What is Wellens' syndrome? And what conditions mimic it?

A 30 year old African American Male presented to the ED with chest pain that occurred the day before.  It had been 6-7/10 in intensity and lasted for about 10 minutes, and was associated with strenuous activity.  It radiated to the left arm and was associated with SOB.  There was no pain on the day of presentation.

Here is the ED ECG:

What do you think?

Since this is a young (30 years old!) patient, so it can't be acute MI, right?  And the patient is African American, so it must be one of those normal variants in blacks, right? 

Wrong!! 

See our article: Walsh, B., Macfarlane, P. W., Prutkin, J. M. and Smith, S. W. (2019) Distinctive ECG patterns in healthy black adults. Journal of Electrocardiology, 56, pp. 15-23. (doi:10.1016/j.jelectrocard.2019.06.007)  

(Full text here: https://eprints.gla.ac.uk/189824/7/189824.pdf)

The ECG above is diagnostic of Wellens' syndrome (full reference below):

1) Episode of anginal chest pain that is resolved (GONE!)

2) preserved R-waves

3a) Terminal T-wave inversion (biphasic T-waves).  This is Pattern A.  

3b) Deep symmetric T-waves (Pattern B)

What does it mean? ----It is a reperfusion pattern!!

It means that the patient had full occlusion at the time of the chest pain, but that there was spontaneous reperfusion ("recanalization") resulting in resolution of pain and what I call "reperfusion T-waves"

That these T-waves are due to reperfusion was published by Wellens' himself (as senior author) a decade after he described Wellens' waves.

Wehrens XH, Doevendans PA, Ophuis TJ, Wellens HJ. A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty. Am Heart J 2000;139(3):430–6.

Doevendans PA, Gorgels AP, van der Zee R, Partouns J, Bar FW, Wellens HJJ. Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol 1995;75(17):1206–10.

  

    

Yet very few know about this.

But the PMCardio Queen of Hearts AI Model knows that this is a reperfused OMI:

Here is a demonstration (Case 2):

First ED ECG is Wellens' (pain free). What do you think the prehospital ECG showed (with pain)?

This male in his 40's had been having intermittent chest pain for one week.  He awoke from sleep with crushing central chest pain and called ems.  EMS recorded a 12-lead, then gave 2 sublingual nitros with complete relief of pain.  He arrived in the ED and had this ECG recorded:

There are Wellens' waves, type A (upsloping ST segment then inversion of the terminal part of the T-wave - terminal T-wave inversion, or biphasic T-waves) in V2-V4, and aVL.  Type B waves are deeper and symmetric.



When the patient had chest pain, prior to nitroglycerine, what do you think the ECG showed?  

Here is the prehospital ECG, recorded in the presence of pain:

Hyperacute anterolateral STEMI


The medics had activated the cath lab and the patient went for angiogram and had a 95% stenotic LAD with TIMI-3 flow.  A stent was placed.  The peak troponin was only 0.364 ng/mL (equivalent to 364 ng/L).  So even a massive STEMI, if it reperfused quickly, can result in a relatvely low troponin (in contrast to the next case!)

Here is a case that shows how Wellens' pattern evolves from a subtle OMI (Case 3):

Paramedics make a great call

A middle-aged male called 911 for chest pain.

Here was the first prehospital ECG with pain at 5/10:

Computerized QTc is 418 ms.  There is nondiagnostic ST elevation in V1-V4.
If you use the 3 variable formula, you get 25.15, (> 23.4, which is all but diagnostic of LAD occlusion).
The medics did not use the formula, as far as I know.
Now we use the 4 variable formula

Or, better yet, the PMCardio Queen of Hearts AI app:

 

Medics were worried, and gave nitroglycerine, then repeated the ECG at 5 minutes with pain at 2/10:

 Less ST elevation

And they repeated again with pain at 1/10 at 9 minutes:

Near Normal 

Medics asked for physician interpretation on arrival. Physicians were worried and activated the cath lab.   The first (and only) ED ECG is here:

QTc 386.  Most ST elevation is resolved.  Formula value is now down to a very low value of 19.352

A 90% thrombotic LAD lesion was found and stented.  There was pre-procedure TIMI-3 flow (perfect flow)

Door to balloon time was 25 minutes.

Peak troponin I was 17 ng/mL (this is quite a large infarct).

IMPORTANT: notice that an LAD Occlusion can have TIM-3 flow at angiogram because it opens spontaneously, AND that the troponin is often very high and indicative that the artery was indeed occluded at the time of the first ECG.

Subsequent Echo showed EF of 56% and distal septal, anterior, apical, and

anteroseptal hypokinesis (wall motion abnormality).

Here are post PCI EKGs, this one at 29 minutes after arrival:

You can see the beginning of terminal T-wave inversion in V2 and V3.
Had there been no prior ECGs, this patient who is now pain free would be suspected of Wellens' syndrome

The next one was done at 10 hours after the first:

Evolving T-wave inversion, classic Wellens pattern B morphology

And then the next day:

Full blown Wellens' Pattern B terminal T-wave inversion.

Learning Points

1. This was diagnosed as a NonSTEMI.

2. The artery was occluded, or nearly so, at the time of the first ECG.

3. Serial ECGs demonstrated dynamic changes diagnostic of ACS (transient STEMI)

4. This facilitated rapid treatment of a potentially life threatening LAD thrombus.

5. This also demonstrates how Wellens' ECG morphology is a representation of the post occlusion state, after spontaneous reperfusion (although it also looks that way after therapeutic reperfusion)
6. Finally, Transient STEMI should be taken emergently to the cath lab.  Failure to do so can result in Disaster: Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death

PseudoWellens Patterns: all of the below were recorded in patients with active pain (which is reassuring!)

What is this strange looking ECG in a young woman?

Normal Variant

Is it important to recognize LVH Pseudo-infarction patterns?

LVH

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

LVH

Finally, Wellens Pattern A evolves over time to Wellens Pattern B.  See this amazing series of ECGs over time:

Classic Evolution of Wellens' T-waves over 26 hours

Wellens' Original Study from 1989

Chris de Zwaan, Frits W. Bär, Johan H.A. Janssen, Emiel C. Cheriex, Willem R.M. Dassen, Pedro Brugada, Olaf C.K.M. Penn, Hein J.J. Wellens,

Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery,

American Heart Journal, Volume 117, Issue 3, 1989, Pages 657-665, ISSN 0002-8703,

https://doi.org/10.1016/0002-8703(89)90742-4.

(https://www.sciencedirect.com/science/article/pii/0002870389907424)

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MY Comment, by KEN GRAUER, MD (4/2/2025): 

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Sometimes it's easy to get fooled. Today's case by Dr. Smith illustrates one of those times.

• As per Dr. Smith — the fact that the patient whose ECG is shown in Figure-1 is a young adult African American male who presented with short-lived chest pain (lasting only ~10 minutes) the day before — is potentially as misleading as can be, given that the overwhelming majority of times that this type of history will be associated with some form of repolarization variant that is so commonly seen with this demographic. But not this time!
• The diagnosis of Wellens' Syndrome is clearly made more difficult by the presence of LVH. This is not to say that Wellens' Syndrome cannot occur when LVH is present — but rather that assessment of ST-T wave abnormalities may be complicated if there are ST-T wave abnormalities as a result of LV "strain". That said — although the S wave in lead V2 measures 21 mm — R wave amplitudes in the lateral chest leads of ECG #1 are modest, such that voltage criteria for LVH are not met (For quick review of ECG criteria for LVH — Click on the Tab in the lower row of the Menu at the top of each page in this ECG Blog). Given the young age of today's patient ( = 30 years old) — even greater amplitudes are required to satisfy LVH voltage criteria than those cited in the above Menu bar.
• A similar pattern of T wave inversion is seen in no less than 5/6 of the chest leads. ST-T wave changes of Wellens' Syndrome are most characteristically seen in leads V2,V3,V4 — but less commonly in leads V1 and V5 (as seen in today's case).

The above said, as per Dr. Smith — Today's case does satisfy criteria for Wellens' Syndrome in this patient whose CP (Chest Pain) had totally resolved by the time ECG #1 was recorded — with preservation of precordial r waves. Additional CLUES to the diagnosis of Wellens' Syndrome include:

• The very straight and steep T wave descent (highlighted by the slanted RED lines that are best seen in leads V2 and V3). This generally is not seen with LV "strain" or repolarization variants.
• Straightening of the ST segment takeoff in leads V3 and V4 (double RED arrows in these leads) — with an unusually wide base to the T waves in these leads.
• Lack of many criteria cited by Drs. Smith and Meyers as characteristic of BTWI (Benign T Wave Inversion) — including: i) Lack of prominent J-point notching that is characteristic of repolarization variants; ii) Greatest T wave inversion in V2,V3,V4 instead of V5,V6 as is seen with BTWI; iii) Lack of ST elevation in most of the leads with T wave inversion (as is typically seen with BTWI); iv) Lack of tall R waves in the lateral chest leads; — and, v) Lack of T wave inversion being also seen in the inferior leads (See My Comment at the bottom of the page in the June 30, 2023 post for review of these characteristic findings with BTWI).

The above said — it is easy to be fooled by today's tracing ...

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

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P.S.: For those interested — I review the history of Wellens' Syndrome, going back to the original 1982 manuscript by de Zwaan, Bär & Wellens in My Comment in the August 12, 2022 post). 

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Everyone sees ST depression, but what does it mean?

Written by Willy Frick

A man in his 70s with hypertension and type 2 diabetes mellitus presented with chest pain which awoke him from sleep around midnight. He described it as substernal, non-radiating, 7 out of 10 intensity. His ECG obtained around 4 AM is shown.

ECG 1

What do you think?

I texted this ECG to Dr. Smith without any information and he immediately replied: "combination of precordial swirl and South African Flag sign, with Swirl predominating.  Occlusion proximal to septal perforator AND first Diagonal."

The Queen of Hearts easily diagnoses OMI. Her confidence is 0.99, almost maximal. In particular, we see:

• Precordial swirl

• STE and hyperacute T waves (HATW) in V1, V2
• Reciprocal STD in the lateral precordium, V4-6

• (Most of) South African Flag

• STE and HATW in aVL and V2 (less apparent in lead I)
• Reciprocal STD in III

This is diagnostic for LAD OMI involving the septal perforators (precordial swirl) and major diagonal (South African Flag). This patient should be taken for immediate angiogram. 

The ECG was interpreted as showing "mild ST depressions in leads II, III, aVF, V4, V5, V6." The patient received aspirin 325 mg and nitroglycerin 0.4 mg sublingual. According to documentation, his pain resolved (but there was no short interval repeat ECG to assure normalization). First troponin I (cTnI) was 0.049 ng/mL (ref: < 0.033 ng/mL). 

The next update in the chart is at 8:10 AM, when repeat cTnI was 3.788 ng/mL, already a sizable infarct. After this resulted, repeat ECG was obtained:

ECG 2

Compared to the first, there is obvious improvement, but it is not normal and one must wonder whether there could be ongoing ischemia. The admitting service described the ECG as having "ST depressions in II, III, aVF, V4-V6," and documented that his pain was significantly improved to 2/10 and resolved during the interview.

PAUSE

Two thoughts:

First, there either is ischemic chest pain, or there is not. "Nearly gone" means unresolved. To use an analogy, would you be happy to drink water with nearly all the sewage filtered out?

Second, when evaluating a patient with ischemic chest pain, it is the clinician's job to elicit symptoms. The specific questions we ask encourage various responses. If you tell the patient "This nitro should help with the pain...Are you feeling better?" they might give you reassurance.

When I treat patients with suspected ACS, I tell them: "Your symptoms are critically important to me. If you feel absolutely normal, we can safely wait until the morning. On the other hand, if you have ANY chest discomfort [or whatever symptom the patient was experiencing] I need to know immediately. Please tell me or tell your nurse, because that would be an emergency."

Back to the case:

The patient was started on continuous heparin infusion and taken for echocardiogram. Apical views are shown below, first 4 chamber, then 2 chamber, then 3 chamber.

The apex is akinetic. It almost looks like takotsubo except we know from ECG and history that it is LAD OMI. The LVEF is ~45% Around this time, the patient was evaluated by the cardiology consult service. The consult note describes the ECG as showing "STD in the inferolateral leads," making this the third interpretation to overlook diagnostic STE and HATW in V1, V2, and aVL.

The patient was taken for cath. I have included the RAO cranial and RAO caudal projections here. Have a look at them and see if you can figure out the diagnosis before watching the video that follows where I explain. As always, you can read more in the angiography guide.

RAO cranial

RAO caudal

Narrated Video Explanation

Color scheme for cath films by Willy Frick.

The angiogram shows exactly what the ECG predicted: LAD occlusion involving the septal perforators and the major diagonal vessel. This is considered a type 2 MI since it is not due to atherosclerotic plaque disruption.

At around 12:30 PM, the patient received intracoronary nitrogylcerin with resolution of vasospasm. Repeat cTnI was still rising when last checked, 6.607 ng/mL.

Discussion:

Cases like this should infuse us with humility. Documentation said the patient's chest pain resolved after NTG, but the next note said he had only "2/10 pain." By the time he got to cath 8 hours after his first diagnostic ECG, his LAD remained severely spastic with very poor flow. If the first ECG had been a STEMI, he would likely have been treated emergently. But instead, it was the red-headed stepchild, NSTEMI. And this turned into another case of supervised, in-hospital anterior wall infarction. Cases like this make it hard to feel comfortable delaying intervention due to symptom improvement. If the patient comes in with ACS symptoms and ECG showing OMI -- just get them to the lab. 

This also brings up the general topic of non-atherosclerotic causes of myocardial ischemia and infarction. JACC published an elegant trial called CorMicA, in which investigators took patients with angina and no obstructive coronary disease (also called ANOCA or angina with non-obstructive coronary arteries) and performed comprehensive coronary evaluation with vasospasm provocation testing and microvascular evaluation. The patients were then randomized to routine care (in which the treating clinician was blinded to the results of the comprehensive assessment) vs stratified medical therapy according to the results of the invasive diagnostic procedure.

CorMicA, JACC 2018

Patients in the intervention arm had significant improvement in symptoms (the primary endpoint) and quality of life. In addition, patients in the control arm were 12.5 times more likely to have a missed diagnosis!

Patients with vasospasm should be strongly supported in their efforts to quit smoking which is a known risk factor for vasospasm. In addition, they should receive calcium channel blockers and long-acting nitrates to prevent recurrent spasm.

Learning points:

• It is your job to ELICIT symptoms of refractory ischemia. Delay intervention at your own peril.

• "Much better" is not the same as "completely resolved"

• Coronary vasospasm classically occurs in the middle of the night or early morning

• Help patients quit smoking, and treat with calcium channel blockers and long acting nitrates

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MY Comment, by KEN GRAUER, MD (3/30/2025):

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As per Dr. Frick — "Today's case should infuse us with humility" — as there are many aspects of this patient's care that could have (and should have) been improved. Filling us with humility is the frequency with which cardiac catheterization (as it is currently performed in most institutions) fails to identify all-too-many patients with a significant component of either microvascular and/or vasospastic angina (Results cited in Dr. Frick's above discussion, taken from the CorMicA Trial by Ford et al: JACC, 2018).

• The problem is not simple — as these non-atherosclerotic causes of CP (Chest Pain) run the gamut of symptomatology — and may be seen either in patients with pure coronary spasm — or — in patients with variable degrees of underlying atherosclerotic disease, upon which either a microvascular or vasospastic component is superimposed in any one or more of the major coronary branches (Matta et al — J Interv Cardiol, 2020 — and — Slavich and Patel — Int J Cardiol Heart Vasc, 2016).
• And then there is the issue of MINOCA (Acute MI in patients with Non-Obstructive Coronary Arteries) — which is estimated to occur in ~10% of patients initially diagnosed as having a STEMI or NSTEMI — in which microvascular and vasospastic angina are just 2 of the potential causes of an MI for which there is no evidence for a "culprit" vessel (See My Comments in the June 5, 2024 post — and the December 19, 2023 post).

The above said — I focus My Comment today on aspects associated with this patient's presentation and his initial ECG.

• To facilitate comparison of today's initial ECG with the repeat ECG — I've put both tracings side-by-side in Figure-1.

QUESTION:

• How to decide IF (and When) cardiac cath is indicated?

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

A Simplified Approach: When to Cath?

Cardiac cath was not performed in today's case for a full 8 hours after the initial ECG was recorded. As emphasized by Dr. Frick — this delay was entirely unnecessary, since the initial ECG was diagnostic of acute LAD occlusion until proven otherwise!

• Identification of the primary problem in today's case ( = coronary spasm) could not be diagnosed until cardiac cath was performed. But the cause of today's symptoms and ECG changes is not the main issue here. Instead — the principal issue is whether and if so, when cardiac cath should be performed in a patient such as the 70-something year old man in today's case who presented to the ED for severe new-onset CP that awakened him from a sound sleep at 4:00 am.

The Answer to the above clinical question should be simple:

• IF the initial ECG of a patient with new-onset CP is clearly abnormal (and clearly suggestive of an ongoing acute cardiac event) — then nothing else can possibly negate the indication for prompt cardiac catheterization.
• By "clearly abnormal" — this does not mean an ECG that satisfies millimeter-based criteria for a STEMI. This is because at least 30% of acute OMIs do not initially meet STEMI criteria — and many of these acute coronary occlusions that eventually do satisfy STEMI criteria, only do so after many hours of delay (Ricci, Smith, et al — Ann Emerg Med 85(4): 330-340, 2024).
• Although an elevated initial Troponin level may confirm acute infarction in progress — this initial Troponin level is not a part of the initial decision-making process IF the initial ECG is clearly abnormal. This is because the initial Troponin level may be normal in as many as 25% of patients who present with a STEMI (Wereski, Smith et al — JAMA Cardio 5(11):1302-1304, 2020). Therefore, if the initial ECG is clearly abnormal — the decision of whether or not to perform prompt cath remains the same regardless of whether or not the initial Troponin is normal or elevated (since a normal initial Troponin in no way rules out an acute event).
• And although repeat ECGs may demonstrate ongoing evolution of acute infarction — Waiting so that you can repeat the ECG should not be a part of the initial decision-making process IF the initial ECG is clearly abnormal. This is because no matter what a repeat ECG shows (ie, worsening — improvement — or no change at all) — IF in a patient with new-onset CP the initial ECG is clearly abnormal — Waiting only delays the indication for prompt cath that has already been established (and waiting only means that more potentially salvageable myocardium will needlessly be lost).

The Initial ECG in Today's CASE:

As per Dr. Frick — today's initial ECG is clearly abnormal (TOP tracing in Figure-1):

• In today's patient who presents with severe new-onset CP — my "eye" was immediately drawn to the 2 leads within the RED rectangles. In view of the small S wave in Lead V1 (ie, There is no LVH) — there simply should not be the ST segment straightening and the amount of J-point ST elevation that we see in ECG #1.
• In this context — the T wave in neighboring lead V2 is also disproportionately tall. An additional subtle-but-real finding is the presence of a small initial q wave that precedes the small r wave in lead V2 (within the dotted BLUE circle).
• The BLUE arrow in neighboring lead V3 highlights loss of the small amount of gently upsloping ST elevation that is normally seen in lead V3. This is followed by 1-to-2+ mm of flat or downsloping ST depression in lateral chest leads V4,V5,V6.
• The other RED rectangle highlights lead aVL — that manifests ST segment coving with >1 mm of ST elevation. This ST elevation in lead aVL is complemented by clearly abnormal reciprocal ST depression in each of the inferior leads.
• BOTTOM Line: Nothing else is needed in today's case to establish the need for prompt cath as soon as this can be accomplished.

The Repeat ECG in Today's CASE:

4 hours later — a repeat ECG was obtained (ECG #2 in Figure-1). That said — multiple concerns relate to this repeat ECG.

• The patient was given sublingual NTG after ECG #1 was recorded — which chart records indicate resulted in "resolution of the patient's CP". As soon as the patient's CP was resolved — the repeat ECG should have been recorded. Instead — no ECG was repeated until 4 hours later, and only then because an elevated Troponin value returned from the lab.
• With acute ongoing infarction — the initial ECG should be repeated within no more than 15-20 minutes after the initial ECG.
• As per Dr. Frick — 2/10 CP (as was noted at the time ECG #2 was recorded) is not the same as 0/10 CP.
• Rather than description of ECG #2 as having "ST depression in leads II,III,aVF; V4-V6" as was written by the admitting service — there have been "dynamic" ECG changes that become obvious by the side-by-side comparison of ECG #1 and ECG #2 afforded in Figure-1 (ie, in the form of deflation of the ST elevation in leads aVL and V1, and deflation of the hyperacute T waves in leads V2,V3). There has also been evolution of reperfusion T waves in leads III,aVF; and in leads V3-thru-V6.
• BOTTOM Line: Demonstration of these "dynamic" ST-T wave changes in association with the reduction in CP severity — confirms an ongoing acute event until proven otherwise. That said — the indication for prompt cath had already been firmly established 4 hours earlier at the time the initial ECG was done.

Even in retrospect, no one could see it.

This was sent to me by a former resident who is outstanding at reading ECGs for OMI.

"Hi Steve wonder what you think of this ecg in a 60 yo woman w cp, known CAD"

Presentation ECG (ECG 1):

Here is her previous from one week prior when she presented with heart failure and trops were "negative" (ECG 2):

My response: "They both look like active ischemia.  The top one (ECG 1) looks like "precordial swirl", which is LAD Occlusion.   The previous ECG also shows active ischemia."

The Queen of Hearts diagnosed "Subendocardial Ischemia"

More explanation: Both have some lateral precordial ST depression which looks like subendocardial ischemia.  However, the presentation ECG (ECG 1) has large, bulky T-waves.  By itself, it is very concerning for LAD Occlusion with Precordial Swirl morphology, but especially when comparing to the old one, those features of hyperacute T-waves really stand out.

He stated later that he gave her 1 sublingual NTG and her pain went down to 1/10.  He did not repeat an ECG.

His response:

"Yeah, that’s what I was afraid of. This is a retrospective ask because with the most recent ECG (ECG 1), I admitted her with new Chest Pain and a modest troponin elevation that I thought was progression of bad multi-vessel disease but she ultimately proved to have acute LAD occlusion that didn’t go to Cath for almost 24 hrs and I’m kicking myself.

Smith: In other words, he saw it in retrospect.

"That is what I was worried about in retrospect. Big MI. They stopped trending trop at 5000 ng/L of hs trop I. EF 20% down from 50%."

"And… they hit the carotid trying to place an Impella, caused a big hematoma where she had precipitous airway occlusion. Just awful all around. I’ll check for updates and other ekgs when I log in later today."

Post cath ekg here. She’s in impella dependent cardiogenic shock w new renal failure. 

Now there is a new intraventricular conduction defect (IVCD) that is very much like true Left Bundle (LBBB).

It is Smith Modified Sgarbossa Negative, but that is because the damage is done.  

Smith: "Sorry about all that."

Former Resident: "Yeah. Me too. Appreciate your feedback. I couldn’t get anyone else to agree with me on the OMI findings even in retrospect and it was driving me crazy."

Smith: In other words, no one else could see the OMI, even in retrospect.  I could see it because Pendell and I have described and coined the term "Precordial Swirl".  We have a paper In Press at the Journal of Electrocardiology that defines it based on a lot of data.  The Queen of Hearts did not diagnose OMI, but she did see ischemia.  

Refractory ischemia needs the cath lab emergently.  

When can you say that the ischemia has resolved and the patient does  not need emergent angiography?  

Both:

1) Pain is resolved completely

2) ST depression is competely resolved

In this case, the pain was still 1/10.  He told me that he did not see any inpatient notes about the presence or absence of pain.  He did not get a repeat ECG after the NTG.

SUMMARY:  This devastating OMI could have been reperfused quickly if the presence of refractory pain had been acted upon, regardless of the ECG.  Troponin was elevated and pain was refractory.  Why was it not acted upon?  I can't say I know for certain.  This former resident is one of the smartest and most diligent I have ever known, but the pressure to not activate the cath lab because of a possible false positive activation is intense.

It is better to have a false positive activation than it is to have a disaster like this, and all members of the team should be encouraged to support taking the patient for angiogram when there is any doubt!!

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MY Comment, by KEN GRAUER, MD (3/27/2025):

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Today’s case by Dr. Smith is subtle — and EASY to overlook because of how abnormal this patient's previous ECG is.

• This 60-year old woman clearly presented to the ED as a higher-risk patient — given her history of known coronary disease, now with new chest pain.
• To facilitate comparison in Figure-1 — I've put today's initial ECG (TOP tracing) — together with this patient's previous ECG from 1 week earlier (LOWER tracing). Of note — Troponin was normal at the time ECG #2 was recorded, so there was no acute infarction in association with this tracing.

PEARL: The KEY for assessing serial tracings is to systematically compare ECG findings by going lead-by-lead. It does not matter if you look first at the previous tracing or at the most current tracing — as long as you then systematically compare one lead in one of the tracings with the same lead in the next tracing — and then repeat this process for each of the 12 leads in both tracings.

• The Clinical Reality: If you do not keep both tracings close to each other as you go lead-by-lead comparing ECG findings — You will miss subtle abnormalities. I believe this was the problem in today's case.

The previous ECG is very abnormal ...

Let's begin with ECG #2 — which is the previous tracing that was recorded ~1 week earlier at the time of a heart failure exacerbation. 

• The rhythm in ECG #2 is sinus at ~75/minute, with several early beats. The PR interval is normal — the QRS is narrow — and the QTc may be borderline prolonged.
• There is marked left axis, consistent with LAHB (Left Anterior HemiBlock).
• Voltage criteria for LVH are satisfied (R wave in lead aVL ≥12 mm).
• There is poor R wave progression with delayed transition (The R wave does not get taller than the S wave is deep until between leads V5-to-V6).
• Regarding ST-T wave findings — There is fairly diffuse ST segment flattening with slight depression in multiple leads — with ST coving and slight elevation in lead aVR.
• Impression: Although the downsloping ST depression in high lateral leads I and aVL could reflect LV "strain" — the overall picture in this tracing is that of DSE (Diffuse Subendocardial Ischemia). That said — We are told that Troponins were negative at the time this ECG was recorded. So, while ECG #2 may be indicative of significant (even multi-vessel) coronary disease — it is not diagnostic of acute coronary occlusion.

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

Why an Acute Event was Not Diagnosed in ECG #1:

Note that both the frontal plane axis and precordial lead QRS morphology for the 2 tracings in Figure-1 are very similar (with the exception of predominant positivity for the QRS in lead V6 of ECG #2 — whereas transition never occurs in ECG #1). As a result of this similarity in axis and overall QRS morphology — any slight changes in ST-T wave morphology are likely to be "real".

• What differences do YOU see between the 2 tracings?

ANSWER:

The heart rate is somewhat faster in ECG #1. Once again there are some early beats that appear to be supraventricular.

• The most concerning difference in ST-T wave morphology between ECG #1 and ECG #2 — is seen within the RED rectangle. In this patient with new CP (Chest Pain) — Isn't it much easier to appreciate the taller T waves in leads V1,V2,V3 with these 2 ECGs placed next to each other?

Other changes are more subtle.

• I thought the ST-T waves in each of the 4 leads highlighted by BLUE arrows looked more acute (ie, with more angled and deeper ST depression).
• Lead aVR shows more ST elevation.

Impression: As per Dr. Smith — New ST elevation in anterior leads V1,V2 — with more ST depression in lateral chest lead V6 — is consistent with precordial swirl (See the October 15, 2022 post — for multiple examples of Swirl — and My Comment at the bottom of the page for qualitative summary of ST-T wave changes with this entity). The increased ST depression in multiple leads in ECG #2, with more ST elevation in aVR — is consistent with severe underlying coronary disease with worsening ischemia.

• Isn't it much easier to recognize subtle-but-important differences between 2 serial tracings by putting both ECGs next to each other, and then going lead-by-lead in your assessment?