ECG Blog #487 — A "Normal" ECG?

I was given the ECG in Figure-1 — knowing only that the patient was a woman with "CP" (Chest Pain). Many of my colleagues interpreted this tracing as "normal".

• QUESTION: Do you agree? Explain your answer.

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

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MY Initial Thoughts on Today's Tracing:

On seeing the ECG in Figure-1 — I instantly knew that this tracing was not "normal". Instead, given the history of new CP — my instinct was that providers should activate the cath lab!

• Why do I say this?

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Looking Closer at ECG #1:

The rhythm for the ECG in Figure-1 — is sinus (despite the baseline artifact — We see upright P waves in lead II, with definite P waves showing a constant and normal PR interval in other leads).

• My "eye" was immediately drawn to lead V3 (within the RED rectangle in Figure-2). Normally, there should be slight, gently upsloping ST elevation in leads V2 and V3. Instead, there is obvious ST segment straightening, with slight shelf-like ST segment depression in this lead V3, that finishes with terminal positivity.

PEARL #1: In a patient with new CP — the ECG "picture" of the ST-T wave that we see in lead V3 indicates acute posterior OMI until proven otherwise.

• This is the concept of pattern recognition. Similar to entities such as a Brugada pattern ECG, which the experienced "eye" should recognize within 2 seconds on seeing (as in ECG Blog #244) — the ECG "picture" within the RED rectangle in Figure-2 in a patient with new CP should prompt the diagnosis of acute posterior OMI until proven otherwise.
• To assist with "engraving" the ECG picture of acute posterior OMI in one's memory — use of the "Mirror" Test may be helpful (See ECG Blog #317).
• 
  
• NOTE: Before deciding that the cath lab needs activation — I seek confirmation of my initial impression in other leads.

Figure-2: I've labeled today's initial ECG.

Confirmation of Posterior OMI from Other Leads:

My 2 favored ways for solidifying my initial impression of acute posterior OMI (with need to immediately activate the cath lab) are based on: 

• i) Awareness that with posterior OMI — ST depression in the chest leads tends to be maximal in lead V2 and/or lead V3 and/or lead V4; — and, 
• ii) Awareness that there is usually a common blood supply to the inferior and posterior walls of the left ventricle. As a result, if there is posterior OMI — then we'll often see limb lead evidence of either acute inferior OMI (if the "culprit" artery is the RCA) — or — of acute high-lateral OMI (if the "culprit" artery is a branch of the LCx).

Looking Closely in Figure-2 for posterior OMI confirmation:

• Support that there is an ongoing posterior OMI is forthcoming in Figure-2 — from similar ST segment straightening and depression with prominent terminal T wave positivity in leads V4 and V5, but not in lead V6 (as seen within the BLUE rectangle).
• PEARL #2: Unfortunately — leads V1 and V2 have almost certainly been placed too high on the chest because: i) There is an rSr' complex in lead V2, which is usually not seen as an isolated finding, especially in the absence of an rSr' in lead V1; — ii) There is significant terminal negativity of the P wave in lead V1; — and, iii) The QRST complex in leads V1 and V2 looks similar to the QRST in lead aVR (See ECG Blog #274 — for more on quick recognition of V1,V2 misplacement).
• The importance of quickly recognizing lead V1,V2 misplacement — is that this invalidates our diagnostic use of these leads for confirming posterior OMI (ie, lead V2 especially should show similar ST segment flattening and depression as we see in lead V3 when there is posterior OMI). 
• Clinically: IF the diagnosis of acute posterior OMI was in doubt — I would immediately repeat the ECG on seeing the picture of leads V1,V2 that is present in Figure-2 (within the GREY dotted rectangle). That said — I don't feel that is necessary in today's case, since the ECG in Figure-2 is so clearly diagnostic of acute posterior OMI.

There is further support of posterior OMI from the limb leads:

• Although limb lead findings in Figure-2 are more subtle — they are nevertheless diagnostic. Despite the baseline artifact — we see: i) ST segment straightening in each of the inferior leads (BLUE arrows in leads II,III,aVF), with a hint of ST depression in III and aVF — and with prominent terminal T wave positivity in leads II and aVF; — and, ii) Straightening and slight elevation of the ST segment takeoff in high-lateral leads I and aVL.
• To Emphasize: In the absence of the chest lead findings that we see in Figure-2 — I would be less cerain about acute posterior OMI from the subtle ECG findings that I see in the limb leads. But given the history of new CP and the absolutely diagnostic findings of posterior OMI within the RED and BLUE rectangles of Figure-2 — I interpreted the overall ECG pattern in today's initial ECG as diagnostic of acute infero-lateral OMI.

PEARL #3: What about lead V6?

• At this point in our interpretation — We can go back and take another look at lead V6. As opposed to the chest leads V3,V4,V5 which all showed ST segment straightening with slight ST depression — lead V6 lacks this ST segment straightening. Instead —  Doesn't the T wave in this lead look a bit "bulkier" than would usually be expected?
• Whereas I would probably not interpret the ST-T wave in lead V6 as abnormal if it was an isolated finding — in the context of our overall findings suggesting acute postero-lateral OMI — I interpreted the slight "bulkiness" of the ST-T wave in lead V6 as a hyperacute finding in further support of lateral OMI.

PEARL #4: It should be apparent from the above description of my "process" — that optimal clinical interpretation of ECGs is like "telling a story". The story makes sense when multiple pieces of the story "fit". 

• In today's "story" — 3/12 pieces are diagnostic ( = leads V3,V4,V5 — that in today's patient with new CP, so strongly suggest acute posterior OMI). 
• 6/12 additional pieces ( = leads I,II,III; aVL,aVF; V6) although much more subtle — do support the hypothesis of the first 3 pieces. 
• Of the remaining 3/12 pieces — 2 of them are invalid ( = leads V1,V2 — which are placed too high on the chest). 
• Isn't it difficult to negate our hypothesis when 9 of the 10 available leads to us all point to the same hypothesis?

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Putting It All Together:

In today's patient with new CP — the ECG picture of acute postero-lateral OMI usually suggests acute occlusion of a branch in the LCx (Left Circumflex) as the "culprit" artery.

• CASE Follow-Up: Cardiac cath revealed complete occlusion of the distal OM (Obtuse Marginal) branch of the LCx. Peak Troponin attained a value over 22,000 ng/mL.

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An ECG was obtained after PCI (Figure-3).

• How does the post-PCI ECG in Figure-3 — compare to today's initial tracing?

Figure-3: Comparison of today's initial ECG — with the repeat ECG that was recorded after PCI.

The Post-PCI ECG:

Lead-to-lead comparison in Figure-3 of today's initial ECG with the post-PCI tracing — shows obvious improvement (deflation of ST-T wave findings) in each of the 9 leads that I highlight above as supportive of my diagnosis of acute postero-lateral OMI.

• PEARL #5: The BEST way to hone your ECG interpretation skills for picking up the subtle findings that I highlight in today's case — is to follow the course of serial ECGs correlated to the course of events. Seeing the improvement after PCI in each of the 9 highlighted leads confirms the validity of the subtle abnormalities pointed out in Figure-1.
• NOTE: Leads V1,V2 remain suggestive of too high electrode lead placement (not uncommon with female patients).

Final Learning Point: To emphasize that while STEMI criteria never came close to being satisfied — 9/10 of the leads available to us in this patient with new CP decisively told us the answer within seconds of seeing the initial ECG.

• To delay prompt cath waiting for ST segments to rise or Troponins to come back would only serve to diminish the chance to save viable myocardium.

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Acknowledgment: My appreciation to David Didlake (USA) for allowing me to use this case and these tracings.

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ADDENDUM (7/11/2025):

• For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-6: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
• In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
• 
  
• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.

• As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
• BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
• The Clinical Reality: Many acute coronary occlusions never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.

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ECG Blog #486 — Unusual Coupling

The ECG in Figure-1 is from a middle-aged man — who presented to the ED (Emergency Department) with on-and-off CP (Chest Pain). The patient was hemodynamically stable at the time this ECG was recorded.

QUESTIONS:

• How would you interpret this ECG in Figure-1?
•    — What is the rhythm?
•       — Would you activate the cath lab?

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 Initial Thoughts on Today’s CASE:

This is a challenging case — in that both the rhythm and the 12-lead tracing manifest complexities, which are important to resolve in time-efficient fashion in this patient who presents to the ED with new CP.

• In time-sensitive cases such as this one — I favor beginning my interpretation with a quick look at the long-lead rhythm strip (ie, that appears at the bottom of Figure-1). 
• To Emphasize: Precise interpretation of the rhythm is not initially needed. But it is helpful to establish if the underlying rhythm is sinus — and to determine if any initial management measures might be needed for the rhythm.
• After this quick look at the rhythm (and after verifying that the patient is hemodynamically stable) — I focus my attention on a quick survey of the 12-lead (ie, In today’s patient who presents with new CP — we want to determine as rapidly as possible IF prompt cath, thrombolytics or other emergency treatment measures are needed).
• NOTE: Although I describe my initial thoughts in "slow motion" — in most cases, the total time I spend for my initial Survey of the rhythm and 12-lead — should be less than 1 minute (and often less than 30 seconds).

The Cardiac Rhythm in Today’s Tracing:

The underlying rhythm in today’s tracing, as seen in the long lead II rhythm strip — is sinus (RED arrows in Figure-2 that highlight upright P waves in this lead).

• There are frequent PVCs ( = beats #3,5; 8,10; 13,15; and 18) — but no repetitive PVC forms are seen (ie, There is never more than 1 PVC in a row).
• NOTE: There is more to see in today’s rhythm — but since this patient is hemodynamically stable, we do not need to assess any more than the above for our initial Survey of the rhythm (that should have taken no more than seconds to complete).

Figure-2: I've labeled sinus P waves with RED arrows. 

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The 12-Lead ECG:

At this point — I turn my attention to the 12-lead ECG. Given today’s clinical presentation (ie, New CP in a middle-aged man — who manifests sinus rhythm with frequent uniform PVCs) — our principal task with initial Survey of the 12-lead ECG is to determine if prompt cath is needed.

• PEARL #1: Given the frequent PVCs — we need to focus our attention on ST-T wave appearance in the sinus-conducted beats ( = beats #2,4,6; 7,9,11; 12,14,16; and 17 — in Figure-3).
• My attention is immediately drawn to the 3 leads within the RED rectangle in Figure-3 ( = leads V2,V3,V4). Note that ST depression is maximal for sinus-conducted beats in these 3 leads — compared to ST depression seen in other chest leads (large BLUE arrows in leads V2,V3,V4).
• PEARL #2: In a patient with new CP — the finding of ST depression that is maximal in leads V2 and/or V3 and/or V4 indicates acute posterior OMI until proven otherwise!
• PEARL #3: Although it is always more difficult to assess the clinical significance of ST depression in PVCs — there are times in which the morphology of ST depression in PVCs is clearly abormal. I thought this was the case for the PVCs within the RED rectangle in Figure-3 ( = beats #13, 15, 18) — which show even more ST depression than is seen for sinus beats #11,12,14,16,17.
• PEARL #4: Because of a common blood supply — acute posterior OMI is often associated with acute inferior MI. And although there is no ST elevation in the inferior leads in Figure-3 — there is straightening of the ST segment takeoff in leads II,III,aVF (angled BLUE lines above the ST segments in these leads). There is also reciprocal ST depression seen in lead aVL (BLUE arrow in this lead) — such that these subtle hyperacute signs of acute inferior OMI serve to confirm my impression of the marked ST depression that immediately caught my "eye" in the chest leads (within the RED rectangle).
• 
  
• BOTTOM Line: Within less than 1 minute — I knew this middle-aged man with new CP and frequent PVCs — was evolving an acute infero-postero OMI — for which prompt activation of the cath lab was clearly indicated!

Figure-3: My attention was immediatey drawn to the maximal ST depression in sinus-conducted beats within the RED rectangle (BLUE arrows in leads V2,V3,V4). 

PEARL #5: Note that there is ST segment flattening, but no more than minimal ST depression of sinus-conducted beats in lead V1 of Figure-3. Given how much ST depression we see for sinus-conducted beats in neighboring leads V2,V3,V4 — the most logical explanation for not seeing more ST depression in lead V1 (that typically also manifests ST depression with posterior OMI) — is that there is associated acute RV involvment (RV MI often manifests ST elevation in right-sided lead V1 — which will attenuate any ST depression that otherwise would have been seen in lead V1 from posterior OMI).

• Clinically — It's important to be aware of acute RV MI because of its different hemodynamics (See ECG Blog #190 — for more on ECG diagnosis and clinical implications of acute RV MI).
• The way to confirm if acute RV MI is (or is not) present — is to obtain right-sided leads (which will show ST elevation in leads V2R,V3R,V4R).
• Anatomically — detection of acute RV MI localizes the "culprit" artery to the proximal RCA (Right Coronary Artery) — since the LCx does not supply the RV.

PEARL #6: Taking another "overview look" at ST-T wave morphology for sinus-conducted beats in Figure-3 — there are ST-T wave abnormalities in virtually all leads in this tracing. As a result, in addition to a proximal RCA "culprit" artery that I'd predict on cardiac cath — I would not be surprised if the patient also had significant underlying multi-vessel coronary disease.

• To Emphasize: Specific findings on cardiac cath will be interesting to learn — but are not needed for my rapid initial Survey decision-making — that as described above, should allow recognition of the need for prompt cath with PCI in this patient with new CP, frequent PVCs — and clear evidence of acute infero-postero OMI.

CASE Follow-Up:

Cardiac catheterization was performed in timely fashion. It revealed proximal RCA occlusion.

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Beyond-the-Core: The fascinating aspect of today's case for me — relates to the coupling intervals for the PVCs that we see in ECG #1.

• Because of our focus on treatment — We often ignore consideration of the mechanisms of cardiac arrhythmias. But awareness of these mechanisms (that although there is overlap, tend to fall within the 3 categories of increased automaticity — reentry — and "triggered" activity) — will at times provide important insight for optimal treatment selection. (Please check out my ADDENDUM below — in which I've excerpted the brilliant brief review of these concepts from Dr. S Venkatesan's website on Expressions in Cardiology — Nov. 2, 2020).
• As per Dr. Venkatesan — the usual mechanism for most ischemic VT rhythms is increased automaticity (especially when the ECG shows a polymorphic morphology with variable coupling intervals). This is in contrast to scar-related and idiopathic VT rhythms, that tend to circulate through the ventricles over a constant path, because they originate from a well defined site (ie, scar) — or in the case of idiopathic VTs (fascicular VT; RVOT VT) — from a specific anatomic location. It follows that QRS morphology will usually be monomorphic — the coupling interval tends to be constant (a result of the repeating re-entry pathway) — and there is generally less chance of deteriorating to VFib. 
• As a result, I find it helpful to look at coupling intervals (ie, the distance from sinus QRS complexes to the onset of the PVC) — with awareness that deterioration to VFib seems to be less common with isolated, monomorphic PVCs that manifest fixed coupling intervals (Hamon et al — Circulation: Arrhythm & Electrophysiol 10(4):XXX, 2017) — and — deVries et al — J Interv Card Electrophysiol 51(1):25-33, 2018).
• With the exception of parasystole (an uncommon independent focus ventricular arrhythmia that is often benign) — many (most) uniform PVCs that I see manifest fairly fixed coupling.
• Today's ECG is an exception ...  

Wenckebach Coupling?

The frequent PVCs that we see in ECG #1 in today's case are monomorphic (similar QRS morphology in each of the 12 leads for beats #3,5; 8,10; 13,15; and 18 — with the exception of minor differences due to artifact).

• As shown below in Figure-4 — a pattern of group beating is seen for these PVCs (repetition of this pattern showing 2 PVCs within each 5-beat grouping for beats #2-thru-6; 7-thru-11; and 12-thru-16).
• As shown by the colored double-arrows — the coupling interval increases within each group (YELLOW double-arrow — to PINK double arrow) — until there is a pause without any PVC (ie, within the R-R intervals between beats #6-to-7; 11-to-12; and 16-to-17) — after which the cycle (with the next YELLOW double arrow) begins again. 
• This timing of group beating with PVCs in today's tracing — to me suggests that the reentry cycle for coupling intervals of these PVCs manifests Wenckebach periodicity (Hansom et al — Curr Cardiol Rev 17(1):10-16, 2021). I have not previously observed this phenomenon of Wenckebach timing for PVC coupling intervals.
• My Theory: Whereas fixed coupling (reentry mechanism) of PVCs tends to be associated with somewhat lesser risk of deterioration to VFib — the obvious acute ischemia in today's ECG predisposes to other arrhythmia mechanisms (increased automaticity; "triggered" activity) which manifest here in the form of Wenckebach periodicity for PVC coupling intervals. The concern is potentially higher risk from these PVCs (therefore, all the more reason in today's case for prompt cath with PCI reperfusion).

Figure-4: I've highlighted what appears to be PVC coupling with Wenckebach periodicity!

Today's final Beyond-the-Core Concept: Did YOU Notice the increase in PR intervals for sinus-conducted beats within the 5-beat groupings in today's long-lead II rhythm strip?

• I illustrate this finding in Figure-5 — in which I focus solely on the long lead II rhythm strip. Baseline artifact in the 1st grouping (for beats #2-thru-6) renders assessment of this phenomenon difficult. But an increase in the PR interval of conducted beats is evident in the last 2 groupings (this increase in PR interval being highlighted as we move from the RED — to PINK — to YELLOW arrows in these last 2 groups).
• As per the laddergram illustration in ECG Blog #68 — this increase in PR interval for the next sinus-conducted beat that occurs after a PVC is not the result of Wenckebach. Instead, it reflects the phenomenon of "concealed" conduction — in which retrograde conduction from the preceding PVC, while not enough to block forward conduction of the next sinus beat — is enough to slightly prolong the ensuing PR interval.
• The term "concealed" is used, because we cannot explain this effect on the ensuing PR interval from what is seen on the actual ECG — but instead must infer there is retrograde conduction from the PVC that impedes forward conduction of the next sinus impulse.

Figure-5: The reaon for the increasing PR intervals (PINK and YELLOW arrow P waves) — is the result of "concealed" conduction from the preceding PVCs.

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Acknowledgment: My appreciation to Narveen Sharma (from India) for the case and this tracing.

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ADDENDUM #1 (7/5/2025):

• Review on basic mechanisms of cardiac arrhythmias:

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Figure-6: Mechanisms of Arrhythmias- Part 1 (from Dr. S Venkatesan's website on Expressions in Cardiology — Nov. 2, 2020).

Figure-7: Mechanisms of Arrhythmias- Part 2 (from Dr. S Venkatesan's website on Expressions in Cardiology — Nov. 2, 2020).

Figure-8: What is "Triggered Activity" with respect to arrhythmia mechanisms? (from AI Internet Summary- 2025).

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ADDENDUM #2 (7/5/2025):

• For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-9: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
• In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
• 
  
• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.

• As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
• 
  
• BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
• The Clinical Reality: Many acute coronary occlusions never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.

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ECG Blog #485 — 30 Minutes Later

Today's patient is a previously healthy middle-aged man who reported a brief episode of CP (Chest Pain) while walking, relieved by rest — followed a day later by recurrence of CP, that now was occurring at rest.

• Additional details about the timing and duration of this patient's CP — as well as the relative severity of his CP at the time the ECG in Figure-1 was recorded — are uncertain.
• Initial hs-Troponin was negative. 

QUESTIONS:

• In view of this history — How would you interpret ECG #1?

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

MY Initial Thoughts:

A history of new CP that is severe enough to prompt a visit to the ED (Emergency Department) — is always of concern. That said — it's hard to draw conclusions as to the likelihood of an acute event from the history we are given. That said:

• The initial ECG is not normal.
• The rhythm is sinus at ~90/minute. All intervals and the axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves — absent (There is a small initial positive deflection = an r wave in lead III).
• R Wave Progression — probably appropriate (although the finding of an initial R wave that is taller in lead V2 than in V3 suggests that there may be some anatomic misplacement of these 2 electrode leads).

Regarding ST-T Wave Changes — This is concerning! (See Figure-2):

• In this patient with a history of new CP — I interpreted the ST-T wave in lead V2 as hyperacute until proven otherwise (ie, disproportionately enlarged with respect to modest size of the QRS in this V2 lead).
• In the context of new CP + a hyperacute ST-T wave in lead V2 — I interpreted neighboring lead V3 as also hyperacute (ie, "fatter"-at-its-peak and wider-at-its-base than expected, given modest size of the QRS in this V3 lead).
• PEARL #1: In cases like this — I begin my interpretation by looking for the 1 or 2 leads which I know are clearly abnormal (that being leads V2 and V3, which are clearly hyperacute!). My "threshold" for interpreting other leads in this tracing as abnormal is then lowered, especially for neighboring leads (in this case — for leads V1 and V4!).
• PEARL #2: In a patient who shows no sign of LVH on ECG — the slight-but-real ST elevation with surprisingly tall positive T wave in lead V1 is definitely abnormal! Given new CP + hyperacute T waves now in leads V1,V2,V3 (with this ST elevation beginning in lead V1) — this suggests a proximal LAD "culprit" until proven otherwise.
• PEARL #3: The final "neighboring lead" — is lead V4. If I were to see lead V4 in isolation — I might not necessarily call it "abnormal". BUT — in the context of new CP + hyperacute T waves in leads V1,V2,V3 — I interpreted neighboring lead V4 as also hyperacute (the base of this T wave being wider-than-what-I'd-expect for a normal ST-T wave).
• KEY Point: I find it helpful to always try to tell a "story" when interpreting an ECG. As a result, given the clinical history of new CP + hyperacute T waves in leads V1,V2,V3 — my "threshold" for assessing neighboring lead V4 needs to be lowered. Considering this context — I interpreted the wider-than-expected T wave base that we see in lead V4 as abnormal (ie, making for a 4th consecutive hyperacute T wave from lead V1-thru-to-lead V4).
• PEARL #4: Given the above context — the ST segment straightening and slight-but-real ST depression that we see in lead V6 of Figure-2 is real! This most probably represents Precordial "Swirl" (ie, hyperacute anterior lead ST-T waves with ST elevation beginning in lead V1 + ST depression in lead V6 — as discussed in detail in ECG Blog #380).
• Finally — subtle-but-definitely-present ST segment flattening with slight J-point ST depression is also seen in lead V5. I suspect the reason this lead V5 finding is so subtle — is that this is a "transition lead" that falls in between the hyperacute ST-T waves from leads V1-thru-V4 and the ST depression we see in lead V6.

QUESTION:

What about the limb leads in Figure-2? 

• Take another LOOK at ECG #1. Do YOU see any abnormalities in any of the limb leads that support my suspected diagnosis of proximal LAD OMI?

Figure-2: I've labeled today's initial ECG.

ANSWER:

In the absence of a history of new CP and the above-described ST-T wave findings that we see in the chest leads of ECG #1 — I would probably have called the ST-T wave findings that we see in the limb leads of this tracing "nonspecific". BUT — in the context of today's case — there are definitely abnormal ST-T wave findings in a number of limb leads:

• The most remarkable finding in Figure-2 is in lead aVF. Although the QRS complex is tiny in this lead — there should be no doubt that the ST segment is abnormally flat. There is also subtle-but-real terminal T wave positivity in this lead aVF.
• To a lesser extent — similar ST segment flattening with terminal T wave positivity is also seen in the other 2 inferior leads ( = leads II and III).
• To Emphasize: In isolation — I would have called these inferior lead ST-T wave findings "nonspecific". But in the context of clearly abnormal chest lead findings — these reciprocal ST-T wave changes in the inferior leads support the likelihood of ongoing acute proximal LAD occlusion.
• PEARL #5: Once you identify one or two definitely abnormal leads in a patient with new CP (such as leads V2 and V3) — the more additional leads that manifest abnormal ST-T wave findings — the more this supports the premise of acute OMI. In Figure-2 — at least 9/12 leads manifest an abnormal ST-T wave appearance.

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The CASE Continues:

The initial Troponin in today's case was negative. The decision was made not to activate the cath lab on the basis of the above history, the negative initial Troponin — and the initial ECG shown in Figure-1.

• Over a period of the next ~30 minutes — the patient's CP resolved. At this time — a repeat ECG was obtained (shown below in Figure-3).
• The initial cardiologist contacted did not feel cardiac cath was indicated at this time because: i) Chest lead ST-T wave abnormalities were no longer present in ECG #2; — ii) The patient's CP had resolved; and, iii) The initial Troponin was negative.

QUESTIONS:

• Do YOU agree with the rationale provided by this initial cardiologist for not proceeding with cardiac catheterization?
• How can you explain resolution of the abnormal ST-T wave findings that were seen on the initial ECG?

Figure-3: The repeat ECG — obtained ~30 minutes after ECG #1.

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ANSWERS:

The rationale provided above by the initial cardiologist consulted as the reason not to pursue prompt cath in today's case — highlights a series of KEY points and misconceptions.

• As reviewed by sources noted in the ADDENDUM below — the pathophysiology of acute OMI evolution often includes a period of spontaneous reperfusion that is independent of any treatment measures. This period of spontaneous reperfusion may sometimes only be transient — before spontaneous reocclusion occurs. 
• IF clinicians carefully correlate the presence (and relative severity) of CP with the timing of each serial ECG — we can usually figure out when spontaneous reperfusion has occurred because: i) This is most often accompanied by reduction (if not complete resolution) of CP; and, ii) Acute ECG changes (ie, ST elevation and depression) decrease, if not normalize on the way to developing the typical pattern of reperfusion T waves (ie, T wave inversion in leads that previously showed ST elevation). All the treating clinician(s) need to do — is correlate the presence (and relative severity) of CP symptoms with serial ECGs. Doing so often renders the diagnosis of acute OMI obvious.

Correlating the above concepts to the repeat ECG:

• PEARL #6: To facilitate interpretation of the repeat ECG in today's case ( = ECG #2) — I've placed it next to ECG #1 in Figure-4. The clinical reality is that unless the 2 ECGs you are comparing are reviewed side-by-side — that subtle differences between the 2 tracings will be missed.
• The principal differences between ECG #1 and ECG #2 — are seen in the chest leads. The hyperacute T waves previously seen in the anterior leads have almost completely resolved — with this dramatic improvement in the ECG picture occurring within 30 minutes after ECG #1 was recorded, in association with resolution of CP!
• 
  
• PEARL #7: The near complete resolution of hyperacute ST-T wave changes that we see in Figure-4, corresponding to complete resolution of CP: i) Constitutes a "dynamic" ECG change — which provides further support in favor of an acutely evolving cardiac event; and, ii) Strongly suggests that the "culprit" artery was acutely occluded when the patient had CP (ie, at the time ECG #1 was recorded) — but that the culprit artery has now spontaneously opened in association with this dynamic ST-T wave improvement seen at the same time the patient's CP resolves.
• The "good news" — is that the "culprit" artery is now open.
• The "less good news" — is that what spontaneously opens — may at any time spontaneously reclose unless prompt cath with PCI is performed to ensure that the culprit artery remains open.
• 
  
• PEARL #8: The fact that the initial Troponin in today's case was negative did not rule out an acute event (as was assumed by the initial cardiologist on the case). More than 25% of patients with an acute STEMI have an initial hs-Troponin value ( = high-sensitivity Troponin) below the threshold for acute infarction (Wereski et al — JAMA Cardiology 5(11):1302, 2020).
• The reason an initial Troponin value may be negative despite an ongoing acute infarction — will in large part depend on the duration of time that the "culprit" artery is occluded. If the culprit artery is only briefly occluded (before spontaneous reperfusion occurs) — then serum Troponin might not rise!
• On occasion — the first and the second hs-Troponin may remain within the normal range despite documented infarction. This is because there may be an ongoing cycle of acute coronary occlusion — followed by spontaneous reperfusion — then spontaenous reocclusion — back-and-forth between culprit vessel closure and spontaneous reopening — until a final state of the culprit artery is reached.
• 
  
• KEY PEARL #9: It is precisely because of this potential back-and-forth cycling between spontaneous culprit artery reperfusion and reocclusion — that careful attention to the timing and duration of symptoms, correlated to each serial ECG is so important. For example — IF the initial ECG in today's case had been obtained 30 minutes later than it was (ie, at the time ECG #2 was done) — then providers would have seen a patient whose CP had totally resolved, with an ECG showing no more than minimal nonspecific changes.
• Knowing that your patient's history of symptoms has been stuttering (ie, off-and-on) should prepare YOU to appreciate that a negative initial Troponin and minimal ECG abnormality — might simply reflect spontaneous reperfusion of an acute ongoing infarction. BOTTOM Line: More than 1 Troponin and more than a single ECG may be needed to arrive at the correct diagnosis!

Figure-4: Comparison between today's initial ECG — and the repeat ECG recorded ~30 minutes later (after resolution of CP). Unfortunately artifact precludes interpretation of lead V6 in ECG #2.

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Today's CASE Concludes:

Fortunately — today's patient was transferred to a second hospital, where another cardiologist was consulted.

• This 2nd cardiologist did proceed with cardiac catheterization — which revealed 99% occlusion of the LAD, that was stented.

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

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ADDENDUM (6/27/2025):

• For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).

Figure-5: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs.

• In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
• In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
• 
  
• Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).

P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.

• As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
• BUT — because the cath lab was activated within 1 hour of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
• The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
• The Clinical Reality: Many acute coronary occlusions never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases.

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