60-something with h/o Coronary Bypass has acute chest pain

A 60-something with h/o Coronary Bypass called 911 for acute chest pain.

Here is the first prehospital ECG: 

What do you think?

There is minimal ST Elevation in inferior leads which could easily be normal.  However, aVL has minimal STD supportive of the diagnosis of OMI.  More importantly, the ST depression in V2-4 is diagnostic of posterior OMI.  There is a hyperacute T-wave in V6, which is the lateral part of the posterior wall and a common supportive finding in posterior OMI.

The Zoll algorithm impressively stated: ***STEMI***

A paramedic student had the PMCardio AI Queen of Hearts on his phone and this is what it reported:

New PMcardio for Individuals App 3.0 now includes the latest Queen of Hearts model and AI explainability (blue heatmaps)! Download now for iOS or Android.  (Dr. Smith is a shareholder in Powerful Medical.)

On arrival, an ED ECG was recorded:

Still diagnostic

When a patient has severe chronic coronary disease, findings which appear to be acute can sometimes be chronic, so in this patient with h/o CABG (coronary bypass), it is wise to find a previous ECG if possible.  

Here it is:

This confirms that all findings are new.

The cath lab was activated

The interventionalist disagreed with the assessment, but agreed to do the angiogram.  

Angiogram results are complicated because of the CABG:

Severe three-vessel obstructive coronary artery disease, with chronic total occlusion of the mid LAD, total occlusion of the mid RCA, and severe subtotal occlusion and severe disease in the left circumflex coronary artery mid segment and proximal segment, as well as severe disease in the OM itself. Noteworthy that the LAD and the left circumflex coronary artery share 2 separate ostia with very close proximity to the origin of both vessels and severe

disease in both vessels.

Saphenous vein graft to the RCA is a large in diameter with significant conduit 2 vessel mismatch but there was no severe disease in the vein graft and the anastomosis to the distal RCA appeared to be okay.

Patent LIMA to the LAD the LIMA is anastomosed to the mid LAD after the large LAD D1 and LAD D2.

Saphenous vein graft to the obtuse marginal is small in diameter with severe ostial disease and total occlusion in the proximal body of the graft.  This is most likely the infarct-related artery.

Unfortunately, for technical reasons, it could not be stented.

Should thrombolytics be given?

I would say that, if there are no contraindications, yes.  I have never seen a case in which the artery was unable to be opened for technical reasons and so therefore thrombolytics were given instead.  

Peak Troponin I was 22,000 ng/L (Typical of a moderate STEMI)

Formal Echocardiogram

Normal left ventricular cavity size, mildly increased wall thickness and mildly reduced systolic function; estimated left ventricular ejection fraction 45-50%.

Regional wall motion abnormality: mid anterolateral and inferolateral hypokinesis.  

This is the term that is used for a posterior wall motion abnormality -- this confirms posterior OMI.

The EF just 9 months prior was 64%, so there was significant myocardial loss.

Learning Points: 

1. If you cannot open the artery for technical reasons, consider thrombolytics.

2. In the setting of acute chest pain, ANY ST depression maximal in V1-V4 is acute OMI until proven otherwise.  We have proven this.

Exceptions

One should be circumspect (careful, that is, and not jumping to conclusions because the STD maximal in V1-V4 may NOT be due to OMI), when there is atrial fibrillation or abnormal vital signs:

1. Atrial fibrillation

Great example: 60-something: chest tightness, palpitations, and ST depression V1-V3

Other Examples:

Cardiac arrest, defibrillated, diffuse ST depression and ST Elevation in aVR. Why?

Chest Pain and Cardiogenic Shock with Profound ST Depression & STE in aVR. Activate the Cath Lab?

Atrial Fibrillation w Rapid Ventricular Response and ST Depression Maximal V1-V4: Not always subendocardial.

Does this ST Depression Maximal in V3 Represent Posterior OMI?

Atrial Fibrillation with RVR and Inferoposterior ST elevation (Injury Pattern)

2. Shock/Hypotension:

Hypotension, chest pain, and precordial ST depression maximal in V3. Is this OMI?

3. Tachycardia

Regular, steady, and fast at 170 (wide or narrow?), hypoxic, crackles in lungs, B-lines, unconscious

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MY Comment, by KEN GRAUER, MD (6/12/2025):

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Today's case is of a 60-something man with known coronary disease — who called EMS for new-onset CP (Chest Pain).

• For clarity in Figure-1 — I've reproduced the first 2 ECGs in this case.

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QUESTION:

  — How quickly can you make today's diagnosis?

• Beyond-the-Core: Has there been a change in the repeat ECG?

Figure-1: Comparison of today's initial EMS ECG — with the repeat ECG on arrival in the ED.

ANSWERS:

The purpose of my comment in today's case is to highlight how quickly the diagnosis of acute posterior OMI should be made from ECG #1.

• Knowing this patient's age and his history of known coronary disease — immediately places him in a higher-risk group for an acute coronary event.
• Given this history — it should take no more than seconds to definitively diagnose acute posterior OMI because: i) There is maximal ST depression in leads V2,V3,V4 (RED arrows); and, ii) The shape of this ST depression in these 3 leads looks acute (straightened, "shelf-like" ST segments with terminal T wave positivity). There is a positive "Mirror Test" (See My Comment in the September 21, 2022 post, among many others for more on the "Mirror" Test).

As per Dr. Smith — There is a hint in ECG #1 of ST elevation in the inferior leads, with abnormal ST segment flattening in lead aVL. That said, by itself — this would not be diagnostic because of how subtle these inferior lead findings are — and because the essentially flat ST segment in lead aVL is nonspecific, and not convincing of a reciprocal change.

• There is also ST depression in lead I of ECG #1. Most of the time with acute inferior infarction — the amount of reciprocal ST depression is usually greater in lead aVL than in lead I. Retrospectively (ie, knowing the cath findings) — this ST depression in lead I more likely reflects this patient's severe multivessel disease.

What about the Repeat ECG?

As stated — the diagnosis of acute posterior OMI (and the need for prompt cath with PCI) — should be immediately made on learning the history and seeing ECG #1. That said — I'd add 2 important points related to ECG #2:

• Point #1: There has been improvement in the ECG findings that were seen in the initial EMS tracing. Specifically: i) Although ST depression is still present and maximal in leads V2,V3,V4 — the amount of depression, and its acute appearance is less in ECG #2 (less of a "shelf-like" appearance to ST segments — with decreased height and less peaked terminal T wave positivity in these leads); ii) There is no longer ST depression in lead V5; and, iii) ST depression is less in lead I.
• Point #2: There is no mention of whether this patient's CP was less at the time ECG #2 was recorded. This is relevant — because IF this patient's CP had decreased at the same time that acute ECG findings were improving, this would provide further support of an acute cardiac event, as well as suggesting some degree of spontaneous reperfusion.

Interns are not (yet) poisoned by the STEMI/NSTEMI paradigm

This case was written up by Kuan-Yu (Evan) Lin with some edits by Willy Frick. I (Willy) had the pleasure of working with Evan when he was a medical student. Now as an intern, he is exceptional at EKG interpretation because he was able to learn of the OMI paradigm and importance of pattern recognition before getting poisoned by years of learning STEMI.

A 41-year-old South Asian male with history of hypertension, alcohol use disorder and hyperlipidemia, who has a strong family history of CAD presented with central substernal burning, pressure, and pain with associated diaphoresis.

(When seeing a South Asian patient with chest pain, concern for ACS must be heightened, given their disproportionately higher risk of CAD, despite often lacking traditional risk factors.)

Patient initially presented at 9 PM to a referring facility with hsTnI 13 (ref: < 34 ng/L) then 30, then 60. Patient stated the symptoms began that same day at around 3 PM when he was drinking alcohol. He consumed 6 drinks. He denied any history of similar symptoms.

EKGs from the referring facility were not available. Patient was loaded with aspirin, started on heparin gtt, and transferred to PCI capable center for treatment NSTEMI. He was also given GI cocktail and chlordiazepoxide. Patient arrived at 3 AM and the following EKG was recorded, and a repeat high sensitivity troponin T (hsTnT) was 189 ng/L. From chart review, no additional anti-anginals were given but the patient was described as chest pain free.

EKG 1

What do you think?

EKG 1 interpretation: Normal sinus rhythm, heart rate 60, normal axis, Q waves in III, aVF, with STE and TWI in lead III. There is concomitant STD in aVL and subtle STD in V2-3. This raises the possibility of reperfusing inferoposterior infarct given TWI in the setting of symptom resolution.

Smith: The newest model, which is not available to the public, give an output of "likely reperfusion."

The Queen of Hearts sees almost no evidence for active OMI (active OMI model), which is good model performance. The "entirety of OMI" model (which is also positive for reperfused OMIs) is also negative but, the value 0.29 demonstrates that the tracing has some very concerning features.

Frick: When Evan sent me this ECG with no context, I said, "Not sure if it’s specific for reperfused inferoposterior. Context?" When he told me acute burning chest pain with diaphoresis (now resolved) and rising troponin, I said "Reperfused inferoposterior."

_________

Smith: a reperfused OMI is high risk.  This is really a transient OMI (or transient STEMI if one uses that terminology and it has diagnostic ST Elevation).  Transient STEMI was studied by Lemkes et al. 

Lemkes JS, Janssens GN, van der Hoeven NW, et al. Timing of revascularization in patients with transient ST-segment elevation myocardial infarction: a randomized clinical trial. Eur Heart J [Internet] 2019;40(3):283–91. Available from: http://dx.doi.org/10.1093/eurheartj/ehy651   

Lemkes et al. randomized 142 patients with transient STEMI (whose symptoms and ST elevation had resolved) to emergent vs. next day angiogram and PCI, with all patients receiving aspirin, a P2Y12 inhibitor, and an anticoagulant. While the infarct size by MRI was the same in both groups, “4 patients (5.6%) in the delayed invasive strategy required urgent intervention due to signs and symptoms of reinfarction while awaiting angiography.” Each patient who suffers reocclusion while awaiting delayed cath runs the risk of lack of identification of reocclusion, worsened MI due to the added ischemic time during the delay, and a small but real risk of true deterioration and death between identification of reocclusion and PCI.

Therefore, my opinion is that it is safest to do urgent PCI on such a patient. 

______________

Cardiology recommended urgent TTE (not stat -- i.e., not emergent), serial EKG and troponin, and urgent catheterization in the AM. At time of cardiology evaluation, patient was chest pain free, according to documentation.

The decision and timing to send a patient to cath lab can depend on the convenience. In a patient “without STE” who is currently “chest pain free” or even improvement of chest pain without resolution, the improvement might sway the interventionalist to defer cath to a more convenient time. 

Frick: This is why we often cite Lupu's study which showed that the highest risks NSTEMIs are rarely taken to lab emergently as they should be according to guidelines.

Repeat EKG as below.

EKG 2

Subtle changes but overall pretty similar to EKG 1.

Smith: Looks to me like the ST Depression in V3 is gone

At 8 AM, the patient complained of return of his chest pain which he rated 5/10 in severity. Repeat EKG at that time is shown.

EKG 3

This EKG is absolutely diagnostic for OMI, and highly suspicious for Re-occlusion. The TWI in III has been replaced by STE and upright T waves. Additionally, the T waves in aVL that were previously overly upright due to mirror image reperfusion are now much less prominent.

Here is the PMCardio Queen of Hearts AI Model.  She is very worried about the ECG.  I'm not sure why she thinks it is reperfused, even after looking at the explainability heat map.

New PMcardio for Individuals App 3.0 now includes the latest Queen of Hearts model and AI explainability (blue heatmaps)! Download now for iOS or Android.

There was high clinical suspicion and ongoing symptoms, so the cath lab was activated.

Coronary angiography before and after intervention is shown below.

There was co-dominant circulation, with 90% stenosis of distal LCx and 100% thrombotic occlusion of proximal RCA with TIMI Flow 0. DES was deployed at 9 AM RCA with plan for staged intervention to LCx the next day.

TTE post cath showed preserved EF of 55-60% and hypokinesis of the basal to mid inferior wall of LV. There was no repeat EKG or troponin after intervention. Patient was discharged with diagnosis of NSTEMI.

Frick: If there had been a repeat troponin, it would likely have been very high (like this case where troponin stayed in the hundreds before skyrocketing to 37,000 ng/L after PCI). In the case of TIMI 0 occlusion, troponin gets "trapped" in the ischemic myocardium. 

Learning points:

Prior to looking at EKG, pretest probability trumps everything. Positive QOH interpretation means very little when applied to a patient without chest pain. Similarly, QOH negativity is not completely reassuring if the pre-test probability is very high as in this case.

Ischemic heart disease is more prevalent in South Asian decents. According to a circulation review article,  South Asians are at a higher rate of ASCVD, higher burden with higher. 

Smith: by waiting for PCI in this "Transient OMI," the patient lost a lot of myocardium.  Do not Wait!!

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MY Comment, by KEN GRAUER, MD (6/10/2025):

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Today's case is troubling to me. While there are details of the case that are uncertain — it appears that this 41-year old man presented to the ED (Emergency Department) for CP (Chest Pain) — but that at the time ECG #1 was recorded — Troponin was somewhat elevated and the patient's CP was less than it had been.

For clarity in Figure-1 — I've reproduced this 1st ECG in this case that I saw. Knowing only the information provided above — my thoughts regarding ECG #1 were as follows:

• In a patient who had CP severe enough to prompt a visit to the ED — but whose CP had significantly decreased by the time today's initial ECG was recorded — I found ECG #1 diagnostic of acute infero-postero OMI.
• The rhythm is sinus. 
• The 3 leads that immediately caught my "eye" — are lead III, lead aVL, and lead V2 (within the RED rectangles).
• Lead III immediately raises suspicion. We see a very deep (albeit narrow) Q wave + ST segment coving + terminal T wave inversion (BLUE arrow). There really is not clear ST elevation in the other 2 inferior leads (leads II and aVF) — so by itself, lead III is not definitive. But the mirror-image opposite ST-T wave picture that we see in lead aVL (ie, subtle-but-real ST depression with terminal T wave positivity) in this patient who had new CP that has now decreased — indicates acute inferior OMI until proven otherwise (See My Comment at the bottom of the page in the October 6, 2018 post and in the May 10, 2025 post, among many others — regarding clinical significance of the "magic" mirror-image opposite relationship between leads III and aVL).
• Confirmation that ECG #1 is diagnostic of acute inferior OMI — is forthcoming by clear indication of associated posterior OMI (given the very common blood supply of both inferior and posterior LV walls). As we often emphasize, there is normally slight, gently upsloping ST elevation in both leads V2 and V3. When this is missing (as the RED and BLUE arrows in these leads highlight) in a patient with suspected inferior OMI — this strongly suggests infero-postero OMI until proven otherwise.

BOTTOM Line: Although other leads in ECG #1 are non-diagnostic — the above ECG findings in the 3 leads within the RED rectangles of Figure-1, in this patient with new CP that has now decreased — indicate acute infero-postero OMI until proven otherwise.

• Reduction in CP, in association with the modest but-definitely-present ST-T wave abnormalities that we see in leads III, aVL and V2,V3 — suggest that the "culprit" vessel (probably the RCA) — has spontaneously reopened.
• But as we so often emphasize — What spontaneously reopens, may just as easily at any moment spontaneously reclose.  Therefore, optimal management is not to delay cath until the next morning — but instead entails definitive treatment by prompt cath with PCI.

Figure-1: The 1st ECG shown in today's case.

Hypertrophic Cardiomyopathy with dehydration and chest pain

A middle-aged man with a history of HOCM presented with 24 hours of chest pain, still active.  He stated that he had been dehydrated for a day as well.  The pain was not at all severe, and localized to the left sternal border, without radiation.  The patient was in no distress and had normal vital signs.

Here is his presentation ECG:

What do you think?

I thought it just looked like HOCM.  But because there were the dramatic HOCM findings, I did not look closely enough.

We did a bedside ultrasound:

This shows very thick LV walls and VERY small LV chamber, with high ejection fraction but low stroke volume. 

My impression was that the patient was dehydrated, which can cause poor LV filling in HOCM, and that might result in chest pain and type 2 MI, with minimally elevated troponin.  So we ordered troponins:

The first troponin I returned at 30,000 ng/L!  This troponin is most consistent with acute coronary occlusion, or in this case, subacute occlusion (because the symptoms are so prolonged and the first troponin so high).

I went back to look at the first ECG, and found an old one to compare with:

Can you see anything?

How about if we put the inferior leads and aVL side-by-side:

You can see now that the T-wave in lead III is far larger in the presentation ECG.  In aVL, although the inverted T-wave is the same size in both, the QRS is far larger in the historical ECG.

Therefore, I thought that this must be an inferior OMI.  The 24 hours of pain and the very high initial troponin show that this is a subacute OMI.

I put this through the PMCardio Queen of Hearts AI model, and she did not see OMI. However, she does not have the advantage of seeing an old EKG.  She did say that the ejection fraction was less than 40%. I wonder if she can see low stroke volume, which this patient definitely had due to low chamber volume?

I asked the patient if he still had chest pain and he confirmed that he did. Therefore, Cath Lab activation was indicated. 

I activated the cath lab 88 minutes after ED arrival.  The patient was in the Cath Lab at approximately 114 minutes after arrival.  

Such a delay is not nearly as detrimental as it would be if the OMI was acute (as opposed to subacute).   Almost all of the damage is already done. 

A 100% distal circumflex occlusion was found, opened, and stented.

A formal echo later showed no wall motion abnormality.  EF was 72%.

Learning point:

When the ECG at baseline is very abnormal, it can be very difficult to make an OMI diagnosis on the ECG. One must scrutinize the ECG, even more closely, and always find an old one to compare with.  Fortunately, my Miss, in this case, did not result in more myocardial damage, because it was such a prolonged myocardial infarction. Moreover, we do not know what the ECG would've shown in the acute phase. 

Outcomes of acute myocardial infarction in patients with hypertrophic cardiomyopathy.

I could not find any data on troponin levels in acute myocardial infarction in hypertrophic cardiomyopathy.  But because there is so much more myocardial mass, one might expect that Peak troponins could be much higher. This would not necessarily translate into a worse outcome, however, because there's so much myocardial mess to begin with.  This increased baseline, myocardial mass may explain why, in the above paper, they did not find worse mortality in patients with hypertrophic cardiomyopathy. 

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MY Comment, by KEN GRAUER, MD (6/7/2025):

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We've illustrated the difficulty of recognizing acute OMI in patients with marked LVH (Left Ventricular Hypertrophy) on a number of occasions (See My Comment at the bottom of the page in the February 6, 2020 post, among many others).

• Today's case is perhaps the most challenging that I have seen in regard to appreciating an acute OMI in the presence of marked LVH.

For clarity in Figure-1 — I've reproduced side-by-side the initial ECG and the prior ECG of today's patient.

• As per Dr. Smith — the patient in today's case is a middle-aged man with known HOCM (Hypertrophic Obstructive CardioMyopathy) — who presented with ongoing severe CP (Chest Pain) for the previous 24 hours. 
• ECG #1 ( = the initial ECG in today's case = TOP tracing in Figure-1) shows obvious marked LVH, with greatly increased R waves in all lateral leads and very deep S waves in leads V1,V2.
• In addition — ECG #1 shows deep, symmetric T wave inversion in multiple leads, as well as marked J-point ST depression (WHITE arrows) in virtually all leads manifesting increased R wave amplitude. But this patient has known HOCM — so the above remarkable findings could be completely appropriate for a nonischemic ECG in a patient with HOCM (See my discussion below Figure-1).

In the absence of a prior tracing for comparison — I examined today's initial ECG knowing that none of the above findings were necessarily diagnostic of acute OMI given the known diagnosis of HOCM.

• PEARL: In cases such as this, in which no definite abnormality is seen in most of the 12 leads — I look for 1 or 2 leads that I know look abnormal. Doing so — my "eye" was drawn to the ST-T wave in lead III (within the RED rectangle) — which I thought clearly manifested a "bulkier"-than-expected T wave, given tiny amplitude of the QRS in this lead.
• NOTE: I did not initially think that lead aVL was diagnostic of acute OMI. It was only after I recognized the above definite abnormality in lead III — that I thought the ST-T inversion in lead aVL was more-marked-than-expected given modest amplitude of the R wave in this lead.
• Acknowledgment: I was not at all certain of the diagnosis of acute OMI based on my initial impression of ECG #1, because only 2/12 leads showed changes suggesting acute OMI. But given the history — I thought ECG #1 was clearly suspicious of a hyperacute inferior lead T wave, with reciprocal changes in lead aVL.
• As per Dr. Smith's discussion above — finding a prior ECG on today's patient confirmed the diagnosis of acute OMI, proven and treated by timely cardiac cath.

Figure-1: Comparison of today's initial ECG — with a prior ECG on this patient.

As review — I've excerpted the following from My Comment in the October 28, 2023 post of Dr. Smith's ECG Blog:

ECG Findings in HCM — vs Echo?

The question of what ECG findings to look for when in search of HCM arises often. HCM is estimated to occur in ~1 in 500 young adults, making it among the most common inherited cardiac disorders. It is the most common underlying cause of sudden cardiac death (SCD) in asymptomatic young individuals — which raises the question of whether to screen those involved in regular (high performance) athletic activity? If so — WHO to screen? College and professional athletes? High school athletes? Others?

• Echocardiography is diagnostic. With formal echo — accurate measurement of septal and chamber size can be obtained and followed on a serial basis. Echo also helps to sort through the large "spectrum" of HCM disorders, encompassing "lower risk" HCM (in those with modest or moderate hypertrophy — but without obstruction) — vs higher-risk obstructive forms of HCM.
• Obtaining formal Echo is expensive. It's easier and cheaper to do screening ECGs in athletic individuals — reserving Echo for when ECG reveals any findings potentially suggestive of HCM.

Most patients with HCM do not have a normal ECG. Among the many ECG findings that may be seen in patients with HCM are the following: 

• Increases in QRS amplitude.
• Large septal Q waves (Sometimes known as "dagger" Q waves — because these are deep but narrow Q waves seen in lateral leads). 
• Tall R wave in lead V1 and/or early transition in the chest leads (reflecting increased "septal" forces).
• Abnormal ST-T wave abnormalities.
• Conduction defects (ie, LBBB, IVCD).
• WPW
• Cardiac arrhythmias (especially AFib). 
• 
  
• The Problem: None of the above ECG findings are specific for HCM. It is also interesting (if not confusing) — how much of a variety one may see on the ECG of a patient with HCM (ie, While QRS amplitude and ST-T wave findings of LV "strain" are marked on today's ECG — large septal Q waves are no where to be found).

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NOTE: For readers interested in treatment recommendations for HCM — this October 28, 2023 post adds information on this subject.

• For more on distinction between the apical form of HCM vs other HCM forms — See My Comment in the December 26, 2023 post.

 

The worst thing you can be when you have this ECG is to be a young woman

This was contributed by a great paramedic, Drew Williams.  He now is his agency's "Clinical Improvement Analyst for STEMI performance and quality assurance.”

A 30-something woman called 911 for chest pain.  Medics report this:

They recorded a prehospital ECG:

What do you think?

To me, this is an obvious proximal LAD occlusion.  However, I am always surprised at how what is obvious to me, is completely missed by many other physicians.

There is a hyperacute T-wave in V2 and aVL, STE in V1, and ST depression in I, inferior leads, and V3-V6.  This should never be missed.

This is a classic "Swirl" pattern, which we described for the first time in a recent publication in the Journal of Electrocardiology.

"When defined as a narrow QRS plus STD in V5/V6 plus T wave to S wave amplitude ratio > 0.40 in V2, precordial swirl pattern yielded PPV 70 %, sensitivity 9 %, specificity 98 %. Of the 23 Occlusion MI patients correctly identified by precordial swirl sign, 19 (83 %) had LAD culprit lesions, and 16 (70 %) were missed by STEMI criteria."

Here is the PMCardio Queen of Hearts AI Model's interpretation:

And here is the explainability "heat map" (notice that she sees the hyperacute T-wave in V2 and the inferior ST depression.

Interesting that she does not highlight the ST depression in V3-V6

New PMcardio for Individuals App 3.0 now includes the latest Queen of Hearts model and AI explainability (blue heatmaps)! Download now for iOS or Android.

But the providers in EMS and in the ED did not see it.  

I do not have any ED ECG.  But it is likely that they never developed diagnostic ST Elevation, since this is very common.  

We have a paper In Press at the Eur Ht Journal Acute Cardiovascular Care in which we show that 20/53 TIMI-0 LAD Occlusions did not have diagnostic ST Elevation.  17/20 had hyperacute T-waves.  Both a blinded expert (Smith) and the Queen identified OMI in 20/20 cases.  NONE of the cases with hyperacute T-waves ever developed diagnostic ST Elevation.  Compared with the 33 with STEMI criteria (diagnostic STE), they had longer door to balloon times.

Case continued

3 hours after arrival in the ED she arrested in ventricular fibrillation.

She went to the cath lab:

So, this unfortunate 30-something woman lost half of her heart, had a cardiac arrest, required a balloon pump and vasopressors, all because no one could read her "Non-STEMI" EKG that was a total coronary occlusion.

She will probably have permanent heart failure, if she lives.

Literature

1. If you don't know about this topic, read this recent article we wrote in JACC Advances:

From ST-Segment Elevation MI to Occlusion MI: The New Paradigm Shift in Acute Myocardial Infarction

Full text: https://www.jacc.org/doi/epdf/10.1016/j.jacadv.2024.101314

2.  Here is the seminal article on the Queen of Hearts: 

International evaluation of an artificial intelligence–powered electrocardiogram model detecting acute coronary occlusion myocardial infarction 

3.  There are now reams of data showing that the Queen will identify almost all acute coronary occlusions (and identify mimics).  See the list of publications here.

Learning points:

1. Use The Queen of Hearts, if allowed, to help you recognize acute coronary occlusion.

2. Young Women often have their OMI missed.  "Nah, couldn't be an MI in a young woman!"

3. If you don't have the Queen, you need to spend a lot of time learning this extremely difficult skill of reading the ECG for subtle OMI.

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MY Comment, by KEN GRAUER, MD (6/5/2025):

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Today's case will be frustrating, not only for medical providers familiar with the concept of acute OMI (Occlusion-based Myocardial Infarction) — but even for those who have only been trained in the basics of ECG interpretation for evaluation of the patient with new CP (Chest Pain). This type of case should not be missed.

• Today's CASE: Paramedics were called to the scene where a 30-something woman reported new CP persisting since she awakened in the morning. Regardless of the younger age of this patient — the history of new and persistent CP severe enough to prompt contacting 911 — automatically places this patient in a higher risk group for having an acute event.
• This history in today's case — should by definition mean that the role of EMS and ED providers is to rule out an acute event rather than the other way around.

For clarity in Figure-1 — I've reproduced and labeled the initial EMS ECG.

• Without entering into the more advanced findings of the specific ECG diagnosis in Figure-1 — the basics that have to be appreciated by even less experienced emergency providers are: i) That the QRS is narrow and the rhythm in Figure-1 is sinus (upright P waves with a constant and normal PR interval in lead II ); and, ii) That there is ST depression in multiple leads (ie, in the 8 leads highlighted by BLUE arrows in Figure-1).
• Regardless of whether or not one ascribes to strict millimeter-based criteria of ST elevation ( = the STEMI-paradigm) — or — whether one has embraced the ever-increasing body of literature that we continually document in support of the newer and more comprehensive OMI paradigm (See the OMI Literature Timeline and OMI Facts and References TABS in the upper MENU on the top of every page in Dr. Smith's ECG Blog) — the combination of new and persistent CP, severe enough to prompt notification of 911 and today's ECG showing ST depression in multiple leads — needs to initiate an expeditious evaluation that leads to prompt cath before the ventricular fibrillation episode that this patient developed because these basic concepts were not appreciated.

Looking Closer at ECG #1:

As per Dr. Smith's above discussion — ECG #1 represents an obvious acute proximal LAD OMI. Our "eye" should be immediately captured by leads V1 and V2 (within the RED rectangle):

• In a patient with new CP — it is the disproportionately increased "bulk" of the ST-T wave in lead V2 (with respect to the relatively small S wave in this lead) that indicates hyperacuity.
• In a patient with a narrow QRS and no LVH — the ST-T wave in Lead V1 should never be more than minimally (if at all) positive. Instead, especially in the the context of the disproportionate ST-T wave in lead V2 — the ST coving and elevation that we see in lead V1 in Figure-1 is an equally hyperacute change as the overly "bulky" ST-T wave in V2.
• We've highlighted the concept of Precordial "Swirl" on multiple occasions in Dr. Smith's ECG Blog (See the October 15, 2022 post — with 20 illustrative ECGs by Drs. Smith and Meyers — and with "My Take" at the bottom of the page on some Pearls for quick recognition of a "Swirl" pattern).
• ECG #1 fits perfectly with this Oct. 15, 2022 description of "Swirl" because: i) In this patient with new CP and a narrow QRS and no LVH on ECG — The ST-T waves in leads V1,V2 are clearly hyperacute; and, ii) There is flat ST depression in leads V5,V6.

Additional ECG findings in Figure-1 include:

• Sinus tachycardia (at ~105-110/minute) — which is unusual in a simple MI unless something else is going on (extensive infarction in this case — that shortly thereafter evolved into VFib).
• A hyperacute T wave in lead aVL (which supports the hyperacute ST-T waves that we see in leads V1,V2 — as indication of a proximal LAD location for this "culprit" artery).
• ST elevation in lead aVR — which in association with this Precordial "Swirl" pattern showing ST depression in 8/12 leads, suggests either multivessel disease and/or an extensive ongoing infarction.

Figure-1: I've reproduced and labeled today's initial EMS ECG.