to activate the cath lab, but that was unsuccessful. She was started on a nitroglycerin and heparin drip, and given full dose Aspirin. He was able to lower the BP to 140s systolic, and she became chest pain free. Cardiology did not want to cath her because she was chest pain free after nitro improved her blood pressure. He repeated the ECG again and it looked identical to the first one. 

So the ischemia resolved, by both symptoms and ECG, with nitroglycerin and BP lowering.

The initial hs troponin I returned at 117 ng/L, then rose to 274 ng/L, then 1064 ng/L, then 1681 ng/L.  

An echocardiogram was normal with 65% EF.

Next day angiogram showed: Severe diffuse atherosclerosis - 50-70% stenosis of LAD, prox ramus 70%, OM1 50%, RCA 20-30%.   I do not know whether a culprit was found.  She underwent 3x CABG (LIMA-pLAD, SVG-OM4, SVG-ramus).   TIMI flow is not given, but probably was TIMI-3 flow (good flow) in all arteries.


Our usual criteria for OMI is either an acute culprit lesion with TIMI 0-1-2 flow, or TIMI 3 with culprit and a peak hs troponin I of at least 10.0 ng/mL (equivalent to hs trop of 5000-10,000 ng/L) or troponin T of 1.0 ng/mL.  So this case does not meet our strict criteria for OMI.  Just having an intervenable culprit or lesion is not enough: there must also be <TIMI 3 flow, or a very high troponin.  

Wall motion: if there is very brief occlusion, wall motion can quickly recover.  Absence of a wall motion abnormality does NOT rule out OMI.

----In our study of 808 patients with suspicion for ACS, as the criteria were loosened (peak troponin level lowered), our sensitivity of the ECG for OMI diminished, and specificity increased; as criteria were more stringent (higher peak troponin required), sensitivity increased and specificity decreased).  See Figure 3 for examples.

Nevertheless, it is likely that the artery was occluded, or nearly so, at the time of the 2nd ECG, and then reperfused by the time of the 3rd ECG, which reverted to the non-ischemic 1st LBBB tracing.


MY Comment, by KEN GRAUER, MD (1/31/2022):


Important case by Dr. Smith for illustrating subtle but important differences in the 2 serial LBBB ECGs in this case. For clarity — I have placed the complete 12 leads of both tracings next to each other (Figure-1).

  • Dr. Smith has already drawn attention to the increase in the amount of J-point ST elevation in lead III of ECG #2.
  • As an additional feature to consider — I submit that ST-T wave morphology is clearly different between these 2 tracings — which immediately told me in this patient with typical chest pain that an acute event was in progress.
  • The KEY to comparison of serial tracings is to: i) Interpret the initial tracing first in its entirety; and thenii) Go lead-to-lead in your comparison of each of the 12 leads. 
  • Be SURE to check out QRS morphology in the 2 tracings you are comparing — since IF there has been an axis shift or difference in chest lead placement — this will need to be accounted for.

Applying this approach to the 2 ECGs in today's case (Figure-1):
  • QRS morphology in all 6 limb leads of ECGs #1 and #2 is quite similar! There is a slight difference in QRS morphology in lead V6 of ECG #2 — in that the QRS remains predominantly negative in lead V6 (whereas it was slightly more positive than negative in ECG #1). That said — overall QRS morphology is quite similar, which means that lead-to-lead comparison is valid!

  • Note in ECG #1 that smooth shape of ST-T waves in virtually all limb leads (slightly curved BLUE lines in ECG #1).
  • In contrast — note straightening of the ST segments in these same leads in ECG #2. Together with the increase in J-point ST elevation already noted by Dr. Smith — there is no doubt that at least 4 of the 6 limb leads in ECG #2 (short RED lines) are different. In a patient who clearly has underlying heart disease (virtually all patients with LBBB do!+ new onset "classic" chest pain — these ST-T wave morphology changes merit prompt cath!

Figure-1: Comparison of both 12-lead ECGs in today's case.

Friday, January 28, 2022

A man in his 60s with syncope. In syncope, what are we looking for on the ECG, and why?

 Submitted and written by Rachel Plate M.D., with some edits by Smith and Meyers


A man in his 60s with history of type 2 diabetes, obesity, obstructive sleep apnea requiring nightly CPAP, and hypertension presented for evaluation following a witnessed syncopal episode at home. The patient noted this occurred after standing and he did have prodromal symptoms including lightheadedness. EKG was obtained and shown below.

What do you think?



The ECG shows sinus rhythm a bifascicular block, both a right bundle branch block and a left anterior fascicular block. The P waves are hard to discern with the artifact present, but I believe there is also likely a prolonged PR interval, also called first-degree AV block (when this is present with bifascicular block, some people use the misnomer "trifascicular block").

There was an old ECG on file from years ago:

Only LAFB here, no RBBB. So the RBBB is new compared to prior.

Unfortunately, the clinicians did not recognize the danger of syncope with new bifascicular block (also probably with first-degree AV block). A urinalysis was ordered and it was reported to show UTI, and the patient was discharged home with antibiotics for UTI.

Two days later he had another syncopal episode at home, woke up on the floor, and again called 911. This time his ventricular rate was notably in the 30s in the ambulance. The following EKG was obtained. 


This ECG shows sinus P waves occurring regularly at about 100 bpm, with (most likely) high grade AV block resulting in conduction of only 1 of every 3 P waves, with a resultant ventricular heart rate of about 30-36 bpm. Notice how the QRS occurs at the same distance from the P wave each time - this greatly favors high grade second degree AV block, Mobitz II, over complete heart block with isorhythmic dissociation (in which it just happens to look like the P waves and QRS complexes are associated). Isorhythmic dissociation can be ruled out with a long rhythm strip. 


The distinction between high grade second degree AV block and third degree (complete) heart block is not very important, as this patient has already demonstrated high risk to deteriorate into fatal bradyarrhythmia. 

While the team was preparing atropine and transcutaneous pacing, the patient’s ventricular rate spontaneously improved. This EKG was obtained.


Now, we again note a bifascicular block with 1st degree AV block.


However, an hour later, he subsequently had another syncopal episode associated with asystole lasting 30 seconds after which he spontaneously reverted to complete heart block. No ECG or monitor strip was obtained during asystole.


Following, cardiology was able to place a temporary pacing wire and then a permanent pacemaker later the same morning. The patient was discharged after an uncomplicated hospital course on hospital day 2.


Here is his ECG after receiving a pacemaker:

The ECG starts in sinus rhythm with first degree AV block, then the sinus rate slows below the atrial pacer rate, and the pacemaker begins pacing the atria. The RBBB and LAFB morphology remains, of course. I am not sure why there appear to be two different atrial pacer spike morphologies. 


Learning Points

Syncope + new onset bifascicular block + historical concern for cardiac syncope warrants consideration that the cause of syncope could have been transient further deterioration of the conduction system, including complete heart block and/or asystole. Such a high-risk syncope patient should be recognized and admitted on telemetry for observation of further episodes and consideration of a permanent pacemaker. Deadly bradydysrhythmias due to conduction system failure is an especially preventable cause of death with the availability of the pacemaker.

I teach the "WOBBLER" mnemonic to my learners for syncope ECG evaluation. I believe this mnemonic is attributed to Cliff Reid at ( I find this to be an excellent way to keep the important ECG syncope findings in mind, and systematically search each of the many many syncope/lightheadedness/palpitations ECGs I see each shift.

WOBBLER stands for:


Obstructed AV pathway (meaning AV blocks)


Bifascicular block

LVH (including HOCM and other entities with LVH such as aortic stenosis)

Epsilon wave (ARVC)

Repolarization (both short and long QT)

Dr Smith wrote this fantastic post back in 2015 which I highly recommend for a review of the entire approach to ED syncope: 

Emergency Department Syncope Workup: After H and P, ECG is the Only Test Required for Every Patient.....

In this post he describes many high risk features in syncope on the ECG, including:

Long QT (at least 480-500 msec)
Brugada morphology
RV dysplasia (including epsilon wave)
Non-sinus rhythm
SVT or VT (obviously)
AV blocks
Sinus pauses of 2 seconds or more
RBBB with hemiblock (bifascicular block)
Any acute ischemia
Pathologic Q waves

Click here for 2 more trifascicular block cases:

Tuesday, January 25, 2022

Acute aphasia. What is the likely etiology?

A 60-something man without significant past history presented after sudden onset of aphasia 45 minutes prior.   There was also a report of a few days of abdominal pain, nausea and vomiting, and of not being himself.

BP was 165/80, pulse 110.  He had profound expressive aphasia but his motor exam was intact.

A stroke code was called and the patient underwent a CT stroke series.   Non-contrast scan showed no bleed and no evidence of infarct.  Cerebral CT angiography did not show a large vessel occlusion.

He was rapidly given tPA (alteplase).

An ECG was obtained (ECG-1):

What does it show?  Is this relevant to the stroke?

A previous was available from 6 years prior that was normal:

ECG-1: There is a QS-wave in V2, with ST Elevation and some T-wave inversion.  There is a tiny r-wave in V3, also with STE and TWI.  There is STE in V4 and V5, with some T-wave inversion.  Is this LV aneurysm?  Or acute MI?  Or subacute MI?

If there is a single lead in V1-V4 which has a T/QRS ratio > 0.36, then there is likely acute MI.  If the ratio is <0.36, it is likely old (LV aneurysm) or subacute; symptoms of >6 hours duration suggest subacute, and <6 hours as acute.  The ratio in lead V2 is 3.5/5.0 = 0.70, so this is an acute anterior MI.  The QS-wave suggests that it is nearly complete.  It could also be an old MI with superimposed acute LAD occlusion.

This is diagnostic of Anterior MI, acute or subacute, but not simply an old anterior MI with persistent STE (not just an LV aneurysm -- there is acute ischemia).  Acute transmural anterior MI puts patients at high risk of LV mural thrombus, which then can release thrombi and cause stroke or other arterial emboli.  

I remember the time in the early 1980s, when I was in medical school, when few patients received reperfusion therapy for STEMI/OMI, and thus most anterior MI progressed to completion (transmural) if they did not spontaneously reperfuse.   All of these patients were put on heparin to prevent mural thrombus.

The first hs troponin I returned at 8000 ng/L, confirming subacute anterior MI.

The patient went emergently to the cath lab and was found to have a 99% acute LAD stenosis with thrombus and TIMI III flow.  (Was it open because of the tPA?)  It was stented.  There was mild CAD in the RCA and LCx.

An echocardiogram showed a wall motion abnormality, and EF of 35%, consistent with a large LAD infarct and it showed a "possible" left ventricular mural thrombus.

Cardiac MRI:

Delayed enhancement sequences obtained at 10 mins after gadolinium administration reveal extensive and patchy subendocardial enhancement involving the mid to distal anterior wall and anteroseptal wall involving less than 50% thickness. There is also delayed enhancement in the apex, involving more than 50% of myocardial thickness.


1) Moderately decreased LV function (calculated ejection fraction of 33%) with large wall motion abnormality in the LAD territory.
2) No evidence for left ventricular thrombus. Large area of microvascular obstruction in the apex.
3) Large area of subendocardial delayed enhancement in the mid to distal anterior wall and distal septum, involving less than 50% of myocardial thickness. The LV apex shows transmural enhancement. These findings suggest apart from the apex the rest of the LAD territory is viable

Clinical Course:

The patient had an uneventful hospital course, was transferred to rehab, and later found dead in his bed shortly before discharge.

This illustrates that one of the longer term complications of myocardial infarction is sudden death, and it is not always predictable.  (However, the topic of preventing sudden death after myocardial infarction is a big one and beyond the scope of this blog post).  An autopsy was inconclusive, but did show "transmural infarct of the anterior and lateral walls," contradicting the MRI results, but consistent with the ECG.  

There was also some stenosis distal to the stent, and 80-85% RCA stenosis and 65-70% LCx stenosis.  The autopsy results of the coronaries is different from the angiogram results.  Why?  This probably reflects the problem with autopsy sections of coronary arteries: Because sections can reveal a large amount of extraluminal atherosclerosis, the stenosis appears to be much greater on pathologic section than on angiogram, which tells you only about the lumen of the artery, not the extraluminal plaque..  

I suspect that the patient had an arrhythmic death.

Learning Points:

1. An ECG is helpful in identifying the etiology of acute stroke.  If there is completed anterior MI, LV aneurysm, or atrial fibrillation, the etiology is likely to be embolic.

2. Completed anterior MI results in a profound wall motion abnormality. The resulting "stasis," combined with inflammation of infarction, creates a perfect environment for an LV mural thrombus, which puts the patient at risk for systemic emboli, including stroke and mesenteric ischemia.

3. Beware the risk of sudden arrhythmic death after acute MI, even when the artery has been stented and the acute ischemia has resolved.  That infarcted myocardium is a nidus of arrhythmia.  

4. tPA is not a contraindication to coronary angiography (in fact, tPA at a referral hospital before transfer to a PCI institution is recommended if first medical contact to PCI time will be greater than 120 minutes)

5. Myocardial infarction may have very nonspecific symptoms.  For this patient, they were abdominal pain, "not being himself," and nausea and vomiting.

6. Autopsy coronary stenosis is usually much greater than seen on angiography

Saturday, January 22, 2022

A man in his 40s with chest pain and T wave inversion

Written by Pendell Meyers with edits by Smith

A man in his early 40s with history of HTN presented to the ED for feeling lightheadedness and mild "beating" chest pain off and on last night, but resolved at the time of ED presentation. He still felt some lightheadedness during evaluation. He stated that he used ecstasy yesterday prior to the onset of symptoms. Vitals were within normal limits on arrival.

Here is his ED ECG on arrival:

What do you think?

Sinus rhythm. The narrow QRS with relatively high voltage is overall most consistent with a young healthy heart, less likely pathologic LVH (including HOCM). There are no signs of OMI or hyperkalemia. There are terminal T wave inversions present in V3 and V4. 

Most learners will not be able to distinguish these TWIs from Wellens' waves. But they are distinctly different and it is difficult to describe why we can tell that they are different. The morphology of the QRS complex itself helps me recognize this overall pattern.

First: What is Wellens' Syndrome?  It is: 1) An episode of anginal chest pain that has resolved, or is resolving. 2) An ECG that has preserved R-waves in V2-V4.  3) The ECG shows terminal T-wave inversion in some or all of V2-V4 ("Pattern A") or deep symmetric T-wave inversion ("Pattern B").  But not all T-wave inversions are equal!

This case and ECG was sent out to our little group of EKG nerds and all immediately recognized it as a normal variant, NOT as Wellens' syndrome.

Young people, especially men, can have a wide range of normal variants including normal variant STE ("early repol", etc.) and normal variant TWI ("persistent juvenile T wave pattern", "benign T wave inversion pattern", etc.). Unfortunately for learners, all of these patterns can change over time. Difference from a baseline ECG does not rule out a normal variant pattern.

This pattern in the ECG above does not fit perfectly into a described variant (it approaches the category of benign T wave inversion pattern), but I have seen many cases like it.

Here are some examples of true Wellens (anterior reperfusion) T waves (the first case will make some readers quite irritated because it looks so similar to the case above, but I promise with time and experience they look different):

A 40-something healthy male with transient chest squeezing

Classic Evolution of Wellens' T-waves over 26 hours

Back to the case:

The patient had a prior ECG on file from 6 months ago:

No TWI here. Tiny amount of normal variant STE in lateral leads. 

It is certainly appropriate to measure troponins, and so 3 serial high sensitivity troponin I measurements were all ⋖ 6 ng/L (below the limit of detection, normal 99% URL for men for this assay is 20 ng/L).

Repeat ECG 4 hours after arrival:

The T wave may be a tiny bit deeper in V3, but overall there is not much change.

Side by side is below.

Despite no further chest pain, no evolution of ECG findings, and three serial negative troponins, the ED team was concerned for Wellens. 

3 serial negative troponins should suffice in a case like this to rule out ACS.

However, the providers advised the patient that he should be admitted for further risk stratification. The patient declined and signed out against medical advice.

Learning Points:

There are many causes and patterns of T-wave inversion. And among them, many can mimic Wellens pattern (which is simply anterior reperfusion T wave inversion). There are some clinical features that help distinguish them, and expert ECG interpretation can help a great deal to distinguish them. Bottom line: see a bunch of them, follow up the results, and compare them to the cases we've posted - you will become great at it.

Normal variant patterns can change over time.

True reperfusion T wave inversions must evolve over time (must either progress through the reperfusion sequence of deepening T wave inversions, or resolve due to very brief reversible ischemia, or reocclude!). If any T wave inversion pattern does not evolve at all over serial ECGs, then it is not due to ischemia.

If a patient has reperfusion T waves that are evolving along the reperfusion sequence (becoming full T wave inversion and deeper), then there has been substantial ischemia even though there is some reperfusion, and Dr. Smith and I believe it is almost guaranteed that there will be a rise and fall detected in appropriately timed serial high sensitivity troponins.  

It is possible that this rise and fall in Wellens' might be below the URL; for example: 

Result:  < 6 ng/L  →  12 ng/L → 17 ng/L → 9 ng/L  →  < 6 ng/L 

See these other cases involving Wellens mimics:

A Very Elderly Male with a Fall and no Chest Pain

Comparison post:

More Cases of PseudoWellens:

Is it important to recognize LVH Pseudo-infarction patterns?

Pseudo-Wellens' Syndrome due to Left Ventricular Hypertrophy (LVH)

Tuesday, January 18, 2022

Which ACS had more myocardial damage? The one that meets STEMI criteria, or the one with the 'normal' ECG?

This case comes from Jesse McLaren, with some contribution by Smith.

Dr McLaren (@, is an Emergency Physician in Toronto with a special interest in emergency cardiology quality improvement and education.  He is an Assistant Professor at the University of Toronto.  

2 Cases

Two patients presented with chest pain. How would you interpret their ECGs, and which had the more myocardial damage?


Patient 1: 55yo with 5 days of intermittent chest pain, now constant. Normal vitals. 

Old, baseline, ECG

Today's acute ECG:

There is normal sinus rhythm, normal conduction, normal conduction, normal R wave progression and normal voltages. There is concave ST elevation in all three inferior leads meeting STEMI criteria, along with hyperacute T waves and reciprocal ST depression and T wave in inversion in aVL; ST depression and T wave inversion in V1-2 from posterior MI, and ST elevation and hyperacute T waves in V5-6 from lateral MI. 

This is an obvious infero-postero-lateral STEMI (+) OMI, identified by the machine and recognized by the emergency physician. The patient was treated with dual antiplatelets, heparin and nitro, and the cath lab was activated. 


Two minutes later the chest pain resolved and the ECG was repeated: 

This ECG, if it had been recorded in isolation, would be highly suspicious for acute ischemia, but not OMI

There is resolution of the inferolateral ST elevation but residual reciprocal ST depression in aVL, and mild precordial ST depression. 

Despite having a transient Occlusion, with ST segments that meet STEMI criteria, the patient was still sent to the cath lab, and before the procedure had another episode of chest pain with recurrence of infero-postero-lateral STEMI(+)OMI ECG:

On angiogram there was a 99% circumflex occlusion, but with TIMI-3 flow, which was stented. All troponins were completely normal, at 2 ng/L, just above the limit of detection (LoD).   (Abbott Alinity high sensitivity troponin assay, LoD = 1.6 ng/L; URL = 26 ng/L for men, 16 ng/L for women).   

Notice that we never called this a "STEMI" because it never actually met the definition of acute MI!!

The definition of MI requires at least one elevated troponin, so the patient actually "ruled out" for acute MI!


Post cath ECG:

Returned to baseline, without Q waves or reperfusion T wave inversion. 

By itself, this would be a non-diagnostic ECG.  

Discharge diagnosis: "STEMI" (technically NOT)

Imagine if that first ECG had never been recorded.  This patient could have been sent home, then re-infarcted at home and died.

Unstable Angina Still Exists!!
Unstable Angina may have transient ST Elevation


Patient 2: 65yo with 30 minutes of chest pain and normal vitals. Old then new ECG:


There is normal sinus rhythm, with 1st degree AV block and otherwise normal conduction, normal axis, normal R wave progression, normal voltages. 


Compared to prior there is subtle concave inferior ST elevation which does not meet STEMI criteria. But there are also inferior hyperacute T waves (large relative to the QRS complex and compared to baseline), and there is new primary reciprocal ST depression and T wave inversion in aVL, which is highly sensitive for inferior OMI. There may also be some pseudonormalization of the ST segment in V2 from posterior MI.

Despite being STEMI negative and labeled normal by the machine, the physician was concerned so gave aspirin and the ECG was repeated 20 minutes after the first:


ECG is similar and patient had ongoing pain. Treated with dual antiplatelets, heparin and cath lab activation: 100% mid RCA occlusion. First trop 26 (borderline normal) and peak 55,000, with inferior basal hypokinesis. 

A peak troponin I of 55,000 ng/L is a level that is associated with very large acute MI (lots of myocardial loss).

Discharge ECG: 

Inferior QS waves and reperfusion T wave inversion, with reciprocal large T wave in aVL; and large T wave in V2-3 reciprocal to posterior reperfusion T wave inversion. 




According to the current paradigm based on ECG millimeter criteria, the first patient had STEMI  requiring emergent reperfusion while the second did not have STEMI so could have been treated with delayed reperfusion. But the second patient had a totally occluded artery leading to a large MI despite rapid reperfusion, and admitting them as “NSTEMI” with next day angiography could have been fatal. According to the discharge summaries, which seemed to be based on culprit lesions that received rapid reperfusion, both patients had “STEMI” despite the first never having a rise in troponin and the second not meeting STEMI criteria.


We need to start with the underlying pathology. Both patients presented to the ED with Occlusion MI, i.e. “acute occlusion or near occlusion of a major epicardial coronary vessel with insufficient collateral circulation, resulting in imminent necrosis of downstream myocardium without emergent reperfusion.” Both patients also had ECGs diagnostic of OMI on ED presentation: rather than falsely separating these ECGs into STEMI vs NSTEMI based on ST elevation millimeter criteria, we can see that they both had some degree of inferior ST elevation along with hyperacute T waves and reciprocal change in aVL. Both STEMI(+)OMI and STEMI(-)OMI have similar clinical, laboratory and echocardiographic features.

These cases had different outcomes, not based on which met STEMI criteria, but based on which OMI had rapid reperfusion. 

The first patient presented with STEMI(+)OMI but had such rapid spontaneous reperfusion, followed by angiography, that they avoided myocardial necrosis completely—without a rise in troponin or ECG evidence of infarction or reperfusion. (But if this “transient STEMI” had not had rapid cath lab activation, they might have re-occluded and developed a preventable infarct).   

In fact, this case does not even meet the formal definition of myocardial infarction (!), by the 4th Universal Definition, which requires a rise and fall of troponin with one value above the 99th percentiile.  It is, in fact, ST Elevation Unstable Angina.  Had the patient had ECGs recorded at different moments, this would have been entirely missed 

The second patient presented with STEMI(-)OMI but had a total occlusion that persisted despite initial management and was only relieved in the cath lab—with a resulting significant rise in troponin despite rapid diagnosis, and ECG evidence of infarction and reperfusion. Instead of these patients both having a discharge diagnosis of “STEMI”, the first had unstable angina from “OMI that is so brief or so quickly treated that troponins do not rise, MI prevented”, while the second had STEMI(-)OMI.



Take home

1.     Automated interpretation is unreliable, even those labeled “normal”

2.     STEMI criteria has poor sensitivity for Occlusion MI

3.     Primary reciprocal ST depression in aVL is highly sensitive for inferior OMI, and can highlight subtle inferior ST elevation and hyperacute T waves 

4.     Acute coronary occlusion is a dynamic process that can spontaneously reperfuse and reocclude, and "transient STEMIs" are at risk for reocclusion

5.     Initial troponins are unreliable for STEMI/OMI, and serial troponins can miss unstable angina from transient occlusions

6.     MIs should be classified based on the underlying pathology of OMI/NOMI, not STEMI/NSTEMI criteria, and this should be reflected in the discharge diagnosis to accurately track and learn from cases



1.     Bischof et al. ST depression in aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med 2016

2.     Meyers et al. Comparison of the ST-elevation myocardial infarction (STEMI) vs NSTEMI and Occlusion MI (OMI) vs NOMI paradigms of acute MI. J of Emerg Med 2021


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