What do you think of these 2 ECGs in patients with chest pain? How to approach these?

What do you think of these 2 ECGs in patients with chest pain?  How to approach these?

ECG 1 (sent to my by Sam Ghali @EM_resus)

ECG 2

ECG 1 

This was sent to me with no clinical information and the question "what do you think?"  

My answer was: "sinus rhythm with right atrial enlargement, probable right ventricular hypertrophy, and old inferior MI with inferior LV aneurysm."  The T-wave inversion in I and aVL is reciprocal to the Old inferior aneurysm.

After I sent my answer, I received this history:

66 yo man presented with chest pain

History of CAD [unclear details out of state, stent(s)?]

STEMI alerted pre-hospital

Found to have very elevated lactate

Significant AKI

Aortic thrombus (chronic) on CT

hS Trop T:   1609->2471->1929 ng/L

Cards was planning on  cath when metabolic situation settled

Angiogram: no culprit and all open arteries.

Final diagnosis: type II MI due to illness

The Queen of Hearts said "OMI with mid confidence."  Version 1 of the Queen does not do a good job of recognizing LV aneurysm morphology, whether it is anterior (which for an expert is not too difficult because they almost always have QS-waves) or inferior (which is even very difficult much of the time for me, because inferior aneurysm frequently has QR-waves)

How to approach?  --when the diagnosis could be "ST Elevation due to Old MI" or "LV Aneurysm Morphology", it is essential to look into the old charts and old ECGs, if available.  It is also essential to assess for other etiologies of the symptoms, and in this case the patient had physiological derangement, with elevated lactate and AKI.  This points to another inciting etiology rather than ACS as the primary mover.  

These physiological derangements do not rule out ACS, but make it much more likely that the patients illness was incited by another factor.

ECG 2

I was reading ECGs on the system and came across ECG 2 and said out loud: "This is a fake."  A colleague sitting next to me asked "why?", and I answered that there is a "saddleback" in lead III and well-formed Q-wave.  Saddleback ST elevation is rarely due to OMI. 

However, on very few occasions Saddleback STE actually is due to OMI.

The Queen of Hearts had stated "Not OMI with low confidence"

There was a previous ECG available:

This confirmed my opinion.

I found out later that the patient had gone to the cath lab.  And I found out that the cath lab activation was a result of this follow up ECG:

I find this to be a negative ECG, except that there is now new ST Depression in V4-V6.

However, there is new tachycardia, and that new ST depression could be a result of supply-demand ischemia from tachycardia.

This time, the Queen of Hearts diagnosed this as "OMI with High Confidence."

This Queen interpretation led to a false positive cath lab activation.

Alternative Management: Always look into the patient's chart!! (including the old ECG above, which was not seen)

In fact, I found that I had blogged this patient before (!!!) due to the ECG that looked like inferior aneurysm.  There were many previous similar ECGs.  Here is that post: 

A Patient with Vertigo

Angiogram 3 months ago:

Severe three vessel native CAD with occlusion of the mid-Cx, mid-LAD, and mid-RCA including several areas of in-stent stenosis or occlusion.  4/4 patent bypass grafts (RIMA > dLAD, LIMA > OM, SVG > rPDA, and free radial > rPLA1) with severe native vessel stenosis just beyond the anastomosis in the dLAD, OM, and rPDA

Previous coronary disease and h/o CABG tells you that there probably is an old infarct and that the baseline ECG is likely to be abnormal and that you should read the present ECG in that context.

Previous Echo:

Normal left ventricular cavity size, mildly increased wall thickness and moderate LV systolic dysfunction.

The estimated left ventricular ejection fraction is 35-40 %.

Regional wall motion abnormality- basal inferior akinetic.

Regional wall motion abnormality- basal inferolateral, akinetic.

Regional wall motion abnormality-apex small .

An Akinetic wall can have the same "LV aneurysm" Morphology as a Dyskinetic wall ("diastolic dyskinesis" is the echo definition of aneurysm.)

The cath lab was activated and there was no acute OMI.  False Positive.

Discussion:

These are very complex cases in which there could be OMI or there could be old MI.  These are the kind of cases in which you want to consult your friendly cardiologist and have a discussion.  But that is only if your cardiologists accept the idea of OMI (Acute Coronary Occlusion in the Absence of ST Elevation criteria).  To make such a consultation,  there must be mutual trust that the consultant will not dismiss your concerns or say "Nah, couldn't be."

It can take years to build such trust.

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MY Comment, by KEN GRAUER, MD (7/30/2024):

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The "theme" of My Comment in today's case is — Shape is KEY!

• For clarity and ease of comparison in Figure-1 — I've labeled and put together the initial 2 ECGs in today's case.

MY Thoughts on ECG #1:

This is a complex tracing. I saw the following:

• There is significant baseline artifact. This is relevant to our interpretation given the difficulty it poses for assessment of ST-T wave changes in multiple leads.
• That said — the rhythm is clearly sinus with a normal PR interval.
• QRS morphology is not normal. That said — the QRS is really not wide (ie, not more than 0.10 second). Given the all upright QRS complex in lead V1, with narrow but definite terminal S waves in lateral leads I and V6 — this QRS morphology is consistent with IRBBB (Incomplete Right Bundle Branch Block).
• The QTc is prolonged (I measure the QT at ~0.44 second — which corrected for the rate of ~80/minute, comes out to a QTc ~0.49 second).
• There is marked LAD (Left Axis Deviation) — with entirely negative QRS complexes in each of the inferior leads. This is consistent with LAHB (Left Anterior HemiBlock).
• There is RAA (Right Atrial Abnormality) — as determined by the presence of tall, peaked and pointed P waves in the inferior leads (ie, P waves ≥2.5 mm in amplitude).
• There may be RVH (Right Ventricular Hypertrophy) — which always needs to be considered if there is true right atrial enlargement. Because of the artifiact — we can not tell if QRS morphology in lead V1 is triphasic (rsR') or represents a qR pattern, which could be consistent with pulmonary hypertension (for more on RAA, RVH — See My Comment in the February 12, 2023 post).
• There may be LVH by Peguero criteria (See My Comment in the June 20, 2020 post) — as suggested by the very deep S waves in leads V3 and V4 (with the PURPLE arrow in lead V3 showing that S wave amplitude is cut off in this lead).

Regarding Q-R-S-T Changes:

• More than inferior Q waves — there is marked fragmentation on each downslope of the S wave in the inferior leads (RED arrows in these leads). It is because of this marked fragmentation that the “attempt” to form a positive deflection in each inferior lead never makes it back to the baseline before being overtaken by resumption of S wave negativity. In my experience — this fragmented QRS shape in any one (let alone all 3) of the inferior leads strongly suggests inferior infarction at some point in time.
• Regarding R wave progression — I interpreted the seemingly multi-phasic upright complex in lead V1 as the result of IRBBB rather than RVH because: i) There is marked LAD with no more than modest depth of the S wave in lead I; and, ii) I thought the overall ECG picture more suggestive of coronary disease rather than RVH. Yet predominant positivity never occurs in the lateral chest leads — and I could not rule out the possibility of RVH on this ECG alone.
• The shape of the S-T segments in the inferior leads is coved, of relatively long duration, and shows slight ST elevation. This shape forms a “picture to remember” — that does not look acute. That this inferior lead ST-T wave appearance is unlikely to be acute — is further supported by a lack of reciprocal ST depression in high-lateral leads I and aVL. Instead (as per Dr. Smith) — this “picture” strongly suggests inferior wall aneurysm, especially given the inferior lead S wave fragmentation marker of prior inferior MI described above.
• Finally — there is ST segment straightening and depression beginning in lead V3 beyond that expected for simple IRBBB (BLUE arrows in the chest leads).

BOTTOM Line: Like Dr. Smith — as a single ECG that I interpreted knowing only that the patient had "chest pain" — I thought ECG #1 did not look acute. But there are multiple complexities that beg further explanation.

• I suspected prior inferior MI with IRBBB/LAHB — and now with inferior wall aneurysm. There is ST depression in leads V3-thru-V5 that I thought likely to reflect multi-vessel disease — but with need to explain the reason for RAA, probable LVH, and possible RVH. But – not an OMI.
• As per Dr. Smith — this patient turned out to have Troponin elevation due to Type-2 MI (clean coronaries on cath). Instead — his clinical presentation was dominated by acute renal failure with severe acidosis. We are left with more questions than answers (ie, How severe is his underlying coronary disease? Any RVH or pulmonary hypertension?) — but this is not the ECG of acute coronary conclusion.
• Personal NOTE: I have been fooled more than once by chest pain in the setting of severe underlying disease (ie, acidosis, sepsis). The KEY is to recognize that ECG #1 is unlikely to represent an acute OMI — with clinical priority to treat underlying conditions, and to then reassess symptoms and repeat ECGs as needed.

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

MY Thoughts on ECG #2:

I found today’s 2nd tracing easier to interpret — in that there were far fewer complicating findings.

• The rhythm is sinus — with normal intervals (PR-QRS-QTc). There is LAD (negative QRS in lead aVF) — but an axis not leftward enough to qualify as LAHB (predominant positivity in lead II).
• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• There are very large and wide Q waves in leads III and aVF — with a small-but-present Q wave in lead II (RED arrows in these leads). This patient has had inferior infarction at some point in time.
• R wave progression shows slight delay in transition (the R wave only becomes taller than the S wave is deep between lead V4-to-V5).
• S-T elevation is seen in each of the inferior leads, followed by a prominent upright T wave. That said — the shape of the elevated inferior lead ST segments manifests an upward concavity (ie, "smiley" configuration). As per Dr. Smith — this shape is less likely to represent an acute cardiac event.
• Although both high-lateral leads ( = leads I and aVL) manifest ST depression — the precise mirror-image opposite ST-T wave picture from lead III — is seen in lead aVL (within the BLUE rectangle, in which I merely inverted one QRST complex from lead III). This to me suggested a similar acuity (or lack thereof) for both lead aVL and the inferior leads.
• There is slight, nonspecific ST-T wave flattening in leads V1,V2 and V6.

BOTTOM Line: Once again, as a single ECG that I interpreted knowing only that the patient had “chest pain” — I thought ECG #2 did not look acute. 

• The deep, wide Q waves in leads III and aVF (with small-but-present Q in lead II) — strongly suggest prior infarction. This patient almost certainly does have underlying coronary disease. Clinically, if I was managing this patient — more information would clearly be needed (ie, specifics of the history; repeat ECG; troponins; comparison with prior tracings, etc.). But as a single ECG without the benefit of more information — the shape of these inferior lead ST segments — and the lack in the chest leads of any suggestion of associated acute posterior involvement — suggest this is not the result of acute coronary conclusion.
• As per Dr. Smith — review of this patient's chart told the story. Not surprisingly — the patient had very severe underlying coronary disease — but no acute OMI.

 

Chest pain and a computer ‘normal’ ECG. Therefore, there is no need for a physician to look at this ECG.

Written by Jesse McLaren, comments by Smith

A 55 year old with a history of NSTEMI presented with two hours of exertional chest pain, with normal vitals. Below is the triage ECG, with a computer interpretation (Marquette 12 SL) of “normal” which was confirmed by the over-reading cardiologist.

What do you think? 

Should this patient continue to stay in the waiting room, without interruption of the physician to interpret the ECG, because the computer interpretation is normal?

Interpretation by the GE/Marquette 12 SL conventional algorithm

Smith: This article, published this month (!), tells us that we physicians do not need to even look at this ECG until the patient is placed in a room because the computer says it is normal:

Validity of Computer-interpreted “Normal” and “Otherwise Normal” ECG in Emergency Department Triage Patients

I reviewed this article for a different journal and recommended rejection and it was rejected.  There were zero patients in this study with a "normal" ECG who had any kind of ACS!  This defies all previous data on acute MI which would show that even undetectable troponins do not have a 100% negative predictive value.  So this study is actually worthless.  

On the other hand, if the physician is unable to recognize subtle OMI, as is the case with the overreading cardiologist, then the conclusion would be correct.

_____________

ECG analysis

There’s normal sinus rhythm, normal conduction, normal axis, normal R wave and normal voltages. What sticks out is the ST depression in aVL, which is reciprocal to subtle inferior ST elevation and bulky T waves.  There is also a down-up T-wave in aVL, which makes aVL even more diagnostic.  This is diagnostic is inferior OMI, accompanied by inferior Q waves, and with a flat ST segment in V2 that could indicate posterior extension.

Old ‘NSTEMI’

A history of coronary artery disease and a stent to the same territory further increases pre-test likelihood of acute coronary occlusion, including in-stent thrombosis. It’s also possible that the old inferior MI left residual ST elevation and reciprocal ST depression, which can difficult to differentiate from acute OMI.

The patient had a history of ‘NSTEMI’ a decade prior, with an RCA stent. Does this change your interpretation? 

_________

Smith: Old inferior MI with persistent ST Elevation ("inferior aneurysm") has well-formed Q-waves.  In inferior aneurysm, we usually see QR-waves, whereas for anterior aneurysm, we see QS-waves (no R- or r-wave at all!).  This ECG has Q-waves, but they are not very wide nor very deep, and so I doubt that the inferior STE is due to old MI.

See these posts: 

Chest Pain, ST Elevation, and an Elevated Troponin: Should we Activate the Cath Lab?

Tachycardia must make you doubt an ACS or STEMI diagnosis; put it all in clinical context

Pulmonary Edema, Hypertension, and ST Elevation 2 Days After Stenting for Inferior STEMI

_________________

There’s limited information from the NSTEMI decade ago, except that the cath report describes a critical RCA stenosis treated with a stent, and the following discharge ECG:

This shows inferior Q and inferoposterior reperfusion, corresponding to RCA territory. So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. A couple of years later these ECG changes resolved, except for small inferior Q waves, leaving an almost normal baseline ECG. Below are the baseline and new ECG from the current patient presentation:

This confirms that the new ECG represented acute inferoposterior OMI: the inferior ST segments have straightened, increase the area under the curve of the T waves, there is new ST depression in aVL which is highly sensitive for inferior OMI, and there’s flattening of the ST segment in V2. 

But the ECG was labeled 'normal', and the patient waited to be seen.

 

New ‘NSTEMI’

Two hours later the first troponin I returned at 450 ng/L (normal <26 in males and <16 in females), which flagged the patient to be seen. By this time their pain had spontaneously resolved, and another ECG was done which was also interpreted as normal. What do you think?

On its own this ECG is nonspecific, with in isolated T wave inversion in III. But compared to the previous ECG the inferior T waves have deflated, the ST depression in aVL has resolved, and the ST segment in V2 is no longer flat and has a taller T wave. This confirms that the previous ECG with pain represented inferoposterior OMI, and that the current ECG with resolved pain represents reperfusion.

So the patient had a transient acute coronary occlusion that spontaneously reperfused but is at risk for reocclusion. The patient was admitted as ‘NSTEMI’ which is supposed to represent a non-occlusive MI, but the underlying pathophysiology is analogous to a transient STEMI. Fortunately the patient did not reocclude while awaiting the angiogram. Next day ECG showed ongoing reperfusion:

Angiogram found 90% RCA in-stent thrombus corresponding to the ECG, peak troponin was 12,000 ng/L which is a sizable infarct, and echo showed new inferior wall hypokinesis. This retrospectively confirms the diagnosis of OMI, yet the patient had a discharge diagnosis of ‘NSTEMI’.

Discharge ECGs showed inferior Q waves, and now very obvious inferoposterior reperfusion T wave inversion (the same pattern as after their prior ‘NSTEMI’): TWI in III/aVF with reciprocal tall T waves in aVL, and tall T wave in V2 reciprocal to posterior TWI:

Below are the baseline ECG(#1),  ECG with occlusion (#2), and follow up ECGs with progressive reperfusion – from initial normalization (#3)to progressive reperfusion TWI (#4-5):

STEMI vs OMI

Another study has claimed that computer interpreted ‘normal’ ECGs can “safely wait for physician interpretation until the time of patient evaluation without delaying an acute STEMI diagnosis.” (Deutch et al. Validity of computer-interpreted ‘normal’ or ‘otherwise normal’ ECG in emergency department triage pateints. West J Emerg Med 2024). They compared computer interpretations with cardiologist interpretations and final diagnosis of STEMI, and found a Marquettte 12 12SL had 100% negative predictive value of STEMI. But in this case, the ECG did not meet STEMI criteria and therefore the patient did not get emergent reperfusion and did not have a diagnosis of STEMI, so their ‘normal’ ECG (also by Marquette 12 SL) would be considered valid despite the patient having an acute coronary occlusion that was visible on ECG. Fortunately they spontaneously reperfused, or else they could have had a worse outcome, but deferring all ‘normal’ ECGs will perpetuate delayed diagnosis and reperfusion for STEMI(-)OMI.

As Deutch et al note in the limitations section, their study “does not directly address other outcomes of interest to an emergency physician such as acute coronary occlusion MI (OMI) which may benefit from timely reperfusion therapy…Moreover, there is a growing body of literature supporting a paradigm shift from evaluating ECGs for STEMI vs no STEMI as an indicator of OMI that may benefit from emergent reperfusion to evaluating ECGs for signs acute total OMI (inclusive of STEMI negative OMI) vs non-OMI.”

This same body of literature has highlighted the hazards of computer-interpreted ‘normal’ ECGs – including dozens of cases on this blog and a 7-year retrospective review that found 4% of true positive Code STEMIs presented with an ECG labeled ‘normal’ by computer interpretation—many of which were identified in real time despite the false reassurance of the computer interpretation and had rapid reperfusion. This 4% is underestimation because it only included patients admitted as STEMI not those admitted as NSTEMI like the case above.

Rather that comparing conventional computer interpretations with STEMI criteria, the real goal standard should be patient outcome of OMI, and then AI can be trained to look for subtle signs of occlusion. I sent the first three ECGs to the Queen of Hearts: even without comparison to baseline the first ECG was identified as OMI, the second was called Not OMI because it had normalized, and the third was called ‘OMI’ because the Queen is currently trained to apply this label to reperfused OMI as well. Future versions will be able to integrate serial ECGs, and differentiate between OMI and reperfused OMI.

Let's look at explainability for that first ECG:

You can see that it is aVL which the Queen is most concerned about.

 She diagnoses OMI with high confidence.

She was correct

And this is in an EKG that the conventional algorithm diagnosed as completely normal!!  

That algorithm could at least have given a diagnosis of "Nonspecific ST-T abnormalities", but it could not even do that!!

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Take away

1.     Computer interpretations of ‘normal’ are based on STEMI criteria, which will miss STEMI(-)OMI

2.     ‘NSTEMI’ does not differentiate between occlusion, reperfusion at risk of reocclusion, and non-occlusive MI

3.     Patterns of occlusion and reperfusion can be learned and taught, including to AI

4.  The Queen of Hearts not only recognizes this "normal" ECG as not normal, but correctly diagnoses OMI with High Confidence

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MY Comment, by KEN GRAUER, MD (1/27/2023):

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Superbly illustrated case by Dr. Jesse McLaren — showing that serial ECGs called "normal" and "NSTEMI" were in reality diagnostic of prior and current OMIs, including evolving patterns of reperfusion.

• To Emphasize: In a patient with new CP (Chest Pain) — the oversight of calling the initial ECG in today's case "normal" — is a mistake that should not be made.
• 
  
• For clarity — I've labeled this initial ECG in Figure-1.

Figure-1: I've labeled the initial ECG in the ED.

KEY Findings in the History:

As per Dr. McLaren, despite a past history of prior MI — and a presenting history of 2 hours of new CP — ECG #1 in Figure-1 was interpreted as "normal" by the cardiologist overreading the computer interpretation — and — this patient was left in the waiting room without his/her ECG being immediately interpreted by the ED physician.

• KEY Point: All patients who present to the ED for new CP should promptly have a triage ECG recorded, that is then immediately interpreted by the ED physician. Today's case illustrates what happens when this procedure isn't followed. It literally should take an experienced ED phsyician minimal seconds to interpret the initial ECG of a patient with new CP.
• Cardiologists assigned to overreading the initial ECG of a patient with new CP should: i) Not allow themselves to be biased by what the computer says until they have independently interpreted the ECG; and, ii) Account for the clinical reality that a patient who presents to the ED for new CP is by definition in a "high-prevalence" group with significantly increased likelihood of having an acute event — especially if this patient has a history of a prior MI (as in today's case). As a result — even subtle ECG abnormalities have to be assumed acute — until proven otherwise (which was obviously not done in today's case).

KEY Findings in the Initial ECG:

In a patient with new CP — emergency providers should pick up on the following ECG findings within seconds:

• The shape of the ST-T wave in lead V2 (within the RED rectangle in this lead). As we often emphasize — there normally should be gentle upsloping with slight elevation of the ST segment in leads V2 and V3. When this normal feature is lost in one or both of these anterior leads in a patient with new CP — and is replaced by an isoelectric or slightly depressed ST segment — posterior OMI should be strongly considered until proven otherwise.  
• Not only is the ST segment in lead V2 of Figure-1 isoelectric and straightened — but there is abnormal angulation between this straightened ST segment and the taller-than-expected T wave in this lead V2. The shape of the ST-T wave in this lead V2 is a "face" that should be instantly recognized as abnormal in a patient with new CP.
• Confirmation that the ST-T wave in lead V2 is abnormal — is forthcoming by the obviously "hypervoluminous" T wave in neighboring lead V3 (within the BLUE rectangle in this lead — with the dotted BLUE line showing that this T wave in V3 is even taller than the R wave in this lead).

Abnormal Findings in the Limb Leads of Figure-1:

• I've enclosed within the RED rectangle in lead aVL the KEY limb lead change that should immediately catch your attention. In a patient with new CP — there is no way that the downsloping ST depression with terminal biphasic (down-up) T waves in this lead can be normal (RED arrows in lead aVL).
• The fact that the ST-T wave in lead aVL is definitely abnormal — should heighten your attention to ST-T wave appearance in the inferior leads, since there is so often that "magical" reciprocal (mirror-image opposite) relationship between the ST-T wave deviation in lead aVL vs lead III (as well as in the other 2 inferior leads = leads II and aVF).
• In this context — the subtle-but-real "fattening" of the peak of the T wave in each of the inferior leads (upright BLUE arrows in these leads) — with subtle straightening of the ST segment takeoff and a hint of J-point ST elevation in leads II,III,aVF is abnormal until proven otherwise.

Are the Q waves in the inferior leads of Figure-1 "significant"?

• Over the years — various definitions have been proposed for what should constitute a "significant" Q wave, based on width and/or depth of the Q wave. The obvious implication of such definitions — is that IF a given Q wave is deemed "significant" because it satisfies a certain millimeter-based definition — that this then indicates infarction has occurred at some point in time.
• I feel such definitions are misleading because: i) Rather than some millimeter-based global definition for Q wave "significance" — other factors defy such generalization (ie, Relative size of the QRS in the lead being looked at in context with the presence or absence of Q waves in neighboring leads); ii) Q waves are not necessarily a permanent finding following infarction — in that what used to be a very large Q wave may with time decrease in size (and even disappear); iii) Axis shift and/or inconsistant chest electrode lead placement may influence both the presence and dimensions of any Q waves seen; and, iv) The angle of the bed at the time the ECG was recorded may also a influence whether or not Q waves are seen.
• BOTTOM Line: In my opinion — there is no perfect definition for what constitutes a "significant" Q wave (ie, a Q wave that indicates infarction has occurred at some point in time). Instead — this is a qualitative judgment to be made by the experienced clinician on the basis of a series of factors. My initial impression regarding the inferior Q waves in Figure-1 (which I arrived at before having seen prior tracings on today's patient) — was that these Q waves are not "deep" (considering the relatively tall R waves in leads II,III,aVF) — but that these Q waves are wider-than-I-would-normally-expect — and therefore, provide yet one additional ECG feature consistent with inferior infarction at some point in time. 

Syncope While Driving. Activate the Cath Lab?

A 50-something had syncope while driving. 

He was belted and it was low speed.  He had a prehospital ECG.  He was ambulatory at the scene.  He has a history of STEMI and heart failure.  The medics stated he had been nauseated and diaphoretic, but he did not have any chest pain or SOB. 

They recorded a prehospital ECG:

What do you think?

I read this blinded, with no clinical information, and read it as inferior OMI.  There is STE in inferior leads with a large T-wave and reciprocal ST depression in aVL with a reciprocally inverted T-wave.  It is all but diagnostic of OMI.  

The only alternative is old inferior MI with persistent ST-Elevation, or inferior aneurysm morphology.  Inferior Aneurysm morphology is incredibly hard to differentiate from Acute OMI, but you should suspect it whenever there are well-formed inferior Q-waves.  Unlike anterior aneurysm, a QS-wave is uncommon.   A QR-wave is far more common, just like you would see in inferior ACUTE OMI.   

And especially suspect Old MI when the patient gives a history of MI and has no chest pain or SOB.

The Queen of Hearts interprets it blinded also (no clinical information and no previous ECGs or serial ECGs).  This will be changed for future versions. 

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

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Case continued

The conventional algorithm diagnosed ***STEMI*** and so did the paramedics.

The patient was given full dose aspirin and the medics activated the Cath Lab. 

What do you think about cath lab activation?

On arrival in the ED, the patient denied any symptoms at all. 

No chest pain, no shortness of breath, no back pain, no numbness, weakness, tingling, no seizures or history of seizures, 

First ED ECG

This still shows apparent inferior OMI.

The Queen agrees:

Because the patient had no symptoms, the diagnosis of OMI was doubted, and the providers were able to access a recent previous ECG:

Old ECG, most recent

Also appears to show inferior OMI, though because there is less STE, it appears to NOT be as acute as the above.

And then a slightly more remote past ECG

Old inferior MI

The patient's previous echocardiogram report was viewed:

Decreased LV systolic performance, estimated left ventricular ejection fraction is 35%.

Regional wall motion abnormality- inferior and inferolateral.

A Coronary angiogram from 8 years prior revealed that he had had an inferior posterior STEMI at the time due to 100% occlusion of the proximal RCA.

Here is the ECG from that visit:

Inferior-posterior-lateral OMI, already with well-formed Q-waves

And here is the post PCI next day ECG:

Q-waves persist

Notice the inverted reperfusion T-waves in inferior and lateral leads.

Notice the increased amplitude of the T-wave in V2 (posterior reperfusion)

The T-wave inversion will almost always normalize over weeks to months, leaving only the Q-waves behind.

And that is what we see in the presenting 2 ECGs at the top.

Case continued

The patient underwent an emergency formal echocardiogram and it was unchanged. 

Cath Lab activation was cancelled.

The patient ruled out by serial troponins.

Learning Points:

1.  When the patient has only syncope as a symptom, you should doubt the diagnosis of OMI, and seek other sources of information: Old ECGs, serial ECGs, Echocardiograms, angiogram reports.  

2.  The pretest probability of syncope without any other symptoms, for OMI, is low

3. Inferior aneurysm morphology is incredibly hard to differentiate from Acute OMI, but you should suspect it whenever there are well-formed inferior Q-waves.  Unlike anterior aneurysm, a QS-wave is uncommon.   A QR-wave is far more common, just like you would see in inferior ACUTE OMI.

4. Version 1 of the Queen of Hearts only sees one ECG out of context.  That will be improved in later versions!!

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MY Comment, by KEN GRAUER, MD (12/9/2023):

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Today’s case brings with it an important lesson — namely that the “right answer” (and the “right” clinical action) — will not always be correct. My 1st, 2nd and 3rd impressions of today’s initial ECG (which like Dr. Smith and QOH — I interpreted without benefit of any clinical information) — was, acute OMI until proven otherwise.

• Acute OMI until proven otherwise is the "correct" answer — even though it turns out that this patient was not having an acute OMI.
• 
  
• This brings home a 2nd important lesson in today’s case — namely, that the History (both the past medical history — as well as the history of today’s presentation) — is an essential component of clinical ECG interpretation. Today’s patient has no CP (Chest Pain) — and once prior ECGs were discovered, it became apparent that as acute as today’s initial tracing may have seemed — the changes were not new!

The above said — I thought it may be insightful to review the initial pre-hospital ECG, which has to be interpreted as an acute OMI until proven otherwise.

• Dr. Smith did prove otherwise — and so we all gain from this case the experience of how appearances can be deceiving.
• BUT — the “correct” interpretation of this initial ECG remains, “Acute OMI until proven otherwise” — and IF this patient had with new-onset worrisome CP — strong consideration of prompt cardiac cath would be the "correct" action.

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TAKE another LOOK at today’s initial tracing — that for clarity, I have digitalized and reproduced in Figure-1.

QUESTION: 

• In addition to the large (wide) inferior lead Q waves + inferior ST elevation + reciprocal high-lateral lead ST-T wave depression (in leads I and aVL) — WHAT ELSE did I see that initially convinced me of an acute OMI until proven otherwise?

Figure-1: The initial ECG in today's case — obtained by the EMS team. (To improve visualization — I've digitized the original ECG using PMcardio).

Why ECG #1 Looks Acute ...

In addition to the acute-looking limb lead changes in Figure-1 — I've labeled several chest lead changes that convinced me that this tracing looks acute until proven otherwise. These include:

• Especially the QRST complex in lead V3 (within the RED rectangle) — because of unmistakeable ST segment flattening (instead of the usual gental upsloping slight ST elevation normally seen in this lead) — in association with a disproportionately "hypervoluminous" T wave in this lead (that is "fatter"-at-its-peak and wider-at-its-base than expected given the size of the R wave in this lead).

By the concept of "neighboring leads" — given clear abnormalities in lead V3 — the ST-T waves in leads V2 and V4 are also abnormal.

• Like lead V3 — the ST segment in lead V2 is normally slightly elevated and gently upsloping. Instead — the ST segment in lead V2 is isoelectric and unmistakeably flat (RED arrow in both leads V2,V3).
• By itself — I would not necessarily interpret the ST-T wave in lead V4 as abnormal. But in the context of clearly abnormal leads V2 and V3 — the ST segment in lead V4 looks "straight", which results in accentuation of its intersection with the T wave in this lead. 
• 
  
• BOTTOM Line: In association with the acute-looking limb lead changes in Figure-1 — the above described findings (subtle-but-real) — increase my concern, and clearly suggest acute Infero-Postero OMI until proven otherwise.

"Take Home" Points from Today's Case:

• The "right answer" (and the "right" clinical action) — will not always be correct. This is fine! The 1st STEP in clinical ECG interpretation is to assess the 12-lead ECG in front of you — and then to clinically correlate your impression.
• 
  
• The History is the essential 2nd STEP component of clinical ECG interpretation. So — despite our concern on seeing today's initial tracing — clinical interpretation of this ECG in the context of knowing the patient had no CP, and that prior ECGs were similar (from this patient's prior inferior MI) — provided us with a definite answer (and clear explanation for the abnormal initial ECG).