EXTRA COPY of ECG Blog #519 - LV "Strain" vs Acute MI? - EXTRA COPY

The ECG in Figure-1 was obtained from a patient who presented to the ED (Emergency Department) with typical CP (Chest Pain).

QUESTIONS:

• Given this brief history — How would you interpret this ECG?
• What is in your differential diagnosis?

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

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MY Thoughts on this CASE:

The history in this patient of presenting to the ED with typical CP is clearly worrisome — and immediately places this patient in a higher-risk group for having an acute cardiac event. The "burden of proof" is on us as providers to rule out an acute event — rather than the other way around (ie, We need to assume the abnormal findings on this ECG represent an acute MI until proven otherwise!).

• The rhythm in ECG #1 is sinus at ~80/minute. All intervals (PR,QRS,QTc) and the axis are normal.
• There are deep S waves in anterior leads V2 and V3. This may represent LVH (Left Ventricular Hypertrophy).
• The principal concern in this patient with CP are the tall T waves with ST elevation in these leads V2 and V3 — because when LVH is manifest on ECG by the presence of deep anterior S waves — then LV "strain" from LVH (and not from acute infarction) may be seen in these same anterior leads!

Consider the ECG that I show in Figure-2 — which is from ECG Blog #461:

• The BLUE arrows in Figure-2 clearly show significant ST elevation.

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Figure-2: Tracing from my ECG Blog #461 — in which anterior ST elevation was not because of acute MI, but instead the result of LV "strain" in a patient with marked LVH!

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Figure-3: I've labeled the initial ECG.

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Figure-4: Comparison between today's 2 ECGs.

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Tayfun Dilek Demir (12/26/2025 — FB Messenger)

LV "Strain" or Acute MI?

 

Hello, the first ECG showed hyperacute myocardial infarction (TMI), but PM Cardio couldn't detect it. The second ECG showed an anterior myocardial infarction image. We had already done the upload, so we are referring you for coronary angiography.

MY REPLY:

Hi. I may want to use this for an ECG Blog if you can give me a few more details and your cath results. Am I correct that this patient presented with CP (Chest Pain) — and that the 2nd ECG was done ~30 minutes after the 1st ECG? Do you know if his CP had increased at the time the 2nd ECG was done.

 

The 1st ECG is subtle — but I completely agree that in a patient with new CP, it is highly suspicious. I think te ST-T waves are "disproportionate" in V1,V2 and V3 (the S waves are fairly deep — but still the ST-T waves are taller than what I would expect given the QRS size.

 

In lead V4 — the ST segment is straightened — so I view this as a continuation of the hyperacute T waves in V1,2,3. And then the ST-T waves are flatter than they should be in V5,V6.

 

In the limb leads — there is ST-T wave flattening, but subtle ST dep i the inferior leads — and straightening of the ST segments in leads I and aVL — so yes, sublte BUT I completely agree, strongly suggestive of acute proximal LAD occlusion until proven otherwise. Given the ST flattening in V5,V6 — I would not be surprised if the patient had multivessel disease.

 

And then ECG #2 is completely obvious ...

Let me know what happens! GOOD recognition by you! 

 

TAYFUN:

The patient presented with typical chest pain. We didn't like the ECG results, so we administered oxygen loading and morphine, but the patient didn't feel better. We took a second ECG in 10-20 minutes. Seeing the ECG, we started high-dose nitrates and sent the patient home without inducing ventricular fibrillation. I will obtain the angiography report, sir. Asa clexane loading.

 

MY REPLY:

Tayfun — What do you mean above when you say, "Seeing the ECG, we started high-dose nitrates and sent the patient home without inducing ventricular fibrillation?" Thanks for the follow-up!

 

TAYFUN:

I apologize, there was a translation error We started nitrates immediately when we saw the significant ST elevation in the second ECG. We sent him to a higher-level center that performs coronary angiography

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Acknowledgment: My appreciation to Tayfun Anil Demir (from Antalya, Turkey) for the case and this tracing.

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ECG Blog #461

https://ecg-interpretation.blogspot.com/2024/12/ecg-blog-461-stemi-lv-aneurysm-or.html

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I was sent the ECG shown in Figure-1 — initially without the benefit of any history.

• How would you interpret this tracing?
•    — What is YOUR differential diagnosis of this tracing?

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

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The Obvious Concern:

• I immediately realized the reason that I was sent this tracing: ==> there is ST elevation in the anterior chest leads!

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MY Initial Thoughts on Figure-1:

Looking systematically:

• There is a regular sinus rhythm at ~85/minute (upright P waves in lead II — with a constant and normal PR interval).
• The QRS is narrow (ie, not more than 1/2 a large box in duration).
• The QTc is at most borderline prolonged.
• The Axis is markedly leftward, as per a predominantly negative QRS complex in lead aVF. Criteria for LAHB (Left Anterior HemiBlock) are fulfilled — given the predominantly negative QRS in lead II (ie, indicating a frontal plane axis more negative than -30 degrees).

Regarding Chamber Enlargement:

• Criteria for atrial enlargement are absent (Reviewed in ECG Blog #75). So, although there is a negative component to the terminal P wave in lead V1 — I favor undercalling LAA because of limited specificity for this amount of P wave negativity in V1 as an indication of LAA.
• That said — voltage for LVH is markedly increased!

There is marked LVH:

• I've reviewed criteria for LVH on many occasions (See ADDENDUM below — for review of LVH criteria that I favor — as well as ECG Blog #73 for full discussion).
• As per Figure-5 (in the Addendum below) — S wave amplitude is markedly increased in today's ECG (attaining an S wave depth = 28 mm in lead V2 — and an S wave depth = 28 mm in lead V4 — as shown in Figure-2).
• 
  
• PEARL #1: Sometimes with LVH — instead of seeing tall R waves with LV "Strain" in the lateral chest leads — we see the "mirror-image" opposite picture in right-sided leads V1,V2 (ie, LVH may be manifested by deep anterior S waves — with ST elevation in leads V1,V2 and/or V3). This is precisely what we see in today's case!

Figure-2: Assessment of R wave and S wave amplitude in the chest leads is rendered difficult by marked overlap of complexes in several leads. To facilitate assessment — I've colored in selected R waves and S waves.

Completing our Systematic Approach (with Q-R-S-T Changes):

• Q Waves — There is a tiny septal q wave in lead aVL — which is unlikely to be important. But there are large QS waves in anterior leads V1,V2,V3.
• R Wave Progression — Because of these large QS waves in the anterior leads, there is poor R wave progression (with Transition delayed until between leads V5-to-V6).
• ST-T Waves — I've drawn in the PR segment baseline in leads V1,V2,V3 of today's ECG to highlight the amount of ST elevation (RED arrows in Figure-3 indicating the J-point as the marker for judging the amont of ST elevation).
• Elsewhere, the 3 inferior leads and lead V6 show nonspecific ST-T wave flattening. Finally, lateral leads I and aVL show subtle, shallow T wave inversion — which is consistent with a "strain equivalent" pattern (as I highlight in Panel B of Figure-6 in today's Addendum).

Figure-3: I've labeled the PR segment baseline and J-points in selected chest leads to highlight the amount of ST elevation.

Putting It All Together:

Today's ECG shows a sinus rhythm at ~85/minute — a borderline QTc — LAHB — marked LVH — and — QS waves in leads V1,V2,V3, with no more than a tiny r wave in lead V4 — plus, ST elevation that begins in lead V1 and extends through to lead V5. Clinically — this may indicate any of the following (See Figure-4):

• i) Antero-Septal MI may have occurred at some point in time — as suggesed by QS waves in leads V1,V2,V3.
• 
  
• ii) That there is marked LVH is strongly suggested by the greatly increased chest lead QRS amplitudes (with S waves = 28 mm in leads V2 and V4 — as shown in Figure-4) — with a "strain equivalent" pattern in lateral leads I and aVL (BLUE arrows in these leads).
• The anterior lead ST elevation may simply reflect LV "strain" in a patient with marked LVH, which when manifest by deep anterior S waves (rather than tall lateral R waves) — may produce a vector in which the hypertrophied, posterior-lying left ventricle opposes normal anterior forces, thereby reducing (and sometimes eliminating) anterior r waves.
• PEARL #2: As shown within the RED insert in Figure-4 — In such cases, the ST-T wave changes of LV "strain" (that are usually seen in lateral leads) — may present a mirror-image opposite ST-T wave picture of "strain" in anterior leads. This may account for the anterior ST elevation seen in today's case (BLUE arrows in leads V1,V2,V3).
• 
  
• iii) There could be acute LAD (Left Anterior Descending) coronary Occlusion that is now superimposed on the ECG of a patient with longstanding LVH, perhaps with also previous anterior infarction.
• 
  
• iv) The findings in Figure-4 could reflect LV aneurysm.

Conclusion: As I contemplated today's tracing that I initially interpreted without the benefit of any history — I thought any of the above diagnostic possibilities might be present. Although I suspected that the ECG findings in Figure-4 were not acute — I was not at all certain of that suspicion from this single ECG.

• Clearly — a detailed history would be needed for adequate clinical assessment. Does this patient have a history of cardiac disease? Did the patient have CP? (Chest Pain). If so — When did the CP begin? Was CP still present at the time that the ECG in Figure-4 was taken?
• Can we find a previous ECG on this patient (looking to determine if the QS waves and ST elevation is new or old).
• Especially if CP was ongoing — a repeat ECG is needed (looking for signs of acute evolution) — in addition to Troponins, Echo and further assessment until we can determine if an acute process is in progress. 

Figure-4: I've labeled KEY findings in today's ECG.

CASE Follow-Up:

I later learned the history in today's case — which was that a middle-aged man with diabetes and hypertension — who presented to the ED (Emergency Department) for abdominal pain that had awakened him from sleep.

• The patient was markedly hypertensive in the ED — but he did not have CP.
• Chest X-Ray was normal. 
• Troponins were negative.
• Echo showed significant LVH with normal LV function and no wall motion abnormality.
• Radionuclide scan was negative for ischemia.
• Previous ECGs were found in the patient's chart — which showed similar findings of marked LVH with anterior ST elevation attributed to LV "strain".
• 
  
• In Summary: The patient's abdominal pain was treated. An acute cardiac event was ruled out. Cardiac cath was not done.

"Take Home" Message: Anterior lead ST elevation does not necessarily indicate acute infarction when the patient has LVH that is manifest by deep anterior S waves. In such cases — the anterior ST elevation may simply reflect LV "strain" (as per the "Mirror Test" that is shown within the RED insert in Figure-4).

• Further evaluation may be needed in such cases to clarify what may be "new" vs "old" (ie, To rule out a new acute event that could be superimposed on longstanding LVH).
• KEY Point: Anterior ST elevation is unlikely to represent LV "strain" if anterior S waves are not larger than is usually expected (ie, if there is no LVH). 

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Acknowledgment: My appreciation for the anonymous submission of today's case.

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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 #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
• ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.
• ECG Blog #424 — Another example of when marked LVH may manifest anterior ST elevation.
•  
• For cases similar to today, in which LVH may mimic ischemia — Check out My Comment at the bottom of the page of the following posts in Dr. Smith's ECG Blog — the November 29, 2023 post — June 20, 2020 — March 31, 2019 — March 29, 2019 — and the December 27, 2018 post.
• 
  
• ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
• ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 

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ADDENDUM (12/21/2024): I've added below in Figure-5 and Figure-6 additional material to facilitate ECG diagnosis of LVH and LV "strain".

 

Figure-5: The voltage and other criteria I favor for ECG diagnosis of LVH (Please see ECG Blog #73 for additional details).

Figure-6: Illustration and description of LV “strain” and a “strain equivalent” pattern (See text).

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ECG Blog #380 - Precordial "Swirl"

ECG Blog #380 — What is "Swirl"?

https://ecg-interpretation.blogspot.com/2023/05/ecg-380-what-is-swirl-metodo.html

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The ECG in Figure-1 — was obtained from an older woman with persistent CP (Chest Pain) over the previous day. Her symptoms lessened after Nitroglycerin — so the decision was made not to activate the cath lab. Do YOU agree with this decision?

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

MY Thoughts on the ECG in Figure-1:

In a patient with CP that had been persistent over the previous day (until Nitroglycerin was given) — the initial ECG shown in Figure-1 is extremely worrisome. 

• The rhythm is sinus. Intervals (PR, QRS and the QTc) and the frontal plane axis are normal.
• Voltage for LVH is satisfied — at least by Peguero Criteria (Sum of deepest S in any chest lead + S in V4 ≥23 mm in a woman — as discussed in ECG Blog #73).

Regarding Q-R-S-T Wave Changes: 

• Q Waves — None are seen. 
• R Wave Progression — Transition (where the R wave becomes taller than the S wave is deep) is slightly delayed, occurring between leads V4-to-V5. That said — R wave amplitude is of reasonable size in all anterior leads (with slight reduction in R wave size from V2-to-V3 probably the result of lead placement).

The most significant abnormalities relate to ST-T Wave Changes:

• In the Limb Leads — There is nonspecific ST-T wave flattening, with slight ST depression in multiple leads (ie, in leads I,II,III,aVF).
• In the Chest Leads — Assessment for ST elevation in the anterior leads is especially challenging in ECG #1. This is because there is normally a small amount of upward-sloping ST elevation in leads V2 and V3. That said — in a patient with CP, the amount of ST elevation in leads V2 and V3 looks excessive to me, in association with ST-T waves that look potentially hyperacute. Thus, despite satisfying voltage criteria for LVH — considering the depth of the S waves in leads V2,V3 — the ST-T waves in these leads still look a little bit taller, fatter-at-their-peak and wider-at-their-base than I would expect them to be.
• Support that the ST-T waves in leads V2,V3 are likely to be abnormal — is forthcoming from the appearance of the ST-T wave in lead V1. In the absence of a deep S wave in lead V1 — it is uncommon to see ST elevation in this lead. It is simply not normal to see a full 1 mm of ST elevation in lead V1 (as we do in Figure-1) — especially in view of the ST segment straightening that is present in this lead.
• 
  
• PEARL #1: The above noted findings in leads V1,V2,V3 are subtle! It is for this reason that I'll emphasize that the one lead in ECG #1 that indisputably manifests an abnormal ST-T wave is lead V6. In a patient with new and persistent CP — it is never normal to see the amount of flat ST depression that is present in lead V6. Abnormal ST segment flattening and depression is also seen in neighboring lead V5, but not nearly as marked as in lead V6. 
• KEY Point: It is the fact that I know the flat ST depression in lead V6 is abnormal in a patient with persistent CP — that tells me the ST-T waves in leads V1,2,3 also have to be assumed abnormal until proven otherwise!

BOTTOM Line: The patient in today's case is an older woman who presents with a 1-day history of new and persistent CP. Her initial ECG should be interpreted as highly suggestive of acute proximal LAD occlusion until proven otherwise.

• NEW Concept: In a patient with CP — the ECG findings of anterior lead ST elevation, in association with lateral chest lead ST depression — is consistent with the pattern of Precordial "Swirl" (that I discuss below).

Continuation of Today's CASE:

A prior ECG on today's patient (done ~5 years earlier) was found — and is shown in comparison with the initial ECG in Figure-2. 

• Does this previous tracing strengthen our impression about this patient's initial ECG? 

Figure-2: Comparison of the initial ECG in today's case — with a prior ECG done ~5 years earlier. What do we learn from reviewing this previous ECG?

Comparison of ECG #1 and ECG #2:

IF there was any doubt about whether the ECG findings in today's tracing (ie, in ECG #1) are acute — it should have vanished the moment the prior ECG in Figure-2 was found!

• NOTE: It's important to correlate ongoing circumstances at the time that a prior tracing was done (ie, Was the patient stable and asymptomatic — or were they having chest pain, an exacerbation of heart failure, or some other ongoing process at the time the prior ECG was recorded?). This point is particularly relevant regarding ECG #2 — because sinus tachycardia is seen on this earlier ECG. In addition — there were more prominent anteroseptal forces on this earlier tracing (ie, in the form of an R wave = S wave in lead V1, with similar-looking equiphasic QRS complexes in leads V2-thru-V5).
• The above said — there previously was no indication of any ST elevation, or of any potentially hyperacute ST-T waves in the anterior leads of ECG #2 — nor was the distinct, flat ST depression in lead V6 present in this prior ECG! These differences between the 2 tracings in Figure-1 strongly support our suspicion that the ST-T wave changes in ECG #1 have to be interpreted as acute until proven otherwise!

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What is Precordial Swirl?

In the October 15, 2022 post of Dr. Smith's ECG Blog — Drs. Smith and Meyers introduce the colorfully descriptive term known as Precordial Swirl — as an intriguing ECG sign that facilitates recognition of a unique ECG pattern strongly suggestive of a very proximal site of acute LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia, in addition to anterior wall and apical involvement.

PEARL #2: In the setting of acute LAD OMI (Occlusion-based MI ) — the pattern of Precordial Swirl is recognized by the finding of ST elevation in leads V1 and aVR — and — reciprocal ST depression in leads V5 and V6.

• When considering Precordial Swirl — I like to focus on the ST-T wave appearance in leads V1 and V6.
• Although 1-2 mm of upsloping ST elevation is commonly (and normally) seen in anterior leads V2 and V3 — most of the time we do not see ST elevation in lead V1 (or if we do — it is minimal!). Therefore — I become immediately suspicious of "Precordial Swirl" whenever there is suggestion of LAD OMI — and — in addition, lead V1 looks different than expected!
• 
  
• NOTE: Sometimes recognition that lead V1 looks "different-than-expected" — is only forthcoming after realizing that lead V2 is clearly abnormal.

In Figure-3 — I've selected 6 sets of V1,V2 leads from the series of tracings shown by Drs. Smith and Meyers in their October 15, 2022 post on Precordial Swirl.

• Although admittedly subtle — the ST segment coving with slight but disproportionate ST elevation in lead V1 of A, B and C in Figure-3 is clearly an abnormal appearance for the ST segment in lead V1. In association with neighboring chest leads suggestive of acute LAD OMI — this picture should raise suspicion of Precordial Swirl.
• Example F in Figure-3 is more subtle — because the S wave in lead V1 is deeper. That said — this coved shape of ST elevation in lead V1 of F should still raise suspicion in a patient with new symptoms.
• The ST-T wave segment in lead V1 of example D — closely resembles the "shape" of LV strain in an anterior lead from a patient with LVH. However, the S wave in example D — is not at all deep in either lead V1 or V2 — which in a patient with chest pain should strongly suggest the possibility of Precordial Swirl.
• The ST-T wave shape in lead V1 of example E also appears to be subtly abnormal. Support that this finding is real — is forthcoming from our impression that the T wave in neighboring lead V2 looks more peaked than expected — which in a patient with new symptoms, should strengthen our suspicion of a disproportionately positive T wave in lead V1.

Figure-3: Selected sets of V1,V2 leads from the examples of Precordial Swirl provided in the October 15, 2022 post in Dr. Smith's ECG Blog.

NOTE: It's EASY to get fooled by LVH! This is because LV "strain" with LVH is sometimes more manifest in anterior rather than lateral chest leads — in which case there may be anterior lead ST elevation (ie, the reciprocal of lateral lead ST-T wave depression). The history and associated deep anterior S waves (ie, the reciprocal of tall lateral lead R waves) will suggest LVH rather than Precordial Swirl (See ECG Blog #254 and My Comment at the bottom of the page in the February 6, 2020 and June 20, 2020 posts in Dr. Smith's ECG Blog).

• For additional examples that illustrate this concept of "proportionality" (regarding relative size of ST-T wave deviations compared to QRS amplitude in the respective lead) — Check out the additional examples of LVH that mimic Precordial Swirl which are provided in the October 15, 2022 post in Dr. Smith's ECG Blog.

Precordial Swirl Appearance in Lead V6:

The final component for diagnosing Precordial Swirl — is to see reciprocal ST depression at least in lead V6 (if not also in lead V5):

• Once I've decided that the tracing I am looking at is not an example of LVH that mimics Precordial Swirl — I focus my attention on the shape of the ST-T wave in lead V6.
• 
  
• I've reviewed my approach to the ECG diagnosis of LVH often (See ECG Blog #245 — among many other posts). In Figure-4 — I've reproduced from the above cited June 20, 2020 post my schematic illustration of the ST-T wave appearance that may be seen in one or more lateral leads for demonstrating LV "strain".

PEARL #3: In general, the shape of ST-T wave depression in lead V6 with Precordial Swirl does not look like either C or D in Figure-4. Instead — the depressed ST segment tends to be flatter. Therefore — THINK Precordial Swirl in a patient with new symptoms IF you see: 

• Other signs suggestive of acute LAD OMI.
• The ST-T wave in lead V1 looking "different-than-expected". 
• A relatively flattened appearance to the depressed ST segment in at least lead V6 (if not also in lead V5).

Figure-4: Schematic illustration and description of LV "strain" on ECG.

CASE Follow-Up:

Cardiac cath was performed on today's patient — and complete proximal LAD occlusion was found.

• In Figure-5 — I compare the post-PCI ECG with the initial tracing in today's case.

FINAL QUESTION:

• How would YOU interpret the post-PCI tracing? 
• Based on the ECGs in Figure-5 — Did PCI succeed in opening the "culprit" artery?

Figure-5: Comparison of the initial ECG in today's case — with a post-PCI tracing. Was PCI successful?

Interpretation of the Post-PCI ECG:

There is significant baseline artifact in the limb leads of ECG #3. Despite this artifact — this tracing is still interpretable.

• The frontal plane axis in both of the ECGs in Figure-5 is similar — which means that lead-to-lead comparison will be valid. There are no acute changes in Limb Lead ST-T wave appearance.

In contrast — the Chest Leads show that there has been marked evolution of this patient’s anterior MI:

• There has been significant loss of anterior R wave forces in ECG #3 since the initial ECG. Specifically — the R wave in lead V2 is now smaller — with further loss of R wave from V2-to-V3 — and disappearance of the initial R wave in lead V4 (to form a QS complex in this lead). This loss of anterior forces is consistent with myocardial injury from the large infarction.
• 
  
• PEARL #4: Note change (deepening) of the S waves in leads V3,V4 of ECG #3. This is not indicative of LVH — but instead results from the loss of anterior forces, that now leaves posterior forces “unopposed” (with resultant deeper anterior S waves). 
• KEY POINT: It’s good to be aware that QRS amplitudes may undergo hard-to-predict amplitude changes over the course of acute MI evolution.

Chest Leads also show marked changes in ST-T wave appearance:

• Compared to ECG #1 — there is clearly more ST elevation in leads V2,V3 of ECG #3 — with new ST elevation now present in lead V4. 
• That said — an even more striking change in ST-T wave appearance — is the very steep decline of the descending limb of the T wave in leads V2,V3,V4!
• 
  
• PEARL #5: It's important to appreciate that although this steep T wave decline appearance looks like the anterior T waves seen in Wellens' Syndrome — this is not Wellens' Syndrome, because infarction has already taken place (whereas Wellens' Syndrome occurs in the absence of CP — and serves as an ECG warning sign that appears before a large infarction with QS waves has taken place — as discussed in ECG Blog #254).
• 
  
• Finally — The ST-T wave appearance in leads V5,V6 of the post-PCI tracing ( = ECG #3) — is very different than it was in the initial ECG. Instead of ST segment flattening and depression (that was seen in ECG #1 ) — there is now ST segment coving in lead V5 (a continuation of the ST coving seen in neighboring lead V4, albeit without any ST elevation) — and, there is no longer ST depression in lead V6.

PEARL #6: One of the KEY learning points of today’s case — is the importance of correlating ECG findings with the clinical situation. The more serial tracings recorded (and the better the notation of whether each serial tracing was associated with chest pain — and if so, relative severity of that CP) — the easier it becomes to correlate clinical events.

• For example — We would not normally expect to see more ST elevation after PCI (as we do in ECG #3) — unless reperfusion of the "culprit" artery with the procedure was not successful — or — unless additional ECGs done prior to PCI showed additional ST elevation occurred before angioplasty opened the occluded vessel. In today's case — presumably this latter possibility is what occurred — in which case (assuming no CP after PCI) — the steep T wave descent with deepening T wave inversion in the anterior chest leads of ECG #3 presumably reflects coronary reperfusion. 

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Acknowledgment: My appreciation to Kim Jiwon (from Seoul, Korea) 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 #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 the importance of the term, "OMI" ( = Occlusion-based MI) as an improvement from the outdated STEMI paradigm.
• ECG Blog #367 — for another example of acute LCx OMI. 
• 
  
• ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
• ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.
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• ECG Blog #260 and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamic" ST-T wave changes.
• ECG Blog #230 — How to compare serial ECGs. 
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• ECG Blog #254 — What Wellens' Syndrome is and is not ...
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• ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...
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• ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #80 — reviews prediction of the "culprit" artery (with another case to illustrate the Mirror Test for diagnosis of acute Posterior MI).
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• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post). 
• ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.
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• ECG Blog #350 — regarding T Wave Imbalance in the Chest Leads.
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• ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).
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• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
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• The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.
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• 20 Cases of Precordial Swirl (or "Look-Alikes" ) — Reviewed in the October 15, 2022 post of Dr. Smith's ECG Blog (including My Comment at the bottom of the page).

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ADDENDUM (5/24/2023):

Josep Serra Tarragon wrote me asking whether inverted U waves were present in the lateral chest leads of ECG #1. On taking another look — I have to agree with him that they are! (BLUE arrows in leads V4,V5,V6 — in Figure-6).

• There are 2 QRS complexes in simultaneously-recorded leads V4,V5,V6, in which we see the ST-T wave. I do not see inverted U waves clearly in the first QRS complex — but BLUE arrows that I have drawn into Figure-6 are certainly consistent with inverted U waves for the 2nd QRS complex.
• Inverted U waves are an uncommon, usually ignored phenomenon. That said — when present in the right clinical situation, they are an indicator of significant ischemia (Correale et al — Clin. Cardiol 27:674-677, 2004).
• Attention to negative U waves was first pointed out to me by Dr. Barney Marriott in the mid 1980s. Thereafter — I looked for negative U waves over a period of many years, but very rarely found them. Much of the time, there was simply too much "noise" on the tracing to be certain of their presence — or the heart rate was such that it was difficult to distinguish what was "real" inverted U wave vs terminal ST-T wave, baseline movement, or the next P wave. 
• The mechanism for U wave inversion remains uncertain. Best theory is delayed repolarization of the His-Purkinje system.
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• Bottom Line: The clinical setting in this Blog #380 is certainly consistent with ischemia. I believe Dr. Tarragon is correct that this is highlighted by the BLUE arrows in Figure-6.
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• My THANKS to Dr. Tarragon for pointing this out! 

Figure-6: I've added BLUE arrows to leads V4,V5,V6 of ECG #1 — to indicate inverted U waves.