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Sunday, April 6, 2025

SSmith -DRAFT (KG- Done) RePost from 3-28-2017 (4-6.1-2025) - I_am_DONE

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MY Comment, by KEN GRAUER, MD (4/6/2025):

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I find it interesting to periodically look back at my ECG interpretations (and at the interpretations of others) from a number of years earlier. I fully acknowledge that doing so provides a number of "cringe moments" for me (in which I find myself thinking "How could I have said that?" ). But that was then — and now is now.

Today's case is a "repost" from March 28, 2017 — or just over 8 years ago ...
The "OMI Manifesto" was published by Drs. Meyers, Weingart and Smith shortly after today's repost, in the April 1, 2018 post of Dr. Smith's ECG Blog.
In the 8 years since today's repost — Drs. Smith, Meyers, McLaren and others have published an expanding number of relevant references supporting the OMI Paradigm as proving itself to be far superior to the outdated and insensitive STEMI paradigm (over 80 references already included in this listing, with this number continually increasing — and, with all references conveniently linked for you in Dr. Smith's OMI Literature Timeline, which is found in the TOP Menu Tab of every page in this ECG Blog).

The Initial ED ECG from Today's Case:

As per Dr. Smith — the 3 prehospital ECGs in today's case were "lost", and therefore not seen by ED providers. As a result — initial decision-making was based on the ECG in Figure-1 (which is the 4th ECG shown above in Dr. Smith's discussion — but the 1st ECG that was recorded in the ED). I focus my comments on this initial ED ECG:

Initial decision-making in the ED was most probably influenced by the younger adult age (30 something) of this previously healthy (without risk factors) woman — who presented with trapezius pain radiating to her throat, but not to her chest.
The patient's CP (Chest Pain) resolved completely after receiving NTG.
ECG #4 (in Figure-1) — was obtained very shortly after NTG was given (such that we do not know whether ST-T wave changes might have looked very different after a few more "pain-free" minutes had passed).
AND — Remember that today's case is a repost from 8+ years ago.

I found today's repost insightful for highlighting what we hope has at the very least improved — since practice patterns in 2017.

Figure-1: The initial ECG that was recorded in the ED.

What We Hope has Improved:

It's hard to know how the 3 prehospital ECGs got "lost". Hopefully in 2025, among the 1st things EMS providers do on arrival in the ED when transporting a "Rule Out MI Patient" with clearly abnormal prehospital ECGs — is to debrief and directly show those tracings to the ED provider.
Hopefully in 2025, more providers are aware that as many as 25% of initial Troponin values in STEMI patients may be normal (Wereski, Smith, et al — JAMA Cardiol 5(11): 1302-1304, 2020). As a result, especially in a patient such as in today's case in which the onset of symptoms is so recent and short-lived — it should not be unexpected for the initial Troponin to be normal.
Hopefully serial ECGs (with repeat of the initial ED ECG occurring within 15-30 minutes, and as frequently as needed thereafter) are now routine in the overwhelmingly majority of centers (instead of the 4+ hour delay in today's case until an elevated Troponin finally came back as the prompt to repeat the initial ED ECG).
Hopefully a tracing as abnormal as today's initial ED ECG (especially in a patient with new symptoms) — will be promptly recognized.
And hopefully emergency providers now realize that although being a younger adult woman without risk factors lowers the risk of an acute cardiac event — it does not eliminate such risk (as today's case conclusively proves). This is all the more true given how abnormal today's initial ED ECG is.

Today's Initial ED ECG:

Recognition of acute LAD OMI until proven otherwise — should occur within seconds of seeing the ECG in Figure-1:

After identifying normal sinus rhythm — my "eye" was immediately drawn to the hyperacute T wave in lead V3. The height of this T wave is literally twice that of the height of the R wave in this lead — with a prolonged QTc and an extremely wide T wave base. In a patient with new symptoms — there is no way this giant, hypervoluminous T wave is going to be a normal variant.
My "eye" was next drawn to the ST-T wave in lead V1 — which shows ST segment coving, J-point ST elevation, and terminal T wave inversion. There is no way that this is a normal ST-T wave morphology in lead V1.
Armed with the knowledge in this patient with new symptoms that leads V1 and V3 are clearly hyperacute — it becomes easy to recognize ST-T wave abnormalities in each of the remaining chest leads.
The T wave in lead V2 is taller than the R wave in this lead — and this T wave is clearly "fatter"-at-its-peak and much wider-at-its-base than should be expected, given very modest size of the QRS complex in this lead.
The T wave in lead V4 is still huge (over 10 mm tall). And while relative T wave size is less in leads V5,V6 — I still interpreted these lateral chest lead T waves as overly "bulky" compared to what I would normally expect given QRS appearance in these leads.
A subtle but additional supportive sign is seen in lead aVL, which clearly shows abnormal ST segment straightening.

Impression: In this patient with new symptoms — this initial ED ECG is alreadly diagnostic until proven otherwise of acute LAD OMI regardless of the lack of risk factors — and regardless of the initial normal Troponin.

Since this patient's CP has just been relieved by NTG as ECG #4 was being recorded — repeating this initial ED ECG within the next 10-15 minutes would probably remove any doubt one might still have about the diagnosis, since complete relief of symptoms most likely heralds spontaneous reperfusion, that typically is accompanied soon thereafter by resolution of hyperacute ECG changes.
I know that I have learned a lot about the diagnosis of acute OMIs over these past 8 years.

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

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30 yo woman with trapezius pain. HEART Pathway = 0. Computer "Normal" ECG. Reality: ECG is Diagnostic of LAD Occlusion.

This is a repost of this amazing case:

Echocardiography, even (or especially) with Speckle Tracking, can get you in trouble. The ECG told the story.

A completely healthy 30-something year old woman with no cardiac risk factors had sudden onset of bilateral trapezius pain that radiated around to her throat. It resolved after about 5 minutes, but then recurred and was sustained for over an hour. She called 911.

EMS recorded these prehospital ECGs:

Time 0:

In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 mm at the J-point, relative to the PQ junction. But there are also unusually Large T-waves

Time = 13 min

T-wave in V2 is now taller and fatter, the ST segment is more straight.
T-wave in V3 is no taller, but it is fatter due to a straighter ST segment

These are hyperacute T-waves that are DIAGNOSTIC of LAD Occlusion.

Time = 24 min

S-wave depth is diminishing

These prehospital ECGs were lost and not seen.

The patient arrived in the ED.

The pain completely resolved after nitroglycerine

Moments later, the this ECG was recorded in the ED when she had been pain free for moments only:

Computer read: Normal ECG.

However, T-waves are still unusually hyperacute; the computer almost never sees this.

The T-wave in V2 is smaller. QTc is 444 ms.

How about using the 4-variable formula?
STE 60 V3 = 1.5 mm, R-wave amplitude V4 = 15 mm, QRSV2 = 8.5
Formula value is 19.38, which indicates LAD occlusion

(Most accurate cutpoint is 18.2 -- value ＞ 18.2 has high probability of LAD Occlusion).

This patient has a non-diagnostic ECG by most rules.

However, with attention to subtleties, especially when compared with the unseen prehospital ECGs, it is diagnostic of LAD occlusion with probable spontaneous reperfusion.

The first troponin was below the level of detection (LoD).

If you use something like the HEART score:
1. H History: She has atypical pain (trapezius) (score = 0)
2. E EKG: a negative ECG (score = 0)
3. A Age: = 0
4. R Risk factors = 0
5. T: Troponin = 0 [first troponin (contemporary, not high sensitivity) was less than the level of detection).
Total HEART score = 0. Risk of 30-day adverse events is less than 1.7%. Some might send her home.

But maybe she has an acute LAD occlusion that will get even worse.

The providers did a bedside echo and even used speckle tracking to look for strain:

hyperacute T-waves standard echo nstemi vid 3 from Stephen Smith on Vimeo.

I think maybe there is an anterior wall motion abnormality, but this is very difficult. They read it as normal.

Here are a couple shots with strain, or "speckle tracking" on ED Echo:

hyperacute T-waves speckle 1 x4 from Stephen Smith on Vimeo.

hyperacute T-waves speckle 2 x4 from Stephen Smith on Vimeo.

To, me these look like anterior wall motion abnormality, but I showed them to one of our ultrasound fellows who is very interested in this.

She said:

This is a tough one. I see what you mean, initially when I looked at the image, I also thought there was an anterior wall motion abnormality. But then on closer inspection, I suspect that maybe the anterior wall is just not being tracked well. In systole, you can see the anterior wall come down and outside of the area that is being tracked (more so than the other tracked walls). Even though the strain values are a little off in the graph (so is the posterior wall) it is still a value range (about -18) that would be considered non-ischemic by the cardiology literature, I believe. I have been wrong before though! So it is possible that I am misinterpreting the clip. If it were me, I would get values at the level of the mitral valve, papillary muscles, and apex (all in PSS axis). Also, narrowing the area being tracked helps the walls get recognized much better.

As I wrote, the first troponin was below the Level of Detection.

She remained pain free, and was admitted without further serial ECGs.

When in doubt, one should always get serial ECGs. Bedside echo is not enough.

At time = 240 minutes (4 hours), the second troponin returned at 1.15 ng/mL. That prompted recording of this ECG:

Back to normal for this patient. This demonstrates that all ST elevation of the previous ECGs was ischemic, not normal. She was having a transient STEMI, briefly.

It is very lucky that she spontaneously reperfused her LAD. It did not progress to full STEMI with loss of the anterior wall, as in this case.

Also, persistence of a pain free state does not guarantee an open artery. See this case.

A formal contrast echo was done at this point:

Normal estimated left ventricular ejection fraction, 65%.

Regional wall motion abnormality-distal septum and apex.

She was treated medically for NonSTEMI, pending next day cath, which showed ulcerated plaque and a 60% thrombotic stenosis in the LAD distal to the first diagonal.

It was stented.

Learning Points:
1. Always get serial ECGs when there is any doubt about what is going on.

2. Use the 4-variable formula!!

12 Example Cases of Use of 3- and 4-variable formulas, plus Simplified Formula, to differentiate normal STE from subtle LAD occlusion

3. Always find and look at prehospital ECGs. They give extremely valuable information.
4. Hyperacute T-waves remain for some time after reperfusion of an artery. I always say that "you get hyperacute T-waves both 'on the way up' (before ST segment elevation) and 'on the way down' (as ST elevation is resolving).
5. Wall motion abnormalities are very hard to see, even with advanced Speckle Tracking technology. They require a great bubble contrast exam and expert interpretation.
6. This case does not demonstrate it, but a wall motion abnormality may disappear after spontaneous reperfusion (see this case).
7. Patients with transient occlusion may manifest only transient STEMI on ECG. Subsequent troponins may be all negative and subsequent formal echo may be normal. See this case.

8. Risk scores + EKG and troponin should not be considered negative unless there are 2 troponins.

9. Risk scores should not be used at all in the setting of a diagnostic EKG. These are DIAGNOSTIC of LAD OCCLUSION.

Wednesday, February 12, 2025

I-Movie DEMO for Willy - His "Not Pericarditis" Case (2-12.1-2025)-for_WILLY

Willy — I decided to show you on my "scrap Blogspot Blog" what your cath films can look like with just a few minutes using imovie. It is very easy in just a few minute on imove to load your cath videos and "freeze" in the middle of the vide — cut the video in that precise spot — shot a still screen on imovie at that point — then insert the still there, and leave the still for as long as you want. You can very easily (and quickly) on your computer screen take that still picture you just made and ADD your labels — and then resume the video.

Your 1st video on the "Not Pericarditis" case IS long enough for me to get a feel as to what is going on. You still can TEACH viewers how to see cath findings in REAL TIME by adding a still and then adding a labeled still — and then resuming the video.

Your 2nd video is too short for me to be able to see anything. Even with your description 2-3 seconds is not enough time. So I slowed this down, added a still and then resumed the video. Again, imovie makes perfrect screen shots by selecting "Save Current Frame".

WILLY — I am providing feedback to you because you've indicated that you would like my feedback. But if at ANY point what I provide is "too much" — just tell me and I will stop. I just think you have done soooooo much to facilitate teaching cath film interp. by non-cardiologists — and that the amount of work (and time) that it would take to bring your cath teaching to the "next level" is not much with just a little practice (and OBVIOUS to me from all you've done up to now that you are SKILLED with technical things!

Attached below figure showing how I make a screen shot with imovie. Below that is the Video that I made slowing the video ( = prolonging it) and adding stills. But I did NOT yet add your labeled stills. Ideally these should be done on the screen shots that imovie makes because the "freeze" shot then is PRECISE — and will look so cool when you free — show a blank still — superimposed to your labeled still — and then resume the video — :) This

This screen shots shot shows me freezing the video and selecting "Save Current Frame" to make an imovie screen shot.

This is the little video I made You can make the freezes as long or as short as you like — same for the absolute control you have for slowing down the video — :)

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WILLY Draft (2/12/2025):

Written by Willy Frick

A man in his mid 30s with type 1 diabetes presented with two days of midsternal and epigastric pain, described as both "sharp" and squeezing." There was associated nausea, vomiting, and dyspnea. He said the pain was worse with supination and improved with upright posture.

What do you think?

Despite the noisy baseline, this ECG is easily diagnostic for OMI. The Queen of Hearts diagnoses OMI with 0.99 confidence (near perfect). Here is her explainability.

Here are some of the diagnostic findings:

Very subtle hyperacute T waves (HATW) in lead I

STE and HATW in II > aVF

Subtle STD in V1 and V2

STE and HATW in V5 and V6

Therefore, we have an inferior, posterior, lateral OMI. In fact, even the GE algorithm got this one (partially) right.

The emergency medicine physician documented, "His initial EKG is riddled with artifact and difficult to interpret but does not look like a STEMI." This is a very bold statement in a type 1 diabetic with very concerning sounding chest pain. One wonders why repeat ECG was not immediately performed if artifact was the problem. The patient was treated with aspirin and a GI cocktail and troponin was obtained, which did not help the pain.

Initial hsTnI resulted at 25,994 ng/L (ref. <35 ng/L). At this point, the physician started heparin and gave nitroglycerin, which improved the pain from 7/10 to 3/10 and performed repeat ECG.

Once again, easily diagnostic for inferior, posterior, lateral OMI. Getting rid of the artifact increased the Queen's confidence from 0.99 to 1.0 (perfect). The ECG remains positive for STEMI by GE. The emergency physician consulted cardiology. Despite apparently hearing the above history together with two diagnostic ECGs and a troponin compatible with OMI, the cardiologist thought the ECG represented pericarditis and recommended echocardiogram.

Several hours passed with no documentation as to the reason for delay. Echocardiogram was finally performed five hours after the first ECG showing STEMI (+) OMI. The report indicates LVEF 35-40% with "globally reduced wall motion with regional abnormalities." The cardiologist then recommended emergent transfer to a PCI center.

Upon arrival at the PCI center, he was immediately taken to cath lab. Angiogram showed thrombotic subtotal occlusion of LCx/OM1. Here is an AP caudal view before and after PCI.

The true AV groove LCx was "jailed" by the stent and appears occluded in the post PCI image. The OM is a much larger vessel.

With the delays and recognition and transit, time from first diagnostic ECG to balloon was 15 hours and 47 minutes. This far out, the benefit of PCI is very attenuated. Troponin peaked above the upper limit of quantitation 60,000 ng/L. Echocardiogram showed LVEF 33% with akinesis of the lateral wall.

Here is the wall motion diagram. The view above is enclosed in a red box.

Final diagnosis written in the chart: NSTEMI

Discussion:

It is hard to understand how this can happen, but unfortunately the blog has innumerable similar cases. If I had to guess, I think some of the cognitive errors that may have contributed to this case are:

The patient was young, in his mid 30s. But you are never too young to have an OMI. Even if it is not atherosclerotic, young people can have embolic OMIs.

The ECG was perceived as having diffuse ST elevations. But it is not really diffuse -- it is inferior, posterior, and lateral. The anterior leads clearly show reciprocal change.

The absolute degree of ST elevation (although enough to meet STEMI criteria), was still relatively small.

We also see that in the end the patient was labeled as NSTEMI, despite meeting STEMI criteria and having acute coronary occlusion. So the diagnosis does not reflect the ECG or the pathology. Instead, the diagnosis reflects how urgently he was treated.

Now, when the data are sent to the National Cardiovascular Data Registry, it will appear that the patient was treated appropriately as an NSTEMI! There is no external auditing of diagnoses selected by treating cardiologists, so missed door-to-balloon time metrics can easily be avoided by simply calling cases NSTEMI.

Saturday, January 25, 2025

SCRATCH Post-2 — to Embed PDF into Blogspot (1-25.1-2025)

This is from ECG Blog #272 —

The patient is a man in his 70s — with symptoms for the past 3 days. He presented to the ED with worsening chest pain. His initial ECG is shown in Figure-1.

QUESTIONS:

Should you activate the cath lab?
How many of the 12 leads manifest abnormal ST-T wave changes?
Is the low voltage a relevant finding?

Figure-1: Initial ECG in the ED — obtained from a man in his 70s with 3 days of chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

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NOTE: Some readers may prefer at this point to listen to the 4:00-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on these tracings (that appear below ECG MP-80).

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Today's ECG Media PEARL #80 (4:00 minutes Audio) — Reviews the ECG finding of Low Voltage (and potential clinical implications of low voltage in the setting of acute MI).

NOTE: For more on "Voltage Discordance" (ie, when there is low voltage in the limb leads — but normal voltage in the chest leads) — See the ADDENDUM at the bottom of this page.

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MY Approach to the ECG in Figure-1:

As always — I favor a Systematic Approach for interpretation of every ECG I encounter (This Systematic Approach is reviewed in ECG Blog 205).

Rate & Rhythm: The rhythm is sinus at ~70/minute.
Intervals: The PR, QRS and QTc intervals all appear normal.
Axis: The frontal plane QRS axis is normal (close to zero degrees — as the QRS complex in lead aVF is nearly isoelectric).
Chamber Enlargement: None

PEARL #1: Did YOU note the relatively Low Voltage throughout this tracing? Although strict criteria for low voltage are not quite met in this tracing (ie, the QRS complex in all 6 limb leads is not ≤5 mm — because the R wave in lead I is taller than this). That said — 5 of the 6 limb leads satisfy this low voltage criterion — and all 6 chest leads are of small amplitude!

As we are about to contemplate the possibility of acute or recent infarction — it is helpful to be aware of potential causes associated with low voltage.
Relevant potential causes of Low Voltage to consider in today's case include the following: i) Pericardial effusion; ii) Takotsubo cardiomyopathy; and, iii) A large acute (or recent) infarction, that may result in myocardial "stunning" (See the above Audio Pearl and/or ECG Blog #262 for more on this subject).

Continuing My System — Regarding Q-R-S-T Changes:

Q Waves — Assessment is challenging because of the small amplitude of the beats in lead III, and especially in lead aVF. That said — a QS wave is seen in at least 2 of the 3 beats in lead III. It looks like an ever-so-tiny initial positive deflection (r wave) is present in the middle beat in this lead.
I find it even more difficult to assess lead aVF for the presence of Q waves — as QRS amplitude is tiny (no more than 2 mm) in this lead. What can be said about lead aVF — is that all 3 of the beats that we see in this lead are notched (ie, fragmented).

PEARL #2: The finding of an isolated QS complex in lead III and/or lead aVF is not diagnostic of previous inferior infarction.

Higher specificity for the occurrence of inferior infarction at some point in time is only obtained when Q waves of a "certain size" (ie, larger and/or wider than normal septal q waves) are seen in all 3 inferior leads (ie, leads III, aVF and also lead II).
That said, in my experience — the finding of an isoelectric or predominantly negative QRS complex that is fragmented in one or more inferior leads (as seen in lead aVF in Figure-1) — significantly increases the likelihood that inferior infarction occurred at some point in time.
In Figure-1 — there is no Q wave in lead II. As a result — the question of a QS complex in lead III by itself does not reliably predict inferior infarction at some point in time. However, in association with the tiny, notched (fragmented) complex in lead aVF — I'd suspect an inferior infarction may have occurred at some point. Whether this event began 3 days ago (at the time of symptom onset in today's patient) — or whether the inferior infarction is old and unrelated to the ST-T wave changes we are about to assess in the chest leads — can not be determined from this single ECG.

Continuing My System — Regarding R Wave Progression:

The zone of "Transition" — is said to occur where the height of the R wave becomes taller than the depth of the S wave in the chest leads. Transition is normally seen between lead V2-to-V4. Because of common usage — I've retained the term, "R wave progression" as part of my Systematic Approach to 12-lead interpretation — though defining the zone of "transition" provides us with more useful information (See ECG Blog #269 — for full review on R Wave Progression).

R Wave Progression: In Figure-1 — R wave progression is "poor", because transition is delayed to between lead V4-to V5.
Other than the QS complex in lead V1 — Q waves and/or QS complexes are not seen in other chest leads. That said — the delayed transition is relevant in today's case! This is because the reduced r wave amplitude in anterior leads, and small size of the R waves in leads V5 and V6 — may reflect loss of anterior forces from recent infarction.

Finally — Regarding ST-T Wave Changes:

ST-T wave abnormalities (some subtle — some not subtle) are seen in at least 9 of the 12 leads in today's tracing. For clarity — I've labeled some of these findings in Figure-2:

The most remarkable abnormal ST-T wave findings — are the hyperacute T waves in leads V2-thru-V6. It is challenging to define the term, "hyperacute" in reference to T wave appearance. My definition is that in the "right" clinical setting (ie, in a patient with cardiac-sounding chest pain) — 1 or more T waves take on a "hypervoluminous" appearance — in that they appear taller-than-expected given QRS amplitude in the lead being looked at — as well as being "fatter"-at-their-peak and wider-at-their-base than would normally be expected (See ECG Blog #218, as well as the Audio Pearl in that post for more on defining hyperacute T waves).
The 3 leads in Figure-2 in which T waves are most obviously "hyperacute" — are leads V3, V4 and V5. In each of these leads — T waves tower over the small-amplitude R waves. Not only are these T waves much taller than the R waves — but these T waves are clearly "fatter"-at-their-peak and wider-at-their-base than one would expect, given the size of the R waves (and QRS complex) in these respective leads.

PEARL #3: By the concept of "patterns of neighboring leads" — Since the ST-T waves in leads V3, V4 and V5 are so obviously abnormal — the somewhat less obvious ST-T wave changes in neighboring leads V2 and V6 are also most probably abnormal.

In lead V6 — although the T wave is not taller than the R wave — this T wave in lead V6 is still much taller-than-one-would-expect given small size of the R wave in this lead.
Height of the T wave in lead V2 is not as pronounced as T wave amplitude in lead V3. However, the ST segment "takeoff" is unusually straight (ie, parallel to the slanted RED line in lead V2 of Figure-2). In addition, considering how small the r wave is in lead V2 (ie, 2 mm) — the T wave in this lead is once again "hypervoluminous" (ie, clearly with a much-wider-than-it-should-be base). I would therefore interpret leads V2 and V6 as also being "hyperacute".
ST-T wave changes in lead V1 are subtle — but nevertheless "real". Normally in this lead — there is no more than minimal ST elevation. Although the T wave in lead V1 may normally be inverted (PURPLE arrow in Figure-2) — the shape of the ST segment in this lead (ie, coved or "frowny"-configuration, as schematically shown by the curved RED arc) — in association with the ST elevation seen (with respect to the dotted RED line in lead V1 — showing the PR segment baseline) is not a normal finding (especially given obvious ST-T wave abnormalities in the 5 other chest leads)!

Figure-2: I've labeled some of the abnormal ST-T wave changes from Figure-1.

Regarding ST-T wave Changes in the Limb Leads:

The ST-T waves in leads II, III and aVF are all clearly abnormal. ST segments in each of these inferior leads are "scooped", with suggestion of slight ST depression. That said — the most remarkable finding is the terminal T wave positivity in each of these 3 inferior leads (upward-pointing BLUE arrows in Figure-2 — with the most prominent terminally positive T wave being seen in lead II).
Depending on the clinical situation (and the stage of evolution during an acute cardiac event) — this finding of terminal T wave positivity in association with ST flattening or depression is clearly abnormal, and may represent the beginning reperfusion changes (ie, the mirror-image of inverting T waves in leads which manifested ST elevation).
Without the benefit of a prior (baseline) ECG for comparison — I was uncertain if the ST-T waves in leads I and aVL were abnormal. I thought the apearance of the QRST complex in lead aVR was unremarkable.

PEARL #4: When assessing an ECG for the possibility of acute ischemic heart disease — the more leads that are abnormal, the greater the chance that the abnormalities you identify are real! I find it helpful to start with a few leads that obviously show acutely abnormal ST-T wave findings — and then to apply the concept of "patterns of neighboring leads" as I look closely to identify more subtle findings in the remaining leads.

As described above in Figure-2 — We have identified definite ST-T wave abnormalities in no less than 9/12 leads. This provides strong support in favor of a recent (or still ongoing) cardiac event.

Putting It All Together:

The ECG in Figure-2 shows sinus rhythm — low voltage — a question about a QS in lead III (with a tiny, fragmented complex in lead aVF) — poor R wave progression (with low-amplitude R waves until leads V5, V6) — worrisome hyperacute T waves in leads V2-thru-V6 — with apparent reciprocal ST-T wave changes in the inferior leads (including terminal T wave positivity that probably represents upright reperfusion T waves).

Given the history of 3 days of symptoms in this older man who finally presented to the ED because of worsening chest pain — I interpreted this tracing as suggesting acute and/or ongoing extensive anterior infarction. Although none of the chest leads manifest J-point ST depression — the disproportionately large chest lead T waves are consistent with a deWinter-like T wave pattern (See ECG Blog #183 for "My Take" on this concept). That said — I wasn't certain about WHEN it was during the patient's 3 days of symptoms that acute infarction took place — or whether perhaps there was an ongoing "stuttering" course with spontaneous opening and closure.
The course of acute infarction is not always "all or none". By this I mean — that the "culprit artery" (most likely the proximal or mid-LAD in today's case) — may acutely occlude — then spontaneously reopen — followed by spontaneous reopening and reclosure a number of times until a final state is reached for the "culprit" artery.
Regardless of when during the patient's 3 days of symptoms acute coronary occlusion first occurred — the lack of anterior Q waves, in association wth marked hyperacute T wave changes in this patient who presented to the ED for increased symptoms — strongly suggests that there is still a large area of jeopardized myocardium that may benefit from prompt reperfusion. Cardiac cath was clearly indicated to define the anatomy and guide clinical decision-making.

Case CONCLUSION:

Cardiac cath was performed on the patient in today's case. Not surprisingly, this revealed total occlusion of the mid-LAD (Left Anterior Descending) coronary artery. Minor lesions were found in the LCx (Left Circumflex) and RCA (Right Coronary Artery).

This patient subsequently developed arrhythmias — that I discuss as this case is continued in my next ECG Blog #273.

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Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) for making me aware of this case and allowing me to use this tracing.

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ADDENDUM (1/25/2025):

What is Voltage Discordance?

On occasion there may be low voltage in the limb leads (ie, all QRS voltage in the limb leads ≤5 mm) — but normal QRS voltage in the chest leads. This is called, "Voltage Discordance" (Chinitz et al — J Electrocardiol 41(4):281-286, 2008).
Low voltage isolated to the limb leads will be associated with the same list of potential causes as I noted above under today's Audio Pearl — in only about 50% of cases.
In the remainder of cases of "Voltage Discordance" — the patient will have a dilated cardiomyopathy. Physiologic explanation for why this ECG phenomenon is seen is discussed in the PDF below (this PDF adapted from presentation by Ahmed ElBorae, MSc — 2022, from Cairo University).

NOTE: You may need to allow Cookies to see this embedded PDF below (This PDF should display on Safari and Chrome — but it may not display on Firefox.).