32 yo with right sided chest pain. Zero ST Elevation, but that does not matter.

This was sent by a reader.  He does a nice job of examining the whole case, so I leave it (mostly) in his words.

32 yo M Sudden onset localized, ‘sharp’ right sided chest pain for 1 hr. 7/10 at worst, now 4/10 with some radiation to both arms. no associated symptoms.

PMH - MS, Cholesterol, Smoker.

FH - Father MI 45

Obs - BP 133/83, RR 20, Sats 95%, examination unremarkable. Bloods pending.

Reader's interpretation:

ECG 1

Sinus rhythm approx 65bpm

normal axis

non-specific inter-ventricular conduction delay (IVCD) versus incomplete RBBB. QRS 100ms

Subtle 'sagging' ST depression I, aVL, V6. no ST elevation

Very tall anterior T waves V1-5 that are symmetrical and disproportionately large (particularly in V4) but neither very peaked or blunted.

The QTc is normal to short, around 400ms

The R wave progression is slow with potential pathological Q waves V3, I, aVL

Reader's comment:

Although I felt the anterior T waves may be hyperacute suggesting a STEMI equivalent (OMI) I did not feel this was diagnostic at the time. Given the atypical pain and well looking patient the initial plan was serial ECGs, CXR, morphine and review with initial bloods in an hour. Not for lab unless evolving ST elevation. This plan was agreed with the on call cardiology registrar.

This was recorded shortly later, (The reader does not give the exact timing):

Reader's interpretation

Overall very similar to the first trace.

There is a reduction in the T wave amplitude and T wave in version in aVL.

There is reduced R wave amplitude in V3 and a new narrow Q wave in V4.

There is perhaps 0.5-1mm ST elevation in V1 only.

I felt these changes were due to chest lead positioning, V1-2 were placed too high for the initial ECG.

Clinical course

Subsequent ECGs over the next 2 hours were similar. The patient looked well and the pain was now a mild ache 1/10 (Smith comment: because of the morphine?).  The CXR was unremarkable as were bloods except high sensitivity Troponin I at 110 ng/L (99th percentile 34 ng/L).  (Smith comment: this is diagnostic of acute MI, and even with a negative ECG, is reason to activate the cath lab if there is ongoing pain, which of course morphine might eliminate)

I treated him as an NSTEMI with Clopidogrel (already loaded with aspirin), Fondaparinux and commenced atorvastatin and bisoprolol. He was admitted directly to the cardiac ward and placed on telemetry. 

When I returned to check on him later in the night shift the patient was sleeping and there were no further ECGs to review.

The following morning the ECG below was recorded. This shows QS complexes throughout the anterolateral leads that suggests a completed extensive anterior STEMI. Repeat Troponin was greater than 10,000 ng/L (large MI, we do not have the peak)

Angiogram

The patient was taken to the lab and a total occlusion of the mid LAD (after a large diagonal) was treated successfully with PCI and stenting. There was also bystander disease and a staged PCI to the proximal RCA was planned. The patient did well and was discharged without significant LV dysfunction or other complications.

Discussion

In hindsight I feel there are very few alternative causes for an ECG like this other than an acute LAD occlusion. I believe this is one of those 'subtle STEMI' cases where neither the ECG nor the symptoms are very obvious or severe and the usual evolution is not seen.

I think of these cases as 'insidious infarcts' and I have seen this in all infarct territories and I do not think they are particularly rare. Essentially the patient is fairly comfortable and the ECG is not obvious but the patient ended up with Q waves, huge troponins and we missed the opportunity to reperfuse the artery when it counts. These patients tend to be younger and do well but I have no doubt that their future risk of heart failure, arrhythmias and premature death is greatly increased compared to if they had PPCI and standard STEMI treatment. Needless to say cases like this have had a significant impact on me and make me strive to be better at spotting subtle ECG patterns and advocating for patients like this having emergent angios.

What could have been done differently.

Applying Smith's subtle anterior STEMI v early repolarisation (4 variable) equation to the first ECG gives a score of 20.6 suggesting STEMI (> 18.2). Although this is arguably outside it's indications as there is a fairly clear Q wave in V3 (note there are lots of exclusions for using this equation). (Smith comment: if exclusions are there because they are indicative of acute LAD occlusion.  If any one of the 8 are present, it is LAD occlusion until proven otherwise.  Here is a link to use of the formula).

A bedside echo (especially with speckle tracking if available) may have helped if there were regional wall motion abnormalities. 

Continuous 12 lead monitoring may have also helped.

FOAM resources that promote recognition and early treatment of 'STEMI equivalent' patterns are promoted by Stephen Smith and Pendell Meyers. This is summed up in their proposed OMI/NOMI terminology to replace STEMI/NSTEMI.

https://emcrit.org/emcrit/omi-manifesto/

http://hqmeded-ecg.blogspot.com/2018/04/the-omi-manifesto.html

Links for the anterior STEMI v early repolarisation equation below.

http://hqmeded-ecg.blogspot.com/p/rules-equations.html

https://www.ncbi.nlm.nih.gov/pubmed/28460689

https://www.mdcalc.com/subtle-anterior-stemi-calculator-4-variable

https://apps.apple.com/us/app/subtlestemi/id617146818

https://play.google.com/store/apps/details?id=com.SMITH490.ecg_smith&hl=en

Smith comment:

1. Morphine should never be given until you are committed to the cath lab.  Pain was 1/10 probably due to morphine.

2. One must learn how to recognize hyperacute T-waves.  These ones are the real thing and cannot be anything else.  The first ECG is absolutely diagnostic of acute LAD occlusion and the cath lab should be activated immediately.

3. Young people do have MI!!


Here are 2 recent cases that are similar:

Case 2. This patient was brought by EMS.  The hyperacute T-waves were immediately recognized by the medics and the patient went expeditiously to the cath lab.   1972765.

Diagnostic hyperacute T-waves in V2-V5Even the small ones are hyperacute, as they are huge in proportion to the QRS and they are "Fat" and symmetric.

This was the patients ED ECG:

Again, diagnostic hyperacute T-waves in V1-V5.

Case 3. Here is a case that was diagnosed and treated immediately, but the myocardium was completely infarcted anyway, without ever developing any ST elevation.

Prehospital ECG:

de Winter's T-waves in V2
Hyperacute in V1-V6, II and aVF
They are symmetric and fat, and also tall.  They tower over the QRS.  The T-wave in V6 is not at all large in any absolute sense, but it is huge in proportion to the QRS.

Here is the ED EDG:

de Winter's T-waves in V3, hyperacute from V1-V6.

And the post-reperfusion ECG:

Notice:
Even though there was never ST Elevation, and the patient underwent rapid reperfusion, there are fully developed QS-waves, indicative of profound anterior wall infarction.

Furthermore, a hyperacute T-wave need not be large, or even proportionally large:  Sometimes a hyperacute T-wave is only symmetric, but not large, as Case 3 below:

Case 3.

Small T-waves that are hyperacute just because they are symmetric.  

The T-waves in II, III, and aVF are hyperacute only because of their symmetry.
I recognized these hyperacute T-waves immediately as part of a study we are doing.  No one else saw them at all.  Another clue is of course the slight STD with T-wave inversion in aVL. 
The next day angiogram, and their disappearance after reperfusion, proved that they were indeed hyperacute Ts due to RCA OMI.

Here is the post reperfusion ECG:

Here is how normal assymetric inferior T-waves look:

Hyperacute T-waves:

Ten (10) Examples of Hyperacute T-waves in Lead V2 (a few in V3), due to acute LAD occlusion

10 Cases of Inferior Hyperacute T-waves

Ten cases of hyperacute T-waves in V4-V6

Hyperacute T-waves "On the way down"

Here are 44 cases with hyperacute T-waves: 

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MY Comment by KEN GRAUER, MD (2/18/2020):

===================================

Our most sincere THANKS to the reader who submitted this case. CREDIT to him/her — for his/her soul-searching account! Hindsight is always much easier in the “retrospectoscope”. I’ll focus my comments on a few additional thoughts to those made by Dr. Smith.

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

Figure-1: The first 2 ECGs that were shown above in this case (See text).

MY THOUGHTS on this Case — Although the patient in this case is young (32yo) — he is a smoker — his family history is worrisome (father with MI at age 45) — and, his symptoms are new, and these new symptoms led to presentation in the ED.

• Especially when there are concerning features in the history — The onus has to be on us to rule out (rather than to rule in) the possibility of an acute cardiac event. As a result — IF the initial ECG is not normal, we need to prove that the ECG abnormalities are not acute (rather than the other way around).
• IF in doubt after evaluating the patient the best you can — Err on the side of caution. Better to cath a patient who doesn’t need it — than not to cath someone who does.

Regarding ECG #1 — The reader was systematic in their interpretation, and he/she identified the main abnormal findings. LOOKING CLOSER at ECG #1:

• In the limb leads — larger and wider-than-expected Q waves are present in leads I and aVL. That said, I wasn’t convinced these limb lead Q waves were significant to the case at hand — and I thought overall ST-T wave changes in the limb leads of ECG #1 were nonspecific.
• NOT SO in the chest leads. Starting from a definite R wave in lead V1 (3 mm in amplitude) — there is Loss of R wave from V1-to-V2. That this is real-until-proven-otherwise, is supported by the very wide and deep Q wave in lead V3 (BLUE arrow) This suggests anterior MI has occurred at some point in time.
• The reader correctly identified, “very tall anterior T waves in V1-thru-V5 that are symmetrical and disproportionately large (particularly in lead V4)”. In a patient with new symptoms — especially in association with loss of R wave + the very-large-and-wide Q wave in lead V3 — this description by the reader is how I would define hyperacute anterior T waves.
• I would add that T waves are fatter-than-they-should-be at their peak (at least in leads V1, V4 and V5) — and, that these T waves are wider-than-they-should-be at their base (at least in leads V1, V3, V4 and V5) — therefore, clearly to be assumed hyperacute in a patient with new symptoms until proven otherwise.

Regarding ECG #2 — We are not told how much time passed between the recording of ECGs #1 and #2. The important point, is that although subtle — there has been serial change between these 2 tracings.

• I thought there was no significant change in the limb leads between ECGs #1 and #2.
• BUT — there has been further loss of anterior forces — seen as development of a very wide-and-deep Q wave in lead V2 + a Q wave in lead V4 (RED arrows in ECG #2 denoting Q waves).
• As noted by the reader — T wave amplitude has indeed decreased in multiple leads (ie, the T wave is not as tall in ECG #2 as it was in ECG #1 in leads V1, V2, V3 and V4). Further support that this decrease in T wave amplitude represents a dynamic ST-T wave change — is provided by the unusual short segment of ST straightening that we see in lead V1 (PURPLE arrow) — which replaces the upward-sloping ST segment that we previously saw in lead V1 of ECG #1. This is not artifact. It is real.
• NOTE: While true that there is now a small negative component to the P wave in leads V1 and V2 of ECG #2 that was not present in ECG #1 — one can not attribute all of the dynamic ST-T changes just described (that occurred in each of the first 4 chest leads) simply to positioning 2 leads (ie, V1,V2) too high on the chest. IF thought that these differences between ECGs #1 and 2 were simply due to lead malposition — then ECG #2 should have been immediately repeated after verifying chest lead placement. This clinical point is important — since IF questions persisted as to whether ECG findings were or were not acutely evolving — demonstration of dynamic ST-T wave change proves that they are.

BOTTOM LINE — Soul-searching cases is TOUGH. But it is an invaluable part of optimizing future treatment. We are indebted to the reader who shared this case with us — so that we can all learn from it.

A 53 yo woman with cardiogenic shock. Believe me, this is not what you think.

This was sent by a reader.

A previously healthy 53 yo woman was transferred to a receiving hospital in cardiogenic shock.

pH was 6.9 and K was normal.

Here was the ECG:

There is sinus tachycardia.
This is "Shark Fin" morphology.

Shark Fin has also been called:
"Giant R-wave"
"Triangular QRS-ST-T waveform"

Usually shark fin is in one coronary distribution and represents massive ST elevation that is as high as the peak of the R-wave and therefore fuses the R-wave and ST segment.

So Shark Fin really is just a dramatic representation of STEMI, and can be in any coronary distribution.

It is often confused with a wide QRS due to conditions such as hyperkalemia. But it is very distinct from hyperkalemia (and anything else, including VT), and such confusion can only be due to lack of familiarity, because, if you look closely, its morpholgoy is very different from anything else.


So this is STEMI, right? 

Which artery?

There is ST Elevation in every lead except aVR (STD in aVR).

Well, don't we see diffuse ST Elevation in Myo-pericarditis (with STD in aVR)?  Could this be myopericarditis?

The patient was hypothermic at 90 degrees F (32.2 C) and she was positive for influenza.  Her troponin I was 500.01 ng/mL (equivalent to a high sensitivity troponin I of 500,000 ng/L).  This is among the highest troponin I of which I have ever heard.

Her ejection fraction was 10%.

She was taken to the cath lab and her coronaries were clean!!

There was no MRI, but the presumptive diagnosis is myocarditis.

Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia.  Here is what he wrote:

"This is a marker of coronary perfusion pressure in the context of severe elevated in LVEDP outside the range of coronary auto regulation. I have seen this pattern in severe acute AI also."  In other words, the severely increased end diastolic pressure from the extremely poor LV function caused by the myocarditis results in extremely poor coronary perfusion pressure.

===================================

MY Comment by KEN GRAUER, MD (2/16/2020):

===================================

As per the title by Dr. Smith — this case was not what I thought. I did recognize the Shark Fin morphology of dramatic ST elevation. Shark Fin morphology has been shown on Dr. Smith’s blog a number of times, including:

• In the June 11, 2018 post —
• In the October 4, 2019 post —
• In the November 22, 2019 post —
• in the January, 24, 2020 post —

PEARL — What I did not appreciate when I reviewed this case — was that among the many potential etiologies of acute myocarditis was HypoThermia! 

• I have summarized the major etiologic categories of acute myocarditis and inflammatory cardiomyopathies. A more complete listing of specific etiologic agents can be found on the source I used to prepare Figure-1 (Kühl Uwe & Schultheiss Heinz-Peter: Myocarditis — Deutsches Ärzteblatt Int. 109 (20):361-368, 2012 — CLICK HERE).
• Referring to Figure-1 — this 53-year old woman who presented in extremis with cardiogenic shock and an initial pH = 6.9, had at least 2 potential etiologies for developing acute myocarditis: i) Profound hypothermia (core temperature = 90°F = 32.2°C); and, ii) She tested positive for influenza.

Figure-1: Potential etiologic categories of acute myocarditis (See text).

Our THANKS to Dr. Smith for presenting this case!

A man in his 50s with "gas pain"

Written by Pendell Meyers, sent by Anonymous


A man in his 50s with history of type 2 diabetes, HTN, and HLD presented with one day of off and on chest / upper abdominal pain. It had awoken him from sleep earlier, and he described it as "gas pain," located in the upper epigastrium and radiating upwards. Vitals were within normal limits. The patient presented with active pain, diaphoretic and ill appearing.

Here was his triage ECG (sorry for the quality, unable to obtain better images from sender):

Last ECG on file is below for comparison. First try this ECG without the baseline, then with. What do you think?

Previous ECG on file (never just assume its the baseline, but I think this one looks consistent with a baseline).

The presentation ECG shows sinus rhythm at almost 100 bpm. There is STD in V3-V6 (maximal in V4-5) and lead II, aVF, I, and aVL. Because of widespread STD, there is obligatory STE in aVR (the aVerage Reciprocal lead of the rest of the ECG).

This pattern in isolation would signify diffuse supply/demand mismatch without focal complete occlusion, which would be a very large differential of anything causing severe global supply demand mismatch, including ACS and various other processes. However, there is STE in V1 with a large area T-wave which is hyperacute.

This fits the pattern we have described many times including recently, of subtle STE and hyperacute T-wave in V1 with STD in the lateral precordial leads, indicative of LAD occlusion (more specifically, subtotal occlusion, just before the pattern of full occlusion).

I emailed just the presentation ECG to Dr. Smith, without any history, and he replied "LAD. Not totally occluded. 99%. TIMI 1 flow."

If you don't see it, you must use these links below to see many other examples until you can see why it fits the pattern:

A man in his sixties with chest pain, tachypnea, and hypertension

A 40 year old man with chest pain since last night

A man in his sixties with chest pain at midnight with undetectable troponin

How long would you like to wait for your Occlusion MI to show a STEMI? Sometimes serial ECGs minimizes the delay.

What will you do for this patient transferred to you who is now asymptomatic?

Crushing Chest pain, but the ECG is not obvious; later there is both RBBB and LBBB

35 yo woman with LAD occlusion manifesting with only hyperacute Ts and inferior ST depression, also missed by computer

The pain increased within the first 15 minutes and this repeat ECG was obtained:

What is this?

This is classic de Winter pattern in V3 and V4 (depressed ST takeoff with hyperacute T-wave). V1-V4 have hyperacute T-waves. Reciprocal STD in inferior leads. We believe that the transition from the presentation ECG to this signifies the process of going from near total occlusion (~99% ~TIMI1 flow) to complete occlusion.



The cath lab was activated immediately. They presented to bedside and more serial ECGs were obtained:

25 minutes:

While waiting for the cath lab to be ready, another ECG obtained:

At cath they found and opened a complete proximal LAD occlusion (images unavailable). Unfortunately, peak troponins and echo are also unavailable.

The patient was discharged home in good condition several days later.

Learning Points:

You must learn this pattern of near-total LAD occlusion, as well as de Winter's T-wave pattern.  If you can intervene at this early stage, you will salvage a lot of myocardium. Some patients will not progress (or not as quickly) to obvious STEMI, as in this case.  Nevertheless, they also will get enormous benefit from emergent cath due to preemption of progression to full thickness MI.

Even in a case like this, in which OMI evolves into obvious STEMI, expert ECG interpretation at the earliest stage, beyond the STEMI paradigm, leads to faster reperfusion and limits the extent of this patient's infarction.

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MY Comment by KEN GRAUER, MD (2/14/2020):

===================================

I think this case provides an excellent example of how we can learn by retrospective review of serial tracings.

• CREDIT to Drs. Meyers and Smith, who instantly recognized impending LAD occlusion
• Although I completely agreed on the need for prompt cardiac cath in this 50s man with risk factors and new symptoms — I did not initially recognize the “culprit artery”.

I thought it might be worthwhile to explore WHY it took me longer than I would have liked to recognize the “culprit artery”.

• PEARL — One of the best ways to hone your ECG interpretation skills — is by retrospective review of serial tracings on cases in which you know the anatomy. Going back to ECGs in which you may not have recognized all findings the first time you looked — is often humbling, and tremendously insightful (especially when you know “the answer” as revealed by cardiac cath).
• Cardiac cath in this case confirmed acute proximal LAD occlusion. Correlating evolution of this patient’s symptoms in the ED, with corresponding evolution of serial ECGs tells us (as per Drs. Meyers & Smith) — that the initial ECG in the ED ( = ECG #1 in Figure-1) represented high-grade LAD narrowing, but not yet complete occlusion.
• It was only later (when ECG #3 was obtained) — that complete occlusion of the proximal LAD occurred.

Figure-1: The first 3 ECGs that were shown above in this case. (See text).

MY RETROSPECTIVE THOUGHTS on this Case — I encourage review of the 7 cases that Dr. Meyers provides links to above — each showing ECGs with acute LAD occlusion. NO 2 ECGs are ever the same — so the more one’s eye reviews patterns in which we “know” the answer — the better (and faster) one gets at recognizing these KEY patterns of acute LAD occlusion.

That said — I had an easier time recognizing the “culprit artery” in each of these 7 cases, than I did for ECG #1. ECG findings that helped me to recognize LAD OMI in these 7 cases included:

• In addition to inferior lead ST depression — some of these 7 tracings showed ST elevation in lead aVL (which is often a great clue to proximal LAD occlusion). Note that there is no ST elevation in lead aVL of ECG #1 in Figure-1.
• Some of these 7 tracings showed subtle-but-definite ST segment straightening and/or elevation in at least 2 (if not all 3) anterior leads. Note that there is no ST elevation in leads V2, V3 or V4 in ECG #1.
• The shape of the abnormal ST elevation in lead V1 in some of these 7 tracings was clearly coved (ie, “frowny”-configuration). The ST segment in lead V1 of ECG #1 is not coved (ie, it is upward-sloping = a “smiley” configuration). Dr. Meyers astutely noted that there is indeed ST elevation in lead V1 of ECG #1 with a “large-area T wave that looks hyperacute”. PITFALL — Perhaps because amplitude of the QRS complex in lead V1 of ECG #1 is so small, it is easy to overlook that the J-point in this lead is indeed 1 mm elevated above the PR segment baseline. Normally, the T wave in lead V1 may be positive — but it should not be as disproportionally large as it is in ECG #1 (and the T wave in lead V6 should normally be larger than the T wave in lead V1 — and this is not the case in ECG #1!).
• Some of these 7 tracings showed at least one (or more) anterior T waves that were more obviously fatter-at-their-peak and/or wider-at-their-base than what we see in ECG #1. Clearly, the T wave in lead V3 of ECG #1 is taller and more pointed than is usually seen — but it is narrow at its peak, and relatively narrow at its base.

THOUGHTS on ECG #2 (the Baseline Tracing): As per Dr. Meyers — the diagnosis of impending LAD occlusion in this patient with new symptoms can (and should) be made on the basis of ECG #1 alone. That said — having access to a Baseline tracing (that is shown in ECG #2) confirms that the ECG findings in ECG #1 are acute:

• The diffuse ST depression seen in ECG #1 was not seen in the earlier tracing!
• The ST-T wave in lead V1 of ECG #2 was completely flat. This confirms that the hyperacute appearance of the ST-T wave in lead V1 of ECG #1 is new!
• The disproportionally tall and remarkably pointed T waves in leads V2, V3 and V4 of ECG #1 are all new!

THOUGHTS on ECG #3: The reason ECG #3 was obtained just 15 minutes after ECG #1 — was because of an increase in the patient’s chest pain. As per Dr. Meyers — ECG #3 now shows a classic de Winter T wave pattern. Note the following:

• Starting from several millimeters of J-point depression (most marked in leads V3 and V4 of ECG #3) — an upward-sloping ST segment rises to very prominent T waves (with a giant T wave in lead V3). Note how fat-at-their-peak and wide-at-their-base the T waves in most chest leads have become compared to what they were in ECG #1.
• DID YOU SEE the marked loss of R wave in the anterior leads of ECG #3? R waves in leads V2, V3 and V4 were tall in ECG #1. The fragmented initial part of the QRS complex in leads V2 and V3 (with initial Q in V2) + the classic de Winter T wave pattern — tells us that the high-grade proximal LAD narrowing is now completely occluded.

GOING BACK to ECG #1: In view of what the baseline tracing on this patient looked like — and, now knowing what the ECG will look like in 15 minutes (ie, in ECG #3) — it becomes much easier to see:

• That the subtle-but-real ST elevation with disproportionately large T wave (considering small size of the QRS) in lead V1 of ECG #1 provides early indication of the more obvious hyperacute ST straightening and T wave fattening that we see in lead V1 of ECG #3.
• That in retrospect, the T waves in leads V2, V3 and V4 of ECG #1 are all clearly hyperacute — and together with clearly abnormal J-point depression in leads V3, V4 of ECG #1 — we are seeing early indication of the frank de Winter T wave pattern that is about to evolve. BOTTOM LINE: Rather than non-localized diffuse ST depression with ST elevation in lead aVR — the overall picture in ECG #1 provides clear indication of impending proximal LAD occlusion. This case is highly insightful as to HOW the pattern of de Winter T waves may develop.

Our THANKS to Dr. Meyers for presenting this instructive case!