Saturday, April 29, 2023

A 50-something with acute chest pain, a computer "Normal" ECG, and a HEART score of 3 (low risk)

A 50-something with no previous cardiac history and no risk factors presented to the ED with acute chest pain (pressure) that radiated to the left arm.  

An ECG was immediately recorded:

Computer read: Normal ECG
Veritas algorithm
What do you think?

There is ST depression in V1-V3.   We showed that this is diagnostic of OMI (of the posterior wall)

Moreover, there is ST elevation in V6 (which is getting close to the location of posterior lead V7).  Thre is also absence of S-wave in V6, which is not entirely abnormal, but is suggestive of OMI (when this finding is in V2 or V3 in the setting of STE in V2 or V3, we call this "terminal QRS distortion", and it rules out normal STE)

Later, it queried the PM Cardio AI bot ("Queen of Hearts," a deep neural network trained by Pendell and me), and its diagnosis was "OMI with High confidence"

Case continued

The faculty physician in triage was very suspicious of OMI and took the patient to the critical care area.  Another very astute faculty physician immediately recognized that the ECG is diagnostic of posterior and lateral OMI, and activated the cath lab.

The cardiology fellow came  to the ED.  Another ECG was recorded as the patient's pain was improving.

This one is far more subtle, and if it were the only ECG, it would be difficult to call it diagnostic.
Veritas algorithm

The Queen of Hearts does not know that there were other ECGs, and does not know the patient.  
Nevertheless, it diagnosed:
 "OMI with Mid Confidence"  Amazing!

The cardiology fellow was skeptical of the need for the cath lab, but he took the patient up.

The first troponin I returned at 34 ng/L (URL = 35 ng/L)

The HEART score (also HEART pathway) = 3 (But this is only if you were to think that the ECG is normal, as the computer does)

Cath report: Findings in left circumflex:

LCX: Large, but non-dominant. Supplies a very large OM1. There is no stenosis in the proximal LCX and OM1 but a small to medium sized mid LCX continuation supplying a left posterolateral artery (LPLA) has a 99% stenosis with TIMI II flow 

(Flow was probably TIMI 0/1 during the initial ECG, but there was some spontaneous lysis and it partly opened to TIMI-2 flow (still insufficient, causing ongoing infarction).

It was stented with good results.

Formal Echo next morning:

The estimated left ventricular ejection fraction is 44%.

Regional wall motion abnormality-mid to basal infero-lateral.

Regional wall motion abnormality-basal anterolateral.

Peak hs troponin I over 36,000 ng/L (too high to measure, a VERY large infarction)

Learning Point:

1. There can be a VERY large infarct in a patient with a low HEART score and a "Normal" ECG.

2. If you do not recognize subtle OMI on the ECG, your patient may suffer large myocardial loss, or even die.

3.  YOU must be the one to recognize it.  Your cardiologist might not see it. 

4.  Our AI program from PM Cardio, trained by Pendell and me, is amazing and when it is FDA approved you will be able to use it to make this important and difficult decision to activate the cath lab.


MY Comment, by KEN GRAUER, MD (4/29/2023):


Today's case solidifies the need to add acute posterior OMI to the list of "Must Recognize" ECG patterns for emergency providers. As we've emphasized on many occasions — in a patient with new chest pain, ST depression that is maximal in one or more leads between V2-to-V4 is diagnostic of acute posterior OMI until proven otherwise! This is precisely the picture seen in the initial ECG in today's case ( = ECG #1 in Figure-1) — and — this ECG picture needs to be instantly recognized.

  • More than just the finding of maximal ST depression in V2-to-V4 — is the shape of the depressed ST segment in these leads. Normally, there will often be 1-2 mm of gently upsloping ST elevation in anterior leads V2 and V3. If instead, in a patient with new chest pain — there is "shelf-like" ST depression, similar to the flattened, depressed ST segment seen in leads V2 and V3, but not beyond lead V4 (as is the case in ECG #1) — this should serve as an instant "tip-off" to posterior OMI.
  • As a visual aid to facilitate recognition of the ST-T wave changes characteristic of acute posterior MI — I favor the Mirror Test (See My Comment at the bottom of the page in the September 21, 2022 post in Dr. Smith's ECG Blog). By simply flipping the ECG over, and holding it up to the light — the mirror-image of QRST complexes in one or more of the anterior leads is revealed — which provides insight to the ST-T wave appearance in the posterior LV wall.

  • Doesn't the Mirror Test faciliate appreciation of the abnormal shape of the shelf-like ST depression in leads V2 and V3 in ECG #1? (within the RED rectangle showing this mirror-image in leads V2 and V3).

  • As per Dr. Smith's discussion above — there are other abnormal findings in ECG #1 (ie, subtle-but-real ST elevation in lead V6, with a straightened, hyperacute-looking ST segment in this lead)In addition — there is subtle ST elevation in high-lateral leads I and aVL, with a Q wave in aVL that looks disproportionately wide. But even without these additional findings — the "Must Recognize" ECG pattern in this patient with new chest pain — is the unmistakeable shape of the ST depression in leads V2 and V3!

  • "A picture is worth 1,000 words ... ". I've added links below to 10 cases of posterior OMI in Dr. Smith's ECG Blog — in which I illustrate application of the Mirror Test. There are many other examples throughout Dr. Smith's ECG Blog.

Figure-1: Comparison between the 2 ECGs in today's case.

The 2nd ECG in Today's Case:
I've added the repeat ECG to Figure-1 — to emphasize how much can be learned from this 2nd tracing:
  • As noted by Dr. Smith — the repeat ECG in today's case is more subtle than the initial ECG. That said, if a patient with new chest pain presents with ECG #2 as the only tracing available — I would still be very suspicious of acute posterior OMI for similar reasons as described above for ECG #1. That is, instead of the small, normal amount of gently upsloping ST elevation in anterior leads — there is subtle-but-real "shelf-like" ST depression in leads V2 and V3. ST segment flattening persists in lead V4 — but is not present in lateral chest leads V5 and V6. While not by itself definitive — in a patient with new chest pain, the abnormal ST-T wave shape in leads V2,V3,V4 of ECG #2 should prompt timely repeat tracings, serial troponins, stat Echo — with high likelihood that OMI confirmation would soon be forthcoming.

The Scenario in Today's Case:
We are told that the patient in today's case noted a reduction in chest pain at the time ECG #2 was recorded. How does this correlate with the ECG changes we see between these 2 tracings?
  • Lead-to-lead comparison between ECG #1 and ECG #2 in Figure-1 is valid — because QRS morphology, the frontal plane axis, and R wave progression are all virtually unchanged between these 2 tracings.
  • In association with a reduction in chest pain — there is now beginning T wave inversion in lead III of ECG #2 — and, slight-but-real increase in T wave amplitude in both leads V2 and V3 of this repeat tracing. I interpreted these ST-T wave changes as subtle findings suggesting reperfusion T waves (which in the posterior wall distribution — manifests as increased T wave amplitude in anterior leads). Clinicallly — this would be consistent with the less-than-total coronary occlusion seen on cath.


Selected LINKS for More on the Mirror Test:

  • ECG Blog #246 — Reviews the concept of the "Mirror Test" with a clinical example.

  • The February 10, 2022 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates the Mirror Test in a case with posterior reperfusion waves (ie, tall anterior T waves).

The following posts in Dr. Smith's ECG Blog provide additional examples in My Comment (at the bottom of the page) that illustrate application of the Mirror Test for diagnosis of acute Posterior MI.
There are many more examples of posterior OMIs with positive Mirror Tests sprinkled throughout Dr. Smith's ECG Blog ... 

Tuesday, April 25, 2023

A 20-something with intermittent then acute chest pain

This was sent to me by a partner:

"Curious what you think of this one we had overnight.  Healthy male under 25 years old with a pretty good story for acute onset crushing chest pain relieved with nitro.  He had another episode the day before after exerting himself.  No pericardial effusion on ultrasound."

What do you think?

First, many on Twitter said "Pericarditis".  This is NOT pericarditis, which virtually NEVER has ST depression any where except aVR.  When there is ST depression (as in aVL, V2, V3), then top on the differential is OMI or myocarditis.

See our publication: ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis

There is STE in inferior leads, high lateral leads, and V4-V6.  And there is ST depression in V2 and V3, all but diagnostic of posterior OMI.

My response was: "OMI until proven otherwise"

#PMCardio AI Bot (AKA: "The Queen of Hearts"): OMI

The young age always makes one suspicious of myocarditis.  The STE in II >III is also suggestive of myocarditis.  But the stuttering pain and sudden onset suggest acute coronary occlusion (Occlusion MI, or OMI).  And it would be dangerous to assume this is myocarditis.   

Therefore, emergent cath is indicated, and the cath lab was activated.


"Acute onset chest pressure with diaphoresis." 

"ECG diffuse ST elevation, but lacking pericarditis features, and very concerning for acute injury."

"Cath lab activation by the ED and I agree with coronary angiography emergently."

Result: no angiographically significant obstructive coronary artery disease .

Medical Rx. Aggressive risk factor modification.

The initial hs troponin returned at 6700 ng/L.  It peaked at 21,000 ng/L

Post angiogram ECG:

The fact that there is near normalization suggests that this may have been a thrombus with complete lysis.  
How would the ECG findings of myocarditis resolve rapidly and nearly completely?

Formal Echo:

The estimated left ventricular ejection fraction is 47 %.

Regional wall motion abnormality-distal septum anterior and apex .

Regional wall motion abnormality-distal inferior wall .

Stress induced cardiomyopathy (Takotsubo like LV dysfunction) possible 

The appearance of wall motion abnormalities in some apical views suggest possibility of stress mediated cardiomyopathy.

A normal angiogram does not necessarily mean that there was no OMI.  There can be non-obstructive lesions that fissure and thrombose, with complete lysis of the thrombus. So MRI is necessary to confirm myocarditis.  Especially with resolution of the ECG findings, OMI is more likely that it otherwise would be.

MRI confirmed Myocarditis.  Viral studies were positive for Rotavirus.

MRI summary:

1) Mildly decreased LV function with no wall motion abnormalities 

2) Normal dimensions of all cardiac chambers 

3) Patchy mid-myocardial and epicardial delayed enhancement in a 

non-coronary distribution, consistent with myocarditis. 

Don't assume that young people don't have OMI!!  2 cases here:

A teenager with chest pain, a troponin below the limit of detection, and "benign early repolarization"

And even more here:

Dr. Smith's ECG Blog: young (

My Comment by KEN GRAUER, MD (4/25/2023):
Today's case is illustrative of the diagnostic path for determining the etiology of new-onset, severe chest pain in a young adult in his 20s. Even after repeat ECG, Echo, troponins and cardiac cath — a definitive diagnosis was not yet attained — with considerations including: i) Acute OMI (with rapid spontaneous reperfusion accounting for the failure of cath to show obstructive coronary disease in this young adult)ii) Takotsubo (Stress) Cardiomyopathy; oriii) Acute Myocarditis.

PEARL: Most patients who present with new chest pain + ECG changes + positive troponin — will not need Cardiac MRI. That said — today's case serves as an insight-providing reminder of the important selective minority of cases in which Cardiac MRI tells us the answer that had alluded us prior to ordering this test.
  • We've previously discussed the all-too-often ignored entity known as MINOCA ( = MI with Non-Obstructive Coronary Arteries) which we detailed in the November 30, 2022 post in Dr. Smith's ECG Blog (See My Comment at the bottom of the page). But cardiac MRI ruled out MINOCA in today's case — because cardiac MRI did not show infarction.

  • Cardiac MRI ruled in acute Myocarditis in today's case — by finding a suggestive acute inflammatory pattern on LGE (Late Gadolinium Enhancement).

  • NOTE: For detailed review regarding use of Cardiac MRI in acute chest pain evaluation — See the extensive article by Broncano et al (RadioGraphics 41:8-31, 2021)

Today's Initial ECG:
For clarity and ease of comparison — I've put the 2 ECGs in today's case together in Figure-1.
  • We've shown on a number of occasions in Dr. Smith's ECG Blog how difficult it may sometimes be to distinguish between acute myocarditis vs acute OMI on the basis of ECG findings and the clinical history (See My Comments in the July 21, 2019 — December 10, 2019 — and January 10, 2020 posts).

  • To Emphasize: Definitive diagnosis was not attained in today's case until cardiac MRI study. That said — there are some ECG findings in the initial tracing that are worthy of mention. These include: i) An unusual distribution of ST-T wave changes (ie, While ST elevation in inferior and lateral chest leads with ST depression in V1-V3 suggest acute LCx OMI — it's unusual with acute OMI to see more ST elevation in lead I than lead III, at the same time there is no ST elevation in aVL)andii) The ST/T wave ratio in lead V6 far exceeds 0.25, consistent with what may be seen with pericarditis (See My Comment in the December 13, 2019 post in Dr. Smith's ECG Blog). ECG findings somewhat atypical for acute OMI in a 20-something year old adult increase suspicion for acute myocarditis.

The Post-Cath ECG: 
Despite an initial ECG picture consistent with acute myocarditis — Uncertainty returned for the follow-up ECG done after cardiac catheterization.
  • As per Dr. Smith — marked reduction in ST elevation and depression so quickly in the post-cath ECG was clearly unexpected in this patient who turned out to have myocarditis! Although there has been a change in the frontal plane axis (which in ECG #2 is now consistent with LPHB, with predominant negativity in lead I) — I don't think this axis shift is enough to explain the resolution of ST elevation in the limb leads.
  • I don't know the significance (if any) of the new Q waves in the inferior leads in ECG #2.
  • In the chest leads — there is no longer anterior lead ST depression. 
  • Lateral chest leads now show narrow Q waves that were not previously present — and the abnormal ST-T wave ratio is no longer present.
BOTTOM Line in Today's Case:
  • Cardiac MRI proved invaluable for determining the diagnosis in today's case.

Figure-1: Comparison between the 2 ECGs in today's case. (To improve visualization — I've digitized the original ECGs using PMcardio).

Friday, April 21, 2023

50 year old with acute chest pain, with ‘normal’ ECG and falling troponin

Written by Jesse McLaren, with comments from Smith

A 50-year old patient on the medical wards developed acute chest pain, with an ECG labeled (see computer interpretation at the top) and confirmed as normal by the over-reading cardiologist. What do you think? 

        (Marqette 12SL algorithm)

There’s normal sinus rhythm, normal conduction, normal axis, normal R wave progression, and normal voltages. Lead aVL jumps out as abnormal because there is a discordant T wave inversion and mild ST depression. This is reciprocal to inferior mild ST elevation and hyperacute T waves (wide based, bulky, and symmetric, and in III taller than the QRS complex), and adjacent to ST depression in V2. 

This is diagnostic of inferoposterior OMI.


I sent the ECG to Dr. Meyers without any other information. He predicted RCA occlusion and tested the AI which he and Dr. Smith are training to identify OMI:

The patient did indeed have a 100% RCA occlusion, with peak troponin I over 10,000 ng/L. So under the OMI paradigm, expert-trained AI would help providers identify OMI and this patient would have had immediate cath lab activation, without any need to wait for repeat ECGs or troponin levels. Now let’s compare this with the existing paradigm to identify multiple preventable delays to reperfusion, which can be improved through the paradigm shift from STEMI to OMI.


1. ECGs labeled ‘normal’


Initially the patient had been on the medical wards for cancer treatment, and had been noted to have on/off chest pain with a troponin I that was mildly elevated around the 300 ng/L range. The day prior to the ECG above, the initial ECG below (ECG #1) showed minimal inferior T wave inversion:

        (Marqette 12SL algorithm)

So the patient was being treated for "Non-STEMI" with anti-platelets and heparin, and was getting troponin levels done every 6 hours. The next day, the patient developed recurring chest pain accompanied by nausea, and an ECG was done (ECG #2, the same ECG from the top of this post, reproduced here to compare with prior):

Compared with the prior ECG,  the ECG with active chest pain now has inferior T waves that are upright (pseudonormalization) and hyperacute, and the reciprocal change in aVL and ST depression in V2 are also new. This confirms infero-posterior OMI with even more certainty.


Many people want to believe that ECGs labeled ‘normal’ by traditional computer interpretation are unlikely to have clinical significance, and sometimes use the cardiologist's final interpretation (rather than patient outcome) as the reference standard. 

But this is one of many cases highlighting this dangerous assumption. This ECG was diagnostic of OMI but was STEMI negative, i.e. STEMI(-)OMI, and was labeled and confirmed by a cardiologist as ‘normal’, so the patient was given nitro and reassessed.

Smith comment: Cardiologists, like all health care professionals who interpret ECGs, are a very heterogeneous group when it comes to ECG interpretation. Some are superb, some not so much.  Cardiologists are indeed very smart and experienced and have a huge knowledge base, and do their best for their patients.  But cardiology is a massive specialty, and ECG interpretation for OMI is a tiny part of it.   It is so small that most cardiologists have never heard of "OMI," even though it is now in their literature (see the OMI literature timeline here).  Reading the ECG for OMI is mostly pattern recognition.  There are no measurements that are reliable.  People who have good pattern recognition skills, know about OMI, and have devoted much time to learning the patterns in patients with known outcomes, are good at this skill whether they are ECG techs such as Vince DiGiulio (who later became an EMT) or whether they are the rare interventionalists, such as Emre Aslanger, who are aware of the many subtle ECG signs of acute OMI.

Therefore, cardiologists in general should not be used as the reference standard for interpreting OMI on the ECG, either in clinical practice or in research papers.


2. Serial ECGs


An hour later, with chest pain persisting, the ECG was repeated (ECG #3) along with a troponin:

This ECG still doesn’t meet STEMI criteria, and now interpreted as “nonspecific” by the computer and over-read, but it is still very specific for inferoposterior OMI. In the STEMI paradigm, patients with ischemic symptoms and ECGs that don’t meet STEMI criteria get serial ECGs. But STEMI criteria has poor sensitivity for acute coronary occlusion. As a result, patients with STEMI(-)OMI can get serial ECGs that are repeatedly diagnostic of OMI but repeatedly fail to meet STEMI criteria.  

Often these ECGs NEVER evolve to meet STEMI criteria; ALWAYS they evolve too late for optimal timing of intervention.  This leads to preventable delays to reperfusion: the patient waited another hour for the troponin results.


3. Initial troponin


But the troponin level decreased from 357 to 179 ng/L, because the previous mild troponin level was falling at the time of occlusion, and the repeat troponin was measured only one hour after symptom onset.


Troponin is like a rear-view mirror, showing damage from the past. Like the initial hemoglobin level in acute hemorrhage, the initial troponin in acute coronary occlusion can be falsely reassuring. This often presents as patients with acute coronary occlusion whose first troponin level is in the normal range, but in this case the troponin was previously mildly elevated and falling at the time of occlusion.

Smith: the definition of MI is based on clinical criteria and troponin. The troponin element is at least one troponin above the 99th percentile URL with rise and/or fall.  So the patient can be diagnosed with acute MI and has recurrent chest pain. Those two elements alone are enough for cath lab activation even if the ECG does not show OMI (or if it does and you do not see it - or the computer does not see it)!!


According to the STEMI paradigm, a patient with serial ECGs labeled ‘normal’ and ‘nonspecific’ does not need reperfusion, especially with a falling troponin. But according to the OMI paradigm the patient had diagnostic ECGs and refractory chest pain, two indications for emergent reperfusion despite early and unreliable troponin.


Despite the troponin level the patient had refractory pain so another ECG was repeated (ECG #4):

Diagnostic of infero-posterior OMI for the third time, and now meets STEMI criteria for the first time two hours later. So the cath lab was activated and found a 100% RCA occlusion, as predicted from the first ECG. Troponin rose above 10,000 ng/L after the angiogram but was not followed to peak.


Below is a look at the 22 hour period surrounding the acute coronary occlusion, showing the troponin lag compared with symptoms and ECGs:


The time prior to the occlusion included ECG #1 and serial troponins from 284 to 269 to 357. When the patient developed acute coronary occlusion they serial ECG #2-4, the last of which led to cath lab activation despite a falling troponin--and the repeat troponin after reperfusion was greater than 10,000. 


Post-angiogram ECG (ECG #5) showed inferior Q waves, with T waves deflating and starting to invert, and resolution of reciprocal change in aVL:

ECG a few days later showed inferior reperfusion T wave inversion:

Take home

1.     ECGs labeled as ‘normal’ by conventional machines (and confirmed by over-reads) can still be diagnostic of OMI, and identified by OMI experts and the AI they train

2.     Serial ECGs looking for STEMI criteria can continually miss STEMI(-)OMI, leading to preventable delays to reperfusion 

3.      Troponin levels lag behind, and can be falsely reassuring early after occlusion


MY Comment, by KEN GRAUER, MD (4/21/2023):


I would add the following Take-Home Point to the excellent discussion of today's case by Dr. McLaren:

  • PEARL: Still all-too-often ignored is the potential benefit derived from correlating the presence and relative severity of CP (Chest Pain) — to the timing of each serial ECG. It's EASY to establish that this invaluable information remains so often ignored — simply by the absence of notation either on each serial ECG or in the medical record, of whether the patient was (or was not) having CP (and if so — how severe?) — at the time each ECG is recorded.

Figure-1 serves as the best way to illustrate the above Pearl — by taking another LOOK and comparing the first 2 ECGs recorded in today's case:

Figure-1: Comparison between the first 2 ECGs that were recorded in today's case. The TOP tracing ( = ECG #2) — is 1st first ECG that was shown above by Dr. McLaren. The BOTTOM tracing ( = ECG #1) — was obtained the day before ECG #2. The patient's CP was "on-off" at the time ECG #1 was recorded (See text).

Taking Another LOOK at the ECGs in Figure-1:
  • Today's case began with us first being shown ECG #2. Even in the absence of clinical information — this tracing has to be viewed as highly suspicious of an acute ongoing event (exactly as it was immediately interpreted by Dr. Meyers and the Queen of Hearts AI program). There is simply no way that the flattened (if not, slightly downsloping) ST segment in lead V2 is ever "normal" (ie, The ST segment in leads V2,V3 should be gently upsloping — and often slightly elevated as a normal finding).
  • As shown in the first illustration of Dr. McLaren's discussion — the computer interpretation of ECG #2 was, "normal ECG". Prior to development of the Queen of Hearts AI program — I had never seen a computerized ECG program sensitive in picking up subtle non-STEMI OMIs, such that: i) Clinicians always need to overread computer interpretations in context with the clinical situation; andii) Given that the patient in today's case was having severe CP at the time ECG #2 was recorded — definitive diagnosis of an acute infero-postero OMI (as per Dr. McLaren) has to be made!

  • BUT — this patient had been admitted to the general medical ward the day before, at which time ECG #1 had been recorded. The reason for this patient's admission to the hospital the day before was for cancer treatment. His symptoms at that time were "on-off" CP — and he had some troponin elevation in association with ECG #1.

  • NOW — Imagine today's case had started with us being shown ECG #1, with the knowledge that the patient was having "on-off" CP — and that an initial troponin value already showed some elevation. Even though there is no ST elevation in ECG #1 — the combination of intermittent CP (reduced at the time ECG #1 was recorded) — in association with shallow T wave inversion in all 3 inferior leads — should at least raise the possibility of spontaneous reperfusionIF the treating clinicians were correlating the history with these subtle-but-real findings in ECG #1.
  • To Emphasize: Even though ECG #1 is not diagnostic by itself of acute OMI — IF the treatment team was correlating ECG findings of this tracing with the history of intermittent CP and, with the fact that there already was an increase in troponin — Then closer observation would clearly be warranted (probably not still on a general medical ward) with repetition of at least several ECGs to ensure no active ongoing process. 

Once ECG #2 was Obtained ...
  • All that should need to be done is — i) To take into account that the reason ECG #2 was obtained, is that the patient was now having increased CP; andii) To compare lead-by-lead the appearance of ECG #2 with ECG #1 (as should be easy to do when you put these 2 tracings together — as shown in Figure-1). As per Dr. McLaren — comparison of these 2 tracings confirms acute dynamic ECG changes — which IF correlated to the history of now severe CP — should mandate prompt cath.

  • The pathophysiology of acute OMI evolution often includes a period of spontaneous reperfusion, that sometimes is only transient before spontaneous reocclusion occurs. IF clinicians carefully correlate the presence (and relative severity) of CP with the timing of each serial ECG — they can usually figure out when spontaneous reperfusion has occurred because: i) This is most often accompanied by reduction (if not complete resolution) of CP; andii) Acute ECG changes (ie, ST elevation and depression) decrease, if not normalize on the way to developing the typical pattern of reperfusion T waves (ie, T wave inversion in leads that previously showed ST elevation). All the treating clinician(s) need to do — is correlate the presence (and relative severity) of CP symptoms with serial ECGsDoing so often renders the diagnosis of acute OMI obvious.

Monday, April 17, 2023

Compare these two ECGs. Do either, neither, or both show anything important?

One case sent by Dr. Sean Rees MD, written by Pendell Meyers, other case by Sam Ghali and Steve Smith

Take a look at these two ECGs below from two patients in the ED, first without any clinical context. Full case details and outcomes are below.

Case 1:

Case 2: 

Case 1:

What do you think?

This was sent to Dr. Smith by SamGhali (@EM_RESUS) with zero other info.  

Smith's response was: "OMI Mimic."

Later, this info was supplied by Sam:

This ECG was recorded in a 23-year-old African American man with a history of psychiatric illness, acute alcohol/drug intoxication, brought in by police officers status post being tazed. He had no symptoms of ACS. This pattern was recognized as an OMI mimic and no further workup was pursued.  The remainder of his Emergency Department stay was uneventful.

The Queen of Hearts correctly says:

Smith: Why is this ECG which manifests so much ST Elevation NOT a STEMI (even if it were a 60 year old with chest pain)?   
--There is even a convex ST segment in V3!! (when there is ST Elevation, convexity in any one of leads V2-V6 is fairly specific sign of LAD occlusion).  
The reasons are: 
1) there is too much voltage in the QRS (deep S-wave in V3 especially).  
2) The T(volume)/QRS ratio is not large enough for the T-waves to be considered hyperacute.  
3) The shape of the T-wave is just "not right".  This is something that is hard to teach, but with hundreds of such cases, we have taught the artificial intelligence algorithm to recognize this.
4) There is well formed J-point notching.

Case 2:

What do you think? In addition to sinus tachycardia, the only abnormalities listed by the computer were "low voltage, precordial leads" and "anteroseptal infarct, old...Q greater than 40mS, V1-V2"

Meyers interpretation: I was sent this ECG with no clinical information whatsoever, and I responded: "Easily diagnostic of acute LAD occlusion." There are hyperacute T waves in V2-V5, I, II, aVL. The STD also present in V2 completes the description of de Winter T waves (hyperacute T wave with depressed ST takeoff). 

Here is the clinical informaton on ECG 2:

A man in his 50s presented to the Emergency Department with acute chest pain that started within the past few hours. He also stated he "just didn't feel well" starting about 14 hours prior to presentation, but the chest pain was only noticed about 2 hours prior to presentation. He was mildly tachycardic (105-110 bpm) and hypertensive (157/92 mm Hg) on arrival.

His triage at 0127 is the ECG above.

Based on approximately 18,000 training ECGs with expert interpretation and outcomes (trained by Smith and Meyers), PM Cardio's Queen of Hearts AI instantly makes this diagnosis on any smartphone, even just by taking a screenshot of a piece of paper in suboptimal conditions:

The ECG was interpreted by the clinicians as "No STEMI." 

His HEAR score (before troponin resulted) was documented at 3, with documentation stating "low suspicion for ACS."

Repeat 0157 with ongoing chest pain:

Basically the same features diagnostic of LAD occlusion. QOH: "OMI High confidence". Physician interpretation: "No STEMI."

Initial troponin I returned elevated at 350 ng/L (not sure exactly which high sensitivity troponin I assay this is, but many of them have a male upper limit of normal around 20-35 ng/L). A troponin this high in a patient with no known chronic troponin elevation, and active acute ACS symptoms, has a very high likelihood of type 1 ACS regardless of the ECG.

Repeat ECG at 0221:
Basically unchanged. QOH: "OMI Mid confidence." Physician: "No STEMI."

With ongoing chest pain and positive troponin, the physician consulted with the cardiologist at the nearby PCI center, who replied that there was no indication for STEMI activation, and no indication for thrombolytics. The patient was transferred to the PCI center non-emergently over the next few hours. 

Upon arrival to the PCI center, the repeat troponin returned at 13,962 ng/L. Chest pain is documented as ongoing.

Repeat ECG at 1624 (shortly before cath):
QS waves now present in V2-V3, with slight STE, showing the pattern of left ventricular aneurysm morphology. No significant signal of terminal T wave inversion to suggest any reperfusion; this MI is in the process of completing. With this ECG alone, and no clinical context, it would be difficult for me to say if this OMI is subacute or old. QOH: "Not OMI, High confidence." (probably because QOH has not had enough training yet to differentiate subacute OMI vs. old LVA morphology, which is very difficult).

Cardiologist interpretation: "Technically does not meet STEMI criteria but concerning for ischemia."

Cath around 1730:

Left main: normal
LAD: prox LAD 30% stenosis immediately followed by a "99-100% thrombus filled occlusion" involving the proximal and mid LAD, as well as a large diagonal branch, with TIMI 1 flow pre-procedure. 
LCX: minimal luminal irregularities 
RCA: minimal luminal irregularities

Aspiration thrombectomy and PCI performed with resultant TIMI 3 flow in LAD and D1.

Next trop 85,528 ng/L (consistent with a massive myocardial infarction), none further measured.

1824 post cath:
Mot much different than the ECG above, but QOH: "OMI, Low confidence."

Echo: EF 40-45%, anterior and apical WMA. 

The patient was discharged 3 days later, and long term follow up is not available. But you could imagine the long term prognosis difference between this patient and one who received reperfusion therapy at the time of OMI diagnosis upon arrival to the initial ED.

Final Diagnosis: "NSTEMI"

Smith:  think about this: the patient had an occluded LAD and lost his entire anterior wall, and yet received a diagnosis of "NSTEMI".  

NSTEMI is worthless garbage diagnosis!  

The diagnosis should be either OMI or Non-OMI.  In this case it is OMI.

Learning Points:

OMI is not solely an ECG diagnosis, but expert ECG interpretation can greatly help to improve recognition of STEMI(-) OMI and conversely to recognize false positive STEMI criteria.

The day seems near when AI ECG interpretation will be a reliable and objective solution for any provider to rapidly differentiate subtle OMI from OMI mimics. 

Ongoing ischemia despite medical management has always been an indication for emergent cath, which is frequently ignored as it was in this case.

According to the 2022 ACC Expert Consensus Decision Pathway on the Evaluation and Disposition of Acute Chest Pain in the Emergency Department (reference below), hyperacute T waves and De Winter sign are both now considered "STEMI equivalents" and warrant the same management as STEMI. 


MY Comment, by KEN GRAUER, MD (4/17/2023):


Today's post by Dr. Meyers (with contributions from Drs. Rees, Ghali and Smith) — serves as a lesson in the recognition of acute OMI — and in distinction from one of the most commonly encountered "OMI mimics".

Like Dr. Smith — I initially viewed the 2 ECGs from Case #1 and Case #2 without the benefit of any history. The Take-Home Point from these 2 Cases lies with how to immediately recognize that Case #1 is an "OMI mimic" — whereas Case #2 shows what should be easily recognizable ECG findings of deWinter T waves, that in a patient with new chest pain should mandate prompt cath.

  • For clarity in Figure-1 — I've reproduced these 2 tracings from today. I focus my comments on a few additional points to the above excellent discussion by Dr. Meyers.

Figure-1: Comparison of the 2 ECGs in Case #1 and Case #2.

CASE #1:
We have presented many examples of LVH that masquerades as an OMI "mimic" (See My Comment in the April 2, 2023 post — and the April 14, 2023 postto name just the most recent examples). Although there are "many variations on this theme" — the basic premise is that although the ST-T wave changes of LV "strain" most often manifest in one or more of the lateral leads — some patients manifest a "mirror-image" of strain in the anterior leads.
  • The first "tip-off" that the ECG in question is unlikely to represent acute OMI — is that one or more of the anterior S waves are disproportionately deep. Whereas in most cases of ECG LVH — the diagnosis is made by tall lateral R waves — the "mirror-image" of this increased lateral lead R wave amplitude is unexpectedly deep S waves in one or more of the anterior leads. For example, in Case #1 — the S wave in lead V3 is 33 mm deep!
  • Doesn't the RED insert of the mirror-image of lead V3 — show precisely what you might expect to see for the ST-T wave of LV "strain" in a lateral chest lead?
  • The other clue that the ST elevation seen in multiple other leads on the Case #1 ECG is unlikely to be due to acute OMI — is the prominent J-point notching in leads II,III,aVF; and in leads V5,V6. In association with upsloping (ie, "smiley"-configuration) ST segments in these leads — this appearance is very characteristic of a repolarization variant (and very unlikely to indicate acute OMI).

  • PEARL #1: I suspect that the ECG in Case #1 represents both benign repolarization changes (J-point notching in the leads with upward sloping ST elevation) — and — probable LVH (ie, extreme increased voltage that surpasses that expected even for a younger adult + LV "strain", as seen in the RED insert in lead V3 in the lead with extreme S wave amplitude). It turns out that the patient whose ECG is shown in Case #1 was a young black male with known alcohol abuse (ie, predisposition to alcoholic cardiomyopathy) — and IF this younger black male had significant longstanding hypertension (common in this demographic) — we would then have an explanation for his abnormal ECG.

  • PEARL #2: Perhaps you were initially concerned not only by the coved ST elevation we see in lead V3 of the Case #1 ECG — but also by the ST elevation and straightening of the ST segment take-off in lead V4? If so — I strongly suspect this ST elevation and straightening in lead V4 simply reflects a "transition" lead between the coved ST elevation in lead V3 (curved RED line in this lead) — and the upward-sloping ST elevation in lead V5 (curved BLUE line in this lead).

  • BOTTOM LINE: Once familiar with how common it is for LVH and repolarization variants to serve as "OMI mimics" — the combination of findings seen in this Case #1 ECG will immediately suggest that this tracing is an "OMI mimic". This impression will then be solidified as soon as you learn that the patient in question is a young black male who is predisposed to both repolarization variants and LVH, and who is without cardiac-sounding chest pain.

CASE #2:
I am more disturbed by learning of the events associated with the ECG in Case #2. As noted by Dr. Meyers in his above discussion — Dr. Meyers instantly recognized the Case #2 ECG as completely characteristic of deWinter T waves — which in a patient with new chest pain, has to be immediately recognized as indicative of acute LAD OMI until proven otherwise.
  • There are certain patterns in ECG interpretation that emergency providers must be able to instantly recognize. Among these patterns are deWinter T waves. In the same way that Brugada-1 ECG patterns — Wellens' Syndrome — acute STEMIs — and Ventricular Tachycardia — must be immediately recognized by emergency providers (to name just a few of these "immediate recognize" patterns) — so it is in a patient with new chest pain who presents with an ECG looking like that seen in Case #2. Yet multiple providers (including at least 1 cardiologist) failed to recognize the deWinter T wave pattern in this acutely ill patient with new, severe and persistent chest pain.

We'll continue to present variations on the "theme" of deWinter T waves. For review — I've copied below my summary of this entity from My Comment in the February 10, 2023 post of Dr. Smith's ECG Blog. Features of deWinter T waves seen in the Case #2 ECG include the following:
  • Disproportionately tall T waves in multiple precordial leads (most marked in leads V2 and V3 — but also seen in leads V4 and V5). These T waves manifest "hyperacute" characteristics of being not only taller-than-expected (given relative amplitude of the QRS in the respective lead) — but "fatter"-at-their-peak and wider-at-their-base than one would expect. For example — the T wave in lead V3 is more than twice the height of the tiny R wave in this lead.

  • J-point ST depression at the onset of the ST segment in leads with tall deWinter T waves (ie, most marked in leads V2 and V3 — but also suggested in the lateral chest leads).

  • PEARL #3: Easy to overlook in this initial ECG in Case #2 — is not only the QS complex in leads V1,V2 — but the fact that the S wave in lead V2 is fragmented (slurred) in the initial part of its downslope, strongly suggesting (much more than a simple QS in this lead would) — that there has already been infarction. This is further supported by the finding of a small-but-present Q wave in both leads V3 and V4! While these Q waves are indeed tiny — the fact that they follow QS complexes in leads V1,V2 in association with deWinter T waves and, in the absence of septal q waves in more lateral chest leads V5,V6 — is indication that infarction has already occurred.

  • PEARL #4: ST-T waves are also abnormal in the limb leads. Although the QRS complex in both leads I and aVL is tiny — the T wave in these leads is clearly hyperacute (ie, disproportionately taller and "fatter" than it should be given the tiny size of the QRS complex). Subtle ST segment flattening with slight ST depression is also seen in the inferior leads. In the context of deWinter T waves in the chest leads — these more subtle limb lead ST-T wave abnormalities confirm acuity of this tracing.

  • BOTTOM LINE: As per Dr. Meyers — the 2022 ACC Expert Consensus Decision Pathway for acute CP Management (on Page 1933 in the J Am Coll Cardiol 2022 manuscript) — now specifically includes deWinter T waves — as potential indication of "proximal LAD occlusion that warrants immediate angiography". Emergency providers need to instinctively recognize this ECG pattern in a patient with new chest pain!


KEY POINTS regarding DWinter T Waves:

In 2008 — Robert J. de Winter and colleagues (Drs. Verouden, Wellens, and Wilde) submitted a Letter to the Editor to the New England Journal of Medicine (N Engl J Med 359:2071-2073, 2008) — in which they described a “new ECG pattern” without ST elevation that signifies acute occlusion of the proximal LAD (Left Anterior Descending) coronary artery.

  • The authors recognized this pattern in 30 of 1532 (~2%) patients with acute anterior MI. Cardiac cath confirmed LAD occlusion in all cases — with ~50% of patients having a "wraparound" LAD. Left mainstem occlusion was not present.
  • This was the authors’ original description of the new ECG pattern: “Instead of the signature ST-segment elevation — the ST segment showed 1-3 mm of upsloping ST depression at the J point in leads V1-to-V6 — that continued into tall, positive symmetrical T waves”.
  • The QRS complex was usually not widened (or no more than minimally widened).
  • Most patients also manifested 1-2 mm of ST elevation in lead aVR.

 For illustrative purposes — I’ve adapted Figure-1 from the original manuscript by deWinter et al, published in this 2008 NEJM citation.
Figure-2: The deWinter T Wave Pattern, as first described by Robbert J. de Winter et al in N Engl J Med 359:2071-2073, 2008. ECGs for the 8 patients shown here were obtained between 26 and 141 minutes after the onset of symptoms. (See text).

In their original 2008 manuscript — deWinter et al went on to describe the following additional features:

  • “Although tall, symmetrical T waves have been recognized as a transient early feature that changes into overt ST elevation in the precordial leads — in this group of patients, this new pattern was static, persisting from time of the 1st ECG until the pre-cath ECG.”
  • Hyperkalemia was not a contributing factor to this ECG pattern (ie, Serum K+ levels on admission were normal for these patients).   


NOTE: Technically speaking — the deWinter T wave pattern as described in 2008 by deWinter et al differs from the finding of simple "hyperacute" anterior T waves — because ECG findings with a strict deWinter T wave pattern persist for an hour or more until the “culprit” LAD vessel has been reperfused. 

  • As I note above (and as illustrated in the example ECGs taken from the deWinter manuscript that are shown in Figure-2) — there should be involvement in all 6 chest leads with the strict deWinter pattern, with most leads showing several mm of upsloping J-point ST depression and giant T waves.

MY OBSERVATIONS regarding De Winter T Waves: Over the past decade — I have observed literally hundreds of cases in numerous international ECG-internet Forums of deWinter-like T waves in patients with new cardiac symptoms.

  • Many (most) of these cases do not fit strict definition of “deWinter T waves” — in that fewer than all 6 chest leads may be involved — J-point ST depression is often minimal (if present at all) in many of the chest leads — and, the number of leads that manifest giant T waves is limited.
  • ECG changes in many of the cases that I have observed are not “static” until reperfusion (as had been initially reported in 2008 by deWinter et al.). Neveretheless, cath follow-up has routinely confirmed LAD occlusion in almost all cases.

 on the Phenomenon of deWinter T Waves: 

I believe there is a spectrum of ECG findings, that in the setting of new-onset cardiac symptoms is predictive of acute LAD occlusion as the cause. I suspect that to a large extent — what is seen on ECG depends greatly on when during the process the ECG is obtained.
  • While many of these patients do not manifest “true" deWinter T waves” (because their ECG pattern does not remain static until reperfusion by coronary angioplasty) — for the practical purpose of promptly recognizing acute OMI — I do not feel that it matters ( = my opinion) whether a “true” deWinter T wave pattern is present — vs the presence of simple “hyperacute” T waves (that are deWinter-like)

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