EXTRA COPY — ECG Blog #543: A 24-Hour Holter was Done- EXTRA COPY

The ECG in Figure-1 was obtained from a previously healthy elderly woman — who presented with dizzyness and fatigue, but no CP (Chest Pain).

• Details of the timing of this patient's symptoms with respect to when the ECG in Figure-1 was recorded are uncertain.

QUESTIONS:

With the above history in mind: 

• How do YOU interpret today's initial ECG?
• Clinically — What would you do?

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

My Thoughts:

The ECG in Figure-1 shows sinus bradycardia at a rate of ~50/minute.

• The QRS is narrow — the PR interval is normal — and the QTc is probably not increased given the slow rate. 
• There may be small U waves in the mid-chest leads (which sometimes occurs in association with bradycardia).
• There is a slight leftward axis — though not negative enough to qualify as LAHB (The QRS is slightly more negative than positive in lead aVF — but mainly positive in lead aVL — which puts the axis at about -15 degrees).
• There may be voltage for LVH (Hard to say for sure if the R in aVL ≥12 mm — given overlap of this R wave with the S wave in lead aVR).

Regarding Q-R-S-T Wave Changes:

• The narrow Q waves in leads I,aVL are probably not abnormal given fairly tall R wave amplitude in these leads.
• R wave progression — looks normal, with transition (where the R wave becomes taller than the S wave is deep) occurring normally beween leads V2-V3.
• There are subtle ST-T wave abnormalities in a number of leads. As shown in lead III and in leads V1,V2,V3 — there is ST segment coving but really no elevation, followed by T wave inversion (the RED arrows in these leads).
• BLUE question marks in a number of other leads highlight ST-T wave segments of uncertain significance — especially given the different ST-T wave appearance between the only 2 complexes that we see in leads aVL and aVL — and our inability to fully see the ST-T wave of the 2nd complex in leads V4,V5,V6 (? what is real vs artifact). That said — there appears to at least be ST segment flattening in lead II, with slight ST depression in leads V4,V5,V6.

Impression: In view of the brief history we were given, but without "being there" — it's hard to know what to think of the above described ECG changes shown in Figure-2.

• It is clearly possible that this elderly woman at some point in time (possibly recently) — had inferior and anterior infarction. That said — the lack of a history of preceding chest pain (and uncertainty about the time of this elderly patient's "dizzyness and fatigue" ) — make it difficult to know whether she may have had a "silent" MI with "chest pain equivalent" symptoms? And if so — when this may have happened? (See ECG Blog #228 — for more on "Silent" MI).
• Without a preceding history of CP that then resolved — this case does not fit criteria for "Wellens' Syndrome". That said — ECG #1 certainly could be the result of infero-antero infarction at some point in time, possibly recent (See ECG Blog #320 and ECG Blog #350 — for more on what Wellens Syndrome is, and what it is not).

Figure-2: I've labeled ECG findings in the initial ECG.

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The CASE Continues:

This elderly woman up until now had not sought out medical care. She lived alone and functioned completely independently. Although she reported dizziness and fatigue as the reason for her ED (Emergency Department) visit — the medical care provider who treated the patient thought she looked remarkably well. As a result — ACS (Acute Coronary Syndrome) was not considered:

• Of note, the patient did not have medical insurance, and she had financial limitation. As a result — she did not want an extensive diagnostic work-up, especially given that she felt good enough to return to her independent living situation at home. 
• Troponin was not ordered.
• Instead, a 24-hour ambulatory Holter monitor was placed — and the patient went home. Follow-up was scheduled for her to return the next day.

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The Patient's Holter Monitor . . .

As you think about the challenging limitations for managing this case — what follows below in Figures-3 -thru-9 are non-sequential rhythm strips from this patient's 24-hour ambulatory Holter moniter that was reviewed the next day.

• NOTE: Each of the 6 non-sequential Holter rhythm strips that are shown below manifest 6 leads — including 1 limb lead (lead aVR) — and 5 chest leads (leads V1-thru-V5).
• As you review these 6-lead rhythm strips — Keep in mind that the only symptoms this elderly woman reported when she was seen several hours earlier, were some "dizzyness" and "mild fatigue" — but no chest pain.
• For ease of comparison in Figure-3 — I've reproduced this patient's initial ECG that was shown above in Figure-2.

Figure-3: Comparison between the initial ECG — and Holter-A, recorded several hours later after the patient had returned home (at 11:16 pm — while the patient was sleeping).

My Thoughts on Holter-A:

Keeping in mind the inevitable slight differences in lead placement with 6-lead Holter monitoring vs the patient's 12-lead — I did not perceive any significant different between these 2 tracings in Figure-3.

13 Minutes Later ...

Figure-4: Holter-B — recorded 13 minutes later (at 11:29 pm) while the patient was still sleeping.

Subsequent Recordings during Sleep ...

Figure-5: Holter-C — recorded ~2 hours later (at 1:23 am).

Figure-6: Holter-D — recorded at 7:30 am the next morning.

Figure-7: A closer look at Holter-D — in which I've labeled regular-occurring P waves that are no longer upright in lead aVF. The vertical RED line marks the end point of the now widened QRS complex in these 6 simultaneously-recorded leads — with the ST segment beginning to the right of this vertical RED line.

Figure-8: 10 minutes after Holter D — We now see a markedly widened agonal rhythm without atrial activity.

Figure-9: 12 minutes later a flat line is seen ...

Editorial Comment:

Today's case is difficult. This elderly woman who lived alone, died at home in her sleep. These Holter tracings were only retrieved afterward.

• Presumably — the initial ECG in Figure-2 did represent recent LAD occlusion and infarction in the form of a "silent" MI in this elderly woman with minimal "CP-equivalent" symptoms, who otherwise looked good — and who wanted to go home.
• Presumably, the reason this patient's initial ECG did not show acute ST elevation — is that there was spontaneous reperfusion of her recent MI, with resolution of what must have been ST elevation several hours earlier. The RED arrows in leads III; V1,V2,V3 — as well as the Blue question marks in her initial ECG represented reperfusion T waves.
• 
  
• I have "been there". As a family medicine Attending and faculty physician for 30 years — we would periodically see elderly patients present a day or more later after some form of symptoms with ECGs similar to that seen in Figure-2. While clearly — hospitalization for a day or two to ensure nothing active is still ongoing would be ideally recommended (and depending on case specifics — serial tracings, Troponins and potentially cardiac catheterization) — but with full informed consent, that is not always the path chosen.

I have also "been there" in the eerie situation of interpreting a Holter monitor on one of our serivce patients who was admitted to the hospital and seemingly doing well on a telemetry-monitored floor. I was downstairs in the hospital ECG station, reviewing the patient's 24-hour Holter recording that had just been placed into my in-box for interpretation. XXXXXXX

I have been there. I'll never forget

Editorial Note:

I have had this same experience myself — that I'll never forget 

Watanabe et al — Heart Rhythm 8:18-25, 2014
https://pubmed.ncbi.nlm.nih.gov/24793460/

Nikolic et al — Circulation 66(1):218-225, 1982
https://www.ahajournals.org/doi/10.1161/01.CIR.66.1.218?doi=10.1161/01.CIR.66.1.218

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Acknowledgment: My appreciation to Passang Jinpa (from Guayaquil, Ecuador) — for allowing me to use this case and this tracing.

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pful ...

In retrospect — the only thing I could say is that subtle change in symptoms (ie, development of some new "fatigue" in recent days in an older person with the initial ECG that you show is suggestive that a recent MI may have occurred, and that we are now seeing reperfusion T waves. What to do with this IF the patient otherwise "seems well" is a difficult question and "Ya gotta be there!" because there is NO certain answer.

In my capacity as hospital Attending for 3-4 months each year — I would read all of our service ECGs and I'd see the Holter Monitors. I will NEVER forget reading ECGs one day — and seeing a Holter monitor of a hospitalized patient, when I suddenly saw on the Holter that the rhythm was getting slower and slower — and then stopped. So I ran up to the floor where this patient was — only to find everyone at the bedside treating her cardiac arrest. It was an EERIE feeling seeing that Holter, and then seeing the patient (just like the eerie feeling that I'm sure you have when you saw these tracings!).

The above said — YES, this is rare to catch this — but I'm not sure you have best exposure by writing an article. Instead — I propose that you let me write an ECG Blog Case that I will publish within a couple weeks. I will show the 12 lead ECG that you sent me and ask the reader how they will interpret this?

There is no right or wrong answer — but the fact that you are soul searching events is sign that YOU are truly a good, caring physician doing the best you can given limited resources for the best you can do for your patients. Many clinicians would not give this case a second thought ....

Is it OK with you that I write this case up as an ECG Blog? I would be happy to acknowledge you if you like? — or the case can be anonymous — JUST LET ME KNOW. It will be published as a Blog post on-line, so it can be referenced by a link to my Blog.

 

EXTRA COPY: ECG Blog #541: Obvious MI — What is the Culprit? — EXTRA COPY

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

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Figure-2: XXXX

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Figure-3: XXXX

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Figure-4: XXXX

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Figure-5: XXXX

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Figure-6: XXXX

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Acknowledgment: My appreciation to Op. Sanooj (from Calicut, India) — for allowing me to use this case and this tracing.

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ADDENDUM:

I have added this Tab on Technical "Misadventures" — to the Menu at the top of every page in this ECG Blog:

— Where to find this LINK in the Top Menu! — 

All-too-often lead reversals, unsuspected artifact, and other "technical misadventures" go unrecognized — with resultant erroneous diagnostic and therapeutic implications. 

• In the hope of facilitating recognition of these cases — I am developing an ongoing listing on this page with LINKS to examples that I’ve published in this ECG Blog, as well as in Dr. Smith’s ECG Blog where I frequently write commentaries.

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O.p. Sanooj ( 10/10/2023 ) — Facebook Messenger

from Calicut, India — I am from Calicut, India. Myself Dr Sanooj Op

— "Obvious MI but WHAT is the Culprit?"

Sure sir, it is a honour for me if you publish this. 

Your earlier advice of giving   IV betablocker and cordarone helped me to kill VT in this case. And also I gave plenty of fluids suspecting RVMI. Thanks from the bottom of my heart sir.

 

THE CASE:

Hi sir, this patient had arrested in cathlab while doing angioplasty. Given CPR for 30 minutes and multiple shocks for VT. Finally after opening RCA, he became stable. Now he is doing well.

 

There is shelf like ST depression in inferior leads, ST elevation in 1, aVL,V6 indicating infero lateral MI. The absence of ST depression in V1 indicates there is RVMI. Am I right sir?

Sir, this is today's ecg. Patient is stable now. There is no occlusion in Lcx. The culprit artery on cath was RCA. I have confirmed it.

MY 1st REPLY (I was initially fooled !!!! — important to tell why!)

Hi. I put the 2 parts together to get a better 12-lead picture. I see sinus rhythm — with as you say MARKED ST elevation in I,aVL and V3-thru-V6. This picture to me is MUCH MORE SUGGESTIVE of acute LCx (Left CircumfleX) occlusion. One of the 2 QRS complexes in lead V2 has slight ST depression (but neither has the usual slight ST elevation) — which to me suggests there is also posterior MI. I am not quite sure why there appears to be slight ST elevation in lead V1 — but everything else on this tracing suggests that the LCx is the "culprit" artery — and the LCx generally does NOT supply the RV ...

 

Are you sure that the "culprit" artery on cath was the RCA? Did this patient have multi-vessel disease ??? — as if he did, then depending on the pattern of collateralization, you may get a different distribution for the ST elevation and depression.

The massive ST depression in leads II,III,aVF is consistent with reciprocal ST depression — which further supports that the main injury is from LCx occlusion.

 

Let me know if you have any follow-up. How is the patient now doing? Any follow-up ECGs? (the distribution of reperfusion T waves might support our theory for what was the "culprit" artery).

MY 2nd REPLY:

NOW I see what is going on !!!! There was LA-LL Lead Reversal on the initial ECG !!!! The usual "clue to this is that the P wave in lead I is larger than in lead II — but that was not at all obvious here, because P waves are almost of similar size. But your post cath ECG shows DEFINITE reperfusion changes in the inferior leads !!! and that would not make any sense if this was an LCx occlusion.

 

I thought lead V1 (as YOU also said) looked funny for LCx occlusion on the original tracing! — and lead II ALSO looked funny, because I would NOT expect reciprocal ST depression — and the AMOUNT of ST elevation in leads I,aVL is more than I've ever seen for LCx occlusion.

BUT — if you make the adjustments that I've made for LA-LL Reversal — then the original ECG fits PERFECTLY with your clinical scenario ( = marked ST elevation in inferior leads with more recip ST dep in aVL than in lead I — and as YOU said, the subtle ST elevation in V1 IS strongly suggestive of acute RV MI! There is also posterior MI which is "masked" because of all the ST elevation in V1,V2 from the RV MI !!!!

And now the post cath ECG makes perfect sense!!!!

I definitely want to use this as an ECG Blog! It may be a month or so until I get to this (because other cases come before) — but do I have your permission to publish this? Please remind me of the city & country from where you are from — as I will acknowledge you and let you know when I publish this. This is a SUPER CASE!

My Blog #396 (https://tinyurl.com/KG-Blog-396 ) is on a lead reversal — but if you scroll down to the bottom of the page — you'll find links to LOTS of lead reversal cases that I've commented on (including a bunch with LA-LL lead reversal) - FASCINATING! — :)

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ECG Blog #375

https://ecg-interpretation.blogspot.com/2023/04/ecg-blog-375-at-least-3-major-findings.html

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The ECG in Figure-1 was obtained from a 50-year old man — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain).

QUESTIONS:

• There are at least 3 principal findings on this ECG — some of which deal with a possible “culprit” artery and/or the location of whatever is going on. How many of these findings can YOU identify?
• 
  
• HINT: Is the rhythm sinus?

Figure-1: The initial ECG in today's case — obtained from a 50-year old man with new chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

As always — I like to start my interpretation of 12-lead ECGs with assessment of the rhythm (as per my systematic approach in ECG Blog-205). Since there is no long lead rhythm strip — I focus my attention on the 3 beats that we see in lead II from the 12-lead ECG shown in Figure-1.

• The QRS complex is narrow — so the rhythm is supraventricular.
• Although we lack a long lead rhythm strip — it appears that the overall rhythm in Figure-1 is Regular — at a Rate between ~80-85/minute (ie, with an R-R interval of between 3-4 large boxes in duration).
• Upright P waves are present in lead II — but there is something unusual about these P waves in lead II. Did you notice this unusual finding that is not typically seen with a normal sinus rhythm?

PEARL #1: Because the overall direction of travel by the electrical impulse with sinus rhythm (as it passes from the SA Node to the AV Node) — is most closely oriented toward the location of lead II in the frontal plane (lead II being located at +60 degrees in the frontal axis plane) — the P wave with normal sinus rhythm should not only be positive in lead II — but also larger in lead II than in lead I (which is oriented at 0 degrees in the frontal plane).

• Note in Figure-1 — that the upright P wave in lead II is clearly smaller than the upright P wave in lead I. While possible that this discrepancy in relative P wave size between leads I and II could be seen with either an ectopic atrial rhythm or certain forms of dextrocardia — this P wave size discrepancy should prompt consideration of the most commonly overlooked form of lead reversal, which is a mix-up of the LA (Left Arm) and LL (Left Leg) electrodes.

What Happens with LA-LL Lead Reversal?

My favorite on-line “Quick GO-TO” reference for the most common types of lead misplacement comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, “LITFL Lead Reversal” in the Search bar — and the link comes up instantly.

• This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and more difficult to predict.
• 
  
• By far (!) — the most common lead reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodes. This lead reversal is usually EASY to spot — because it typically produces global negativity of the P wave, QRS and T wave in lead I — which is something that is virtually never normally seen (See ECG Blog #264 — for an example of LA-RA lead reversal).
• 
  
• In contrast — it is EASY to overlook LA-LL reversal — because the ECG picture seen with this type of lead reversal does not immediately stand out as physiologically “off”. For clarity — I’ve reproduced with slight modification the illustration from LITFL on LA-LL reversal in Figure-2.

Figure-2: LA-LL Lead Reversal (adapted from LITFL).

What Should the Initial ECG in Today's Case Look Like?

For clarity — I've taken the limb leads from the initial ECG in today's case ( = ECG #1) — and inverted lead III — switched leads I and II — and switched leads aVL and aVF. The result is ECG #1a — which is seen in the righthand portion of Figure-3. 

• Note that the chest leads in ECG #1a of Figure-3 — are unchanged from what they were in Figure-1.

QUESTIONS:

Looking at ECG #1a in Figure-3:

• Is the P wave in lead II of ECG #1a now larger than the P wave in lead I (as it should be with a normal sinus rhythm)?
• 
  
• Now that we've established that the 1st KEY finding in today's case is that there was LA-LL Lead Reversal — How would YOU interpret ECG #1a, which shows what today's 12-lead ECG would look like IF lead placement was correct?

MY Interpretation of ECG #1a:

Having accounted for what today's initial tracing would have looked like had lead placement been correct — I see the following in ECG #1a:

• The rhythm is sinus at ~80-85/minute.
• There is dramatic ST elevation in each of the inferior leads. A Q wave is forming in lead II.
• There is equally dramatic reciprocal ST depression in lead aVL (which manifests the mirror-image opposite ST-T wave picture as seen in lead III).
• Significant reciprocal ST depression is also seen in the other high-lateral lead ( = lead I).
• 
  
• In the chest leads — there is significant ST elevation, with a straightened ST segment takeoff in lead V1.
• There is abrupt transition to a surprisingly tall R wave (of ~10 mm) already by lead V2. There is significant ST depression with a positive "Mirror" Test for acute posterior infarction in lead V2. Chest lead ST depression is limited to lead V2.
• There is marked overlap of QRS complexes in virtually all chest leads. The deep anterior S waves and tall lateral chest lead R waves suggest significant LVH.

Putting It All Together: 

After correcting for LA-LL lead reversal — ECG #1a shows sinus rhythm — LVH — and an acute infero-postero STEMI with acute RV involvement.

• PEARL #2: The "culprit" artery in today's case — is almost certain to be the proximal RCA (Right Coronary Artery). As discussed in ECG Blog #141 — ECG features in Figure-3 that strongly support the likelihood of the RCA as the "culprit artery" are: i) ST elevation in lead III>II; ii) Marked reciprocal ST depression in lead aVL; iii) Relatively less (or no) lateral ST elevation, with the amount of ST elevation in lead III > V6; and, iv) Evidence of acute RV involvement. 

PEARL #3: In the absence of an anterior STEMI — acute inferior MI is the result of either acute RCA or LCx (Left Circumflex) coronary occlusion. The LCx does not supply the right ventricle. Therefore, if there is ECG evidence suggesting acute RV involvement in association with inferior STEMI — this is virtually diagnostic of the proximal RCA being the culprit artery. 

• ST elevation in right-sided leads (especially in lead V4R) is clearly the best indicator of acute RV MI. That said — lead V1 is a right-sided lead, and on occasion it may provide insight as to whether or not there is likely to be significant associated RV infarction. 
• Normally the ST segment in lead V1 is flat or slightly depressed. With acute inferior STEMI — ST segments in leads V1, V2 and V3 often show ST depression due to accompanying posterior infarction and/or reciprocal changess due to the inferior STEMI. Typically, such ST depression is maximal in lead V2 — but it should also be present in V1. If ever there is ST segment coving (especially if accompanied by some ST elevation) in lead V1 — there is almost certainly acute RV involvement. This is precisely what we see in lead V1 of ECG #1a.

Figure-3: Comparison of the limb leads from the initial tracing in today's case ( = ECG #1) — with what the initial 12-lead ECG would have looked like ( = ECG #1a) after correction to account for LA-LL Lead Reversal. (To improve visualization — I've digitized the original ECG using PMcardio).

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Acknowledgment: My appreciation to Adem Ahmed (from Nouakchott, Mauritania) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
• 
  
• ECG Blog #190 — When to suspect acute RV Infarction?
• ECG Blog #141 — On acute RCA Occlusion (with RV MI).
• ECG Blog #80 — More on the "culprit" artery.
• 
  
• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery (as well as reviewing why the term "STEMI" — should replaced by "OMI" = Occlusion-based MI).
• 
  
• ECG Blog #285 — and ECG Blog #246 — and ECG Blog #80 — for examples of acute posterior MI (with use of the Mirror Test to facilitate diagnosis). 
• ECG Blog #317 — reviews use (or not) of Posterior Leads.
• 
  
• ECG Blog #184 — and ECG Blog #167 — review the "magical" mirror-image opposite relationship between lead III and lead aVL that helps to confirm acute OMI.
• 
  
• 
  
• ECG Blog #264 — For review of another limb lead reversal (ie, LA-RA lead reversal in a patient with an acute MI).

OTHER Examples of Lead Reversal (from Dr. Smith's ECG Blog):

Technical errors featuring a variety of lead reversal placements remain a surprisingly common “mishap” of everyday practice. As a result — it's important to familiarize ourselves with how best to recognize the various forms of these "misadventures". For review — Check Out My Comment — at the bottom of the page in the following posts on Dr. Smith's ECG Blog:

• The June 4, 2018 post (LA-LL reversal).
• The July 29, 2018 post (LA-RA reversal).
• The November 4, 2018 post (Leads V1,V2 misplacement).
• The February 11, 2020 post (LA-RA reversal).
• The March 18, 2020 post (LA-RA reversal).
• The August 28, 2020 post (LA-LL reversal).
• The November 19, 2020 post (LA-LL reversal).
• The November 27, 2021 post (LA-RA reversal).
• The April 17, 2022 post (Leads V1,V2 misplacement).
• The May 24, 2022 post (LA-LL reversal).
• The May 26, 2022 post (LA-LL reversal).
• The August 17, 2022 post (LA-RA reversal).

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EXTRA COPY — ECG Blog #540: It Doesn't "Fit" ...- EXTRA COPY

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Figure-1: The initial ECG in today's case — obtained from an adult with frequent "palpitations". (To improve visualization — I've digitized the original ECG using PMcardio).

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Figure-2: XXX

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Figure-3: XXX

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Acknowledgment: My appreciation to Paul Carr and Nataliya Szozda (from Toronto, Canada) for contributing this case.

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From Paul Carr

Paul Carr <paul.carr@medportal.ca>  (7/13/2026)

TITLE: — It Does Not "Fit" Clinical —

ME TO ACKNOWLEDGE: — Paul Carr and Dr. Nataliya Szozda (both from Toronto, Canada) 

 

This case is from a rural hospital with no cath lab or stroke thrombolysis capacity.

A 59 year old female was brought by ambulance to the emergency department. She was at a spa and while getting out of the hot tub suddenly became confused and unable to speak. She subsequently had clonic movements and profuse diaphoresis. She was placed in a position of safety.

 

On EMS arrival patient was confused and "post ictal" with ongoing diaphoresis. During transportation she became agitated and combative requiring sedation with midazolam. During transport the monitor showed ECG changes concerning for "STEMI" and so they diverted to my local hospital rather than preceding directly to the nearest stroke centre. On arrival patient was not responsive.

 

The nearest interventional cardiologist was paged and his concern was that with the story not fitting occlusion MI, it was important to work up for other etiologies before considering any medical intervention for possible acute MI.

 

The nearest stroke centre also had interventional cardiology and the stroke team there agreed to take the patient emergently "code stroke".

 

While patient was in transit the initial high sensitivity troponin was 400 (upper limit of normal for our assay is 20).

 

At the stroke centre the patient was found unfortunately to have a necrotic ring enhancing mass with significant surrounding edema favoured to represent a tumour. I do not have a follow-up ECG but my understanding is these ST elevations normalized over 1-2 hours.

 

Paul Follow-Up !!!!

Survived neurologically intact. Now they think might be necrotic transformation of previous stroke rather than tumour. Cardiologist opined may be Takotsubo. Repeat troponin was unchanged.

 

Just saw that they did do a Cath and pristine coronaries with mid-type typical Takotsubo wall motion abnormality.

SSmith! "Clinical does not "fit" OMI. These cases tell you everything you need to know to interpret your case!

Dec. 20, 2021 CASE

https://drsmithsecgblog.com/collapse-ventricular-tachycardia/

 

Feb. 20, 2025 CASE

https://drsmithsecgblog.com/acute-coma-then-sudden-pea-arrest-in-2/

MY REPLY to PAUL — I wrote Steve back the following: THANKS Steve! My Comment on the 2nd case you sent (from Feb. 20, 2025) relates to a subarachnoid hemorrhage causing the pseudo-MI pattern. I hadn’t been aware of brain tumor doing the same, but as per your 1st case — a simple MI should not result in a non-responsive patient — and no flow to the heart as well as the brain + greatly increased catecholamines might raise Troponin and produce bizarre ECG changes that in a patient with CP would say S. Afr. Flag .. — but which in a comatose patient say CNS catastrophe and NO MI. THANK YOU = “Clinical does not fit OMI!” —

 

PAUL — So yes, I DO want to write up this case! I like to acknowledge people — so should I say that the case is from Paul Carr from Toronto, Canada? — or if you prefer, the case can be anonymous — JUST LET ME KNOW! It may be a little while before I publish it as I have other cases to go in front of it.

Otherwise — My wife and I just went on a Tauck tour to Canada's eastern "Capital Cities" and Toronto was our first stop. GREAT CITY! I love the unique skyline! We went up the CN Tower and toured the city. Other stops on the tour were Niagara Falls (Canadian side) — Ottawa, Montréal, Québec — GREAT country, wonderful and friendly people who amazingly still like us Americans after all the mess that our current administration continues to cause (very embarrassing to me!)

Let me know if you find out anything else? Did the patient survive?
I'll let you know when I publish this — :)

 

Paul Follow-Up !!!!

Survived neurologically intact. Now they think might be necrotic transformation of previous stroke rather than tumour. Cardiologist opined may be Takotsubo. Repeat troponin was unchanged.

 

Just saw that they did do a Cath and pristine coronaries with mid-type typical Takotsubo wall motion abnormality.

 

 

MY REPLY (7/14/2026):

Thanks for the clinical & ECG follow-up! Cath very helpful that it ruled out coronary disease and confirmed Takotsubo. That said — although Takotsubo can definitely mimic an acute MI (!) — as Takotsubo evolves, you'll usually see a more prolonged QTc than what we see here ... so would be GREAT if you could find out #1) How much time passed between these 2 ECGs that you have sent me — and #2) Any chance you could check to see if a final ECG was done? (looking to see if the T wave inversion with long QTc finally developed .... GREAT CASE with review of Takotsubo here. THANKS again! — :) Ken

https://ecg-interpretation.blogspot.com/2024/10/ecg-blog-456-woman-with-chest-pain-from.html

 

P.S. You say "Ontario, Canada" — but for "symmetry", is it OK if I say both you and Dr. Szozda are from Toronto, Canada? 

 

P.P.S. It may be a little while until I publish this as I have other cases to go before — but I'll definitely let you know when I do publish it — :)

 

PAUL REPLY (on 7/16/2026):

Thanks as always. Yes Toronto Canada for both is great. There was only about 4 hours between ECGs I believe and I will look for a discharge ECG for completeness. Probably best to have some time before publication to help with anonymity of the case anyway. All the best, Paul

PAUL's COMPLETE CASE !!!!
Hi, Ken, This is Paul Carr writing. Had a very interesting case yesterday I wanted to share in case you wanted to use for the blog.

 

This case is from a rural hospital with no cath lab or stroke thrombolysis capacity.

 

A 59 year old female was brought by ambulance to the emergency department. She was at a spa and while getting out of the hot tub suddenly became confused and unable to speak. She subsequently had clonic movements and profuse diaphoresis. She was placed in a position of safety.

 

On EMS arrival patient was confused and "post ictal" with ongoing diaphoresis. During transportation she became agitated and combative requiring sedation with midazolam. During transport the monitor showed ECG changes concerning for "STEMI" and so they diverted to my local hospital rather than preceding directly to the nearest stroke centre.

 

On arrival patient was not responsive. She was met in the ambulance bay where a formal ECG showed concerning elevation in I and aVL, disproportionately large T waves in I, and reciprocal depression maximal in lead III.

 

The nearest interventional cardiologist was paged and his concern was that with the story not fitting occlusion MI it was important to work up for other etiologies before considering any medical intervention for possible acute MI.

 

The nearest stroke centre also had interventional cardiology and the stroke team there agreed to take the patient emergently "code stroke".

 

I had a broad differential and agreed with the consultant recommendations. Near the top for me was acute aortic syndrome involving the left main coronary with embolic stroke so we did not give any antiplatelet or anticoagulation.

 

While patient was in transit the initial high sensitivity troponin was 400 (upper limit of normal for our assay is 20).

 

At the stroke centre the patient was found unfortunately to have a necrotic ring enhancing mass with significant surrounding edema favoured to represent a tumour. I do not have a follow-up ECG but my understanding is these ST elevations normalized over 1-2 hours.

 

It is important to remember that history is just as important as the ECG itself and that we need to keep an open mind and at least consider a thorough differential for all cases.

 

I'm curious to see what QOH would make of that ECG and also for your expert opinion on the case.

 

Best wishes,

Paul